A system of practical medicine. By American authors. Vol. 2 (part 7 of 8)

A system of practical medicine. By American authors. Vol. 2 (part 7 of 8)

In cases of dropsy of the gall-bladder there are no febrile symptoms, no chills, and the tenderness when present is limited to the pyriform body, the seat of the accumulation of fluid, and no general enlargement of the liver can be made out. At the point of swelling fluctuation may be detected, or if the gall-bladder is filled with calculi the sensation imparted to the touch is that of a hard, nodular body of an area and position corresponding to that of the gall-bladder. Tapping the gall-bladder, an easy and safe procedure, will resolve all doubts. When an impaction of a gall-stone is the cause of abscess, the clinical history is eminently characteristic: there are attacks of hepatic colic, after one of which the chills, fever, and sweats belonging to hepatic abscess occur.

The differentiation of cancer of the liver from abscess rests on the following considerations: In cancer there is slow enlargement, with pain; a more or less nodular state of the organ without fluctuation; usually ascites; no rigors; no fever and sweats. In abscess the liver may or may not be enlarged; there are rigors, fever, and sweating, and the surface of the organ, so far as it can be reached, is smooth and elastic, and it may be fluctuating. Cancer happens in persons after middle life, develops very slowly, and is accompanied by a peculiar cachexia; abscess occurs at any period, very often succeeds to or is accompanied by dysentery and by the usual phenomena of suppuration.

It is extremely difficult to separate an abscess in the abdominal wall, in the right hypochondrium, or a tumor in this region, from an abscess of the liver. The history of the case, the existence of a dysentery or of an apparent intermittent or remittent fever before the appearance of a purulent collection, will indicate the liver as the probable source of the trouble. Attention has already been called to a case in which an abscess of the liver was supposed by an eminent surgeon to be a tumor of the abdominal wall. The history in this case of an obstinate remittent fever, followed by the appearance of a tumor of the hypochondrium and by a preliminary discharge at the umbilicus, clearly indicated the nature of the trouble. In the absence of any history of the case it is extremely difficult to fix the origin of a suppurating tumor originating, apparently, in the depth of the right hypochondrium.

Mistakes are frequently made in the case of an abscess developing in {1020} the convexity of the right lobe of the liver and pushing the diaphragm up to the third, even to the second, rib, and thus producing conditions identical with empyema of the right thorax. Such instances of hepatic abscess are peculiarly difficult of recognition, because, the physical signs being the same as those of empyema, the differentiation must rest on the clinical history. In cases of empyema proper the effusion in the chest is preceded by pain and accompanied by an increasing difficulty of breathing; in hepatic abscess there are, as a rule, symptoms of disturbance in the hepatic functions, fluctuation in the hepatic region, dysentery, etc., long anterior to any disturbance in the thoracic organs. Again, empyema may be a latent affection, without any symptom except some obscure pain and a progressive increase in the difficulty of breathing; on the other hand, abscess of the liver is preceded by symptoms of liver disease and of associated maladies. A dry, purposeless cough is present in many cases of abscess; a painful cough with bloody expectoration occurs when preparation is making for discharge through the lungs.

Errors of diagnosis are liable to occur in the consideration of symptoms unquestionably hepatic in origin. Thus, the intermittent fever accompanying some cases of hepatic colic, like the shivering fits and fever which occur in cases of nephro-lithiasis, may be confounded with the septicæmic fever of hepatic abscess. An attentive examination of the attendant circumstances, especially a careful survey of the right hypochondrium, can alone determine the nature of the symptoms. In all doubtful cases the experimentum crucis of puncture with the exploring-needle becomes a measure of necessity. When all diagnostic indications are at fault, the needle of the aspirator may decide the issue. An abundant experience has shown that a needle of suitable size may be introduced into the right lobe without any ill result--often, indeed, with distinctly good effects when there is no suppuration or when pus cannot be detected. In the present state of our knowledge it cannot be determined why puncture of the organ should be beneficial in cases having the symptomatic type of hepatic abscess when none exists; but of this fact there is no doubt.

TREATMENT.--As the formation of pus is coincident with or causative of the first symptoms, it is obvious that treatment directed to prevent an abscess can rarely succeed. Yet it is probable that now and then an abscess just forming has been arrested and healing effected. At the onset of symptoms some large doses of quinine, with a little morphine (scruple j of the former and 1/8 gr. of the latter), every four or six hours, may have a decided curative effect. During the course of the septicæmic fever, with its chills and febrile exacerbations, quinine in full doses and alcohol according to the conditions present are necessary remedies. As the symptoms develop saline laxatives are useful until the formation of pus becomes evident, when all perturbating treatment of the intestinal canal should cease. If dysentery be present when the hepatic symptoms arise, it should be cured as promptly as possible; and of all remedies for this purpose, ipecac given in the usual antidysenteric quantity offers the best prospect of relief. For the dysentery which succeeds to abscess, and is probably, in part at least, dependent on portal obstruction, the mineral astringents, as copper sulphate, are the most effective remedies. As far as practicable, after an abscess has formed the intestinal canal should be kept quiet, for any considerable disturbance will {1021} endanger the escape of pus into the peritoneal cavity. Persistent vomiting is very significant of pressure by an enlarging abscess in the stomach, and usually signifies an abscess associated with impacted calculus. It is important in such cases to maintain, as far as can be done, a quiescent condition of the stomach, for the purpose of preventing rupture into the peritoneal cavity and to favor the nutrition which is seriously endangered by the repeated vomiting. Effervescent soda powders are very useful; carbolic acid in solution, or creasote-water with or without bismuth, is beneficial; champagne, very dry and highly effervescent, has been, in the writer's hands, remarkably efficient. As food becomes a most important need in such cases, milk and lime-water, wine-whey, egg-nog, and similar aliments must be given in small doses and frequently. Nutrient enemata, prepared from eggs, milk, and beef-juice, with the materials for digestion--acid and pepsin--may be made to supplement the stomach, but such efforts have a very limited utility, owing to the state of the hepatic functions and to the obstruction of the portal circuit. In all cases it is necessary to maintain the strength by suitable aliment and the judicious use of stimulants. The long-continued and profuse suppuration makes an enormous demand on the vital resources of the patient, and this must be compensated by suitable food-supplies.

As the formation of pus has taken place in most cases when symptoms have begun, the question of highest importance is, Shall the pus be evacuated? The statistical evidence relating to this question becomes then an extremely valuable guide. As in almost all cases of puncture of the liver for the evacuation of an abscess some part of the liver substance must be passed through, it is necessary to note how far this can be done without inflicting permanent injury on the organ. Hammond has punctured the liver in eight cases without the presence of an abscess, and of these not one has presented any unfavorable symptom. The author has punctured the liver, penetrating well into the interior, in two cases in which no abscess was discovered, but the symptoms of hepatitis existed, with the effect to improve the symptoms. In Condon's[113] collection of 11 cases there were 8 of abscess evacuated by the trocar, and 3 of acute hepatitis in which abscess had not formed, but in which the puncture procured the most decided amelioration of the symptoms. We have heretofore referred to Hammond's experience in the puncture of the liver in cases of hypochondriasis, this condition appearing to depend in some instances on the presence of abscess. In a number of instances abscesses did exist, but in many others there was no apparent lesion of the liver, but in these cases the puncture of the organ was without any ill result. Testimony to the same effect is given by Ramirez,[114] who asserts that he had not known a single instance in which any ill result followed puncture of the liver. It may therefore be regarded as certain that exploratory puncture of the organ for the purpose of diagnosis as well as for treatment can at any time be performed with suitable precautions in respect to the size, condition, and character of the instrument.

[Footnote 113: "On the Use of the Aspirator in Hepatic Abscess," Dr. E. H. Condon, The Lancet (London), August, 1877.]

[Footnote 114: Du Traitement des Abcès du Foie, Observations recueilles à Mexico et en Espagne, par Lino Ramirez, M.D., Paris, 1867, p. 65.]

The authorities of most experience are agreed that, provided with the {1022} aspirator, the abscess may be punctured as soon as a purulent collection can be ascertained to exist. The obvious reason for tapping the abscess is its tendency to extend in various directions, destroying the hepatic substance. In those examples confined by a limiting membrane, after a time of inactivity ulceration begins, and the pus seeks an outlet in some direction. The early evacuation by a suitable aspirator becomes then a measure of the highest necessity. The good effects of puncture with even such a crude instrument as the trocar is well exhibited in the statistics collected by Waring.[115] In a collection of 81 cases opened by the knife or trocar there were 66 deaths, making the percentage of recoveries 18.5. In these cases the operative procedure was a final measure, and the mischief had been done almost if not quite in its entirety. The statistics of Waring are concerned with a period anterior to 1850. Although they demonstrate the value of the trocar and evacuation of the abscess, as compared with the results of the natural course of the disease, the far greater success of the treatment by the aspirator is shown by the statistics of recent times. Thus in McConnell's[116] 14 cases, also of India, in which the aspirator was used to empty the sac, 8 recovered and 6 died. The statistics of Waring may also be profitably compared with those of Condon,[117] in which, of 8 cases of abscess evacuated by the aspirator, 4 recovered, or 50 per cent. They may also be compared with Sach's[118] cases, 21 in number, of which 8 recovered, or 38 per cent., and with the cases of De Castro[119] of Alexandria, who reports 22 large abscesses operated on, the proportion of cures being 31.8 per 100, and 10 small abscesses, the proportion of cures being 70 per 100. In a case seen in consultation with Collins, in this city, last year, the aspirator was used by us about three months after the symptoms of abscess declared themselves. About a quart of bloody pus was drawn off at once, the opening sealed, and no subsequent accumulation occurred, the patient entirely recovering, for after a year he was seen (December, 1884) in complete health. From these data we draw the important conclusion that early operation is desirable. This fact may be formulated in the expression: In all cases of hepatic abscess use the aspirator whenever the presence of pus is made out. When the abscess is large, and especially when communication is established with the parietes of the abdomen, a free opening, followed by the insertion of a drainage-tube, is the proper method to pursue. If the pus reaccumulates, it is good practice to inject the cavity with tincture or compound solution of iodine after the pus is drawn off, provided the dimensions of the abscess are not too great.

[Footnote 115: An Inquiry into the Statistics of Abscess of the Liver, loc. cit.]

[Footnote 116: "Remarks on Pneumatic Aspiration, with Cases of Abscess of the Liver treated by this Method," Indian Annals of Medical Science, July, 1872, quoted.]

[Footnote 117: Lancet, supra.]

[Footnote 118: Ueber die Hepatitis der heissen Länder, etc., von Dr. Sachs in Cairo.]

[Footnote 119: Des Abcès du Foie des Pays chauds, et de leur Traitement chirurgical, par le Docteur S. V. de Castro (d'Alexandrie d'Egypte), Paris, 1870, p. 59.]

As regards the mode of proceeding, the following are useful rules: Ascertain, if possible, the existence of fluctuation; locate the point where the walls of the abscess are thinnest; insert an exploring-needle, and if the dépôt of pus is reached substitute a trocar having a sufficient calibre to evacuate the contents of the abscess; observe antiseptic precautions in respect to each detail of the operative procedure, and after the removal of the canula or needle, if a drainage-tube is not necessary, close the {1023} wound antiseptically. If drainage is necessary, keep the cavity empty and use proper solutions to prevent septic decomposition. When an abscess of the liver is pointing, the best place to puncture is where the abscess is most prominent and it walls thinnest, but if the accumulation of pus is encysted and there is no attempt at effecting an exit, the exploring-needle should be passed into the interior of the right lobe, the most usual site of suppuration. If pus be reached, a larger trocar may be inserted to evacuate the cavity thoroughly. Repeated insertion of the needle-trocar is preferable when the abscess is small, but when the accumulation is large and sufficiently firm attachments to the abdominal parietes exist, a drainage-tube will be necessary.

In what direction soever discharge of an abscess may take place, the general indications are to support the powers of life by food and stimulants. The utmost quietude should be maintained. It is useful, by the application of a firm flannel bandage, to keep the liver in its proper position and maintain it there. When pointing of an abscess occurs, a large flaxseed poultice is a soothing and a mechanically supporting application.

Acute Yellow Atrophy.

DEFINITION.--By the term acute yellow atrophy is meant an acute affection of the liver, characterized by rapid wasting or degeneration of the organ, accompanied by the systemic symptoms belonging to an acute acholia or cholæmia. It is an acute, diffused inflammation, with atrophy of the proper gland-elements. It has been called icterus gravis, malignant icterus, hemorrhagic icterus, malignant jaundice, etc.

HISTORY.--Cases having a more or less exact resemblance to acute yellow atrophy have been occasionally reported from the earliest period. Amongst English physicians, Bright[120] was one of the first to give an accurate account of the clinical history of some well-defined cases. Rokitansky[121] was really the first to define the disease from the pathological standpoint, and it was he who designated it acute yellow atrophy, this term being intended to signify the nature of the objective changes. The first treatise ever published on the disease as a distinct morbid entity was the monograph of Horaezek,[122] which appeared in 1843. Amongst the French, Ozonam in 1847 was the first to recognize and describe the disease as a distinct affection, although Andral[123] had several years before mentioned an affection of the liver which corresponded in some of its features to this affection. In 1862, Wagner[124] asserted that many of the cases of acute yellow atrophy were only examples of acute phosphorus-poisoning, and that no real distinction exists between the two affections. This statement has been warmly disputed by various German observers, but there is no doubt a close resemblance between the two affections.

[Footnote 120: Guy's Hospital Reports, 1836, vol. i. p. 621.]

[Footnote 121: Handbook of Pathological Anatomy, Am. ed.]

[Footnote 122: Quoted by Legg, On the Bile, Jaundice, and Bilious Diseases, loc. cit.]

[Footnote 123: Clinique médicale, 1839, tome ii. p. 363.]

[Footnote 124: Archiv der Heilkunde, 1862, p. 364.]

CAUSES.--There can be no doubt that acute yellow atrophy is a very rare disease, since so few examples are found post-mortem. In the course of a very large experience in autopsical examinations I have met with but {1024} one characteristic example.[125] According to Legg, it is "one of the rarest diseases known to man."

[Footnote 125: General Field Hospital, December, 1863.]

Several theories have been proposed to explain the occurrence of this affection, but without success. It has been ascribed to an excess in the production of bile, to stasis in the bile, and to a sudden saturation of the hepatic cells with biliary matters contained in the portal vein. That these supposed causes are really influential in producing the malady can hardly be entertained. That there is a peculiar poison which has a causative relation to the disease is rendered probable by the fact that a condition closely allied to this disease is produced by phosphorus, antimony, arsenic, and other poisons. Is it not a ptomaine generated under unknown conditions in the intestine? Especially does the morbid anatomy of phosphorus-poisoning nearly agree in all its details with icterus gravis--so nearly that by many German authorities they are held to be identical.

Age has a certain influence in the causation of this disease. It is rarely seen in early life, Lebert in a collection of 63 cases having found only 2 before ten years of age, yet there has been a well-marked case at three, and Hilton Fagge reports one at two and a half years of age. Nevertheless, much the largest number occur between fifteen and twenty-five years of age, and the maximum age may be fixed at sixty.

The influence of sex in the pathogeny is most remarkable. It is true in Lebert's collection of 72 cases there were 44 men and 28 women, but it is now known that he did not properly discriminate in his selection of supposed examples of the disease. The statistics of all other observers are opposed to those of Lebert. Thus, in Frerichs' collection of 31 cases, carefully sifted to eliminate error, there were 22 women and 9 men. Legg has also collected 100 cases of acute yellow atrophy, and of these 69 were women or girls. The most active period of life--from twenty to thirty years of age--is the usual period for the appearance of this disease. More than one-half of Lebert's cases occurred between fifteen and twenty-five; and of Frerichs', two-thirds happened between twenty and thirty years of age. In Legg's collection of 100 cases, 76 were between fifteen and thirty-five years of age. What is the condition of women at this period in life which renders them so susceptible to this malady? There can be no doubt that pregnancy is the great factor. Of 69 cases especially interrogated on this point, examined into by Legg, in 25 pregnancy was ascertained to exist. In Frerichs' collection one-half were women in the condition of pregnancy. The period of pregnancy at which the disease appears varies from the fourth to the ninth month, the greatest number occurring at the sixth month. So long ago as 1848, Virchow drew attention to the remarkable changes in the liver due to pregnancy. Sinety[126] has studied the effect of lactation on the liver, and has ascertained the existence of fatty degeneration. There is a form of jaundice which accompanies menstruation, as shown by Senator,[127] Hirschberg, and others. These facts indicate a certain relationship between the sexual system of the female and the liver, but they do not indicate the nature of the connection, if any exist, between this condition and acute yellow atrophy.

[Footnote 126: De l'État du Foie chez les Femelles en Lactation, Paris, 1873 (pamphlet).]

[Footnote 127: Berliner klinische Wochenschrift, 1872, p. 615, "Ueber Menstruelle Gelbsucht."]

The influence of depressing emotions has been supposed to be effective {1025} in producing this disease, but it is more than doubtful if such a relationship exists. Lebert, however, refers 13 of his cases to this cause, but Legg, who bases his statements on the study of 100 carefully-recorded cases, is sceptical regarding the effect of such influences. Syphilis has in some instances appeared to be the principal, if not the only, pathogenetic factor, and Legg[128] compares the action of the virus of syphilis to the effect of phosphorus, mercury, etc.

[Footnote 128: On the Bile, Jaundice, and Bilious Diseases, loc. cit.]

PATHOLOGICAL ANATOMY.--The anatomical changes occurring in this disease indicate the existence of a systemic condition: the lesions are not limited to the liver, but involve various other organs. The changes in the liver should be first described, since the name of the disease is derived from the alterations in this organ. As the name indicates, the lesions are atrophic, but not all examples show this. In some cases there is little change in the size of the organ; in others the wasting is extreme; certainly in all typical examples the liver is reduced in size. The variations in size observed are probably due to the stage at which the inspection is made: if early, the organ may not be reduced in size, may be even somewhat enlarged by the deposition of new material; if later, the atrophic changes will be more or less pronounced. When the atrophy has taken place, the size of the liver is reduced to one-half, even to one-third, of its original dimensions; it is then soft, almost like pulp, and cannot maintain its shape, but flattens out on the table. The capsule is much wrinkled and the color of the organ is yellowish, variegated by islets of reddish or brownish-red color, these spots being somewhat depressed below the general surface and having a firm texture. On section the boundaries of the lobules are either lost or have become very indistinct, the line of section being bloodless. The knife with which the sections are made becomes greasy. In some instances ecchymoses are discovered under the capsule, and rarely hemorrhagic extravasations in the substance of the liver. The bile-ducts are found intact, as a rule. The greatest change in the size of the liver is observed in the left lobe. The duration of the disease, as has been indicated above, has a marked influence over the size and condition of the liver. The atrophic shrinking of the liver occurs more decidedly after the ninth day. In general, the tissue of the liver is soft and pulpy in consistence. On microscopic examination the most important alterations are seen to have occurred in the hepatic cells; ultimately, these cells disappear, being replaced by fatty and connective-tissue detritus; but before this stage is reached important alterations have taken place in the form and structure of these bodies: the cells become granular and fatty, and lose their sharpness and regularity of contour, especially at the periphery of the lobule, but ultimately all the cells within the lobule undergo atrophic degeneration. In this atrophic degeneration of the hepatic cells, in their fatty degeneration, and ultimately entire disappearance, consist the real proofs of the disease. The red islets of tissue already alluded to consist of the fatty detritus mixed with crystals of hæmatoidin.

More or less increase of the connective tissue is noted in many of the cases--increase of connective tissue with numerous young cells formed around the vessels and the bile-ducts (Waldeyer[129]). The changes in the {1026} liver would surely be incomplete without some references to the minute organisms which play so important a part in modern pathology. Waldeyer was the first to demonstrate the presence of bacteria in the pigment-remains of the hepatic cells. Other observers have been unable to detect them, so that at present the parasitic origin of this affection remains sub judice.

[Footnote 129: Arch. für path. Anat., 1868, p. 536, Band xliii.]

Important changes also take place in the spleen, but the opinions on this point are somewhat contradictory. Frerichs found the spleen enlarged in most of his cases; Liebermeister, on the other hand, and Legg,[130] find that the spleen is enlarged in about one-third of the cases. When the atrophic changes occur in the liver, more or less swelling of the splenic veins must occur in consequence of portal obstruction. The peritoneum, especially the omental part, is the seat of multiple ecchymoses, and the endothelium is fatty. The mesenteric glands are usually swollen. More or less blackish or brownish fluid, consisting of altered blood, is usually found in the stomach, and the same, assuming a tar-like consistence, in the large intestine. Ecchymoses of rather small size are distributed over the stomach and intestines. The epithelium of the stomach-glands is found granular and disintegrating, and a catarrhal state of the gastro-intestinal mucous membrane exists throughout. The secretions are never normal, and the stools are wanting in bile or present a tarry appearance, due to the presence of blood.

[Footnote 130: On the Bile, Jaundice, and Bilious Diseases, supra.]

Important changes take place in the kidneys. They consist essentially in a granular and fatty degeneration of the tubular epithelium, whence the altered appearance of the cortex. Multitudes of bacteria crowd the pyramids. Ecchymoses also are found in the mucous membrane of the pelvis of the kidney, in the bladder, and indeed all along the genito-urinary tract.

The muscular tissue of the heart is in a state of acute fatty degeneration, beginning with a granular change which may at the outset be of very limited extent and involve but few fibres. The endo- and pericardium are studded with ecchymoses or marked by hemorrhagic extravasations, and the pleura presents similar appearances, but not to the same extent.

The brain does not always show evidences of change, but in many instances there are ecchymoses of the meninges; the walls of the vessels are affected by fatty degeneration.

The tissues of the body are more or less deeply stained with bile. The pathological change on which the jaundice depends has been variously stated, but the most probable explanation is that which refers it to mechanical obstruction of the bile-ducts, either by catarrhal swelling or fatty degeneration of the epithelium. Notwithstanding the prominence of the hepatic symptoms, acute atrophy of the liver is probably only one element in a constitutional morbid complexus.

SYMPTOMS.--Acute yellow atrophy begins in two modes--the grave symptoms preceded by mild prodromes, or the most serious symptoms appear at the onset. The former mode is the more common. The usual prodromes are referable to the gastro-intestinal canal, and consist of loss of appetite, nausea, vomiting, a bitter taste in the mouth, headache, and general malaise. Indeed, the opening attack may be much like an {1027} ordinary bilious seizure or acute gastro-duodenal catarrh or a sick headache. In some cases the initial symptoms--nausea and diarrhoea--appear to be induced by an indigestible article of food. Jaundice never fails to be present at some period, but is usually one of the prodromic symptoms. It has no special characteristics by which the gravity of the approaching seizure may be measured. It is usually rather deep, and all parts are deeply stained, but the coloration may be limited to the body and upper extremities. No change in pulse or temperature, except the usual depression of both functions, is to be observed; the urine is deeply stained with pigment, and the feces are grayish, colorless, or parti-colored.

The period of time elapsing before the serious symptoms come on is not constant; from one week to several months have been the variations observed. In a minority of the cases no prodromes have occurred, but the grave symptoms have declared themselves at once. From the appearance of the jaundice up to the onset of severe symptoms the time has varied from two weeks to several months, but has rarely exceeded three months. During this time there may be nothing to indicate the gravity of the approaching symptoms; in fact, the case then, as at the onset, seems to be one of simple gastro-duodenal catarrh associated with catarrhal jaundice. The onset of serious symptoms is most usually announced by dilatation of the pupil. If, therefore, in a case of apparently simple catarrhal jaundice, especially in a pregnant female, there should occur without apparent reason a marked and persistent dilatation of the pupil, the possibility of the case being one of acute atrophy should be apprehended. This symptom is not, alone, of sufficient value to decide the character of the case, but then an obstinate insomnia comes on, violent headache is experienced, there is more or less confusion of mind, and jactitations or an extreme restlessness occurs. When such pronounced nervous symptoms appear the character of the attack is explained.

Various divisions have been proposed to mark the type of the symptoms: thus, the icteric period embraces the prodromal symptoms with jaundice; the toxæmic period is that stage characterized by profound nervous disturbances. Ozonam has divided the symptoms into those of the prodromal period and those of the serious stage, the latter being subdivided into the symptoms of excitation and those of collapse. There may be no prodromal period, however; without any preliminary symptoms the patient is suddenly seized with delirium and passes into a condition of coma and insensibility, or the first evidence of serious illness may be convulsions. It is probable, however, that in even the most sudden cases mild prodromal symptoms had occurred, but were overlooked. There is much variability in the symptoms of the toxæmic period. There are three symptoms: excitement with delirium, sometimes delirium ferox; coma, less or more profound; and convulsions. Legg has numerically expressed the relative frequency of these symptoms thus: Of 100 cases of unquestionable acute atrophy, 76 had become comatose, 59 were delirious, and 32 had suffered convulsions.[131] According to the same authority, delirium and coma were associated together in about one-half of the cases, but in pregnant women coma often occurs alone (Legg). Usually, when convulsions happen there has been either coma or delirium. With these cerebral symptoms there are often present various {1028} disturbances of motility and sensibility, such as local convulsions, jactitations, hiccough, extreme restlessness, paralysis of the sphincters, and incontinence of urine and feces or retention, grinding of the teeth, exalted sensibility of the skin, or it may be complete anæsthesia, severe itching of the surface, etc.

[Footnote 131: On the Bile, Jaundice, and Bilious Diseases, loc. cit.]

During the toxæmic period, and directly dependent on the retention of excrementitious matters in the blood, hemorrhages occur from the mucous surfaces, from wounds, and into the various serous membranes. A changed state of the blood being present in all cases of this disease, the proportion in which extravasations take place is high--in about 71.3 per cent. according to Liebermeister, and 80 per cent. according to Legg. The latter author regards these estimates as rather low. When hemorrhage occurs in the stomach in small amount, it presents itself as coffee-grounds or as black vomit, and in the intestine in the form of black, tarry stools or melæna. Hemorrhage may also occur from the surface of an ulcer, from a fresh wound, a leech-bite, etc.; but the most usual form of extravasation of blood after the gastro-intestinal is epistaxis or bleeding from the nose. Women who abort, as they are very apt to do when this disease comes on, may suffer from frightful hemorrhage, and deaths have been thus caused. Various opinions have been expressed as to the cause of the hemorrhagic condition--by some attributed to the changes in the composition of the blood; by others to the alterations of the vessel walls; both factors are doubtless concerned.

During the prodromic period the temperature of the body, as in the case of ordinary uncomplicated jaundice, is rather depressed below normal, sometimes as much as two degrees; but when the toxæmic stage comes on the body-heat rises to a variable extent, but usually over 100° F. In some cases no febrile movement can be detected; in others a very considerable elevation of temperature occurs, but very rarely attains to 105° or 106° F. The pulse becomes very rapid, in some instances rising to 140; but without any apparent cause it may fall suddenly to 70 or 80, and these fluctuations may take place several times a day. The rise of temperature and a very rapid pulse may come on in the final coma only; and immediately after death, as Legg points out, the body-heat may attain the maximum elevation.

As the toxæmic period develops the tongue becomes dry, glazed, fissured, sordes form on the teeth and lips, the breath becomes fetid, and the breathing may assume the Cheyne-Stokes type. The nausea and vomiting of the prodromal period persist, and the ominous coffee-grounds appear in the rejected matters, or grumous masses--clots acted on by the gastric juice--are brought up. Black, pitch-like, or tarry stools, the result of hemorrhage, are passed toward the end--involuntarily when liquid. When no blood is present the stools are grayish and without bile. Constipation may be the condition instead of diarrhoea in about one-third of the cases.

Various eruptions have been observed on the skin, such as petechiæ, roseola, eczema, etc., but their very variety, as their occasional appearance, indicates their accidental relationship to the disease.

The urine is much altered in character, but it is usually acid in reaction, although it has been observed neutral or alkaline. The specific gravity is at or nearly normal, and it has a deep-brownish or bilious hue {1029} due to the presence of bile-pigment. The most important change in the composition of the urine is the diminished quantity of urea or its entire disappearance; the phosphates, and especially the chlorides, are also usually diminished in amount; and albumen and leucin and tyrosin appear to a lesser or greater extent, together with hyaline, fatty, and granular casts.

Although the observations are somewhat contradictory, it seems pretty definitely established that the blood is more or less altered in composition, morphological and chemical. The red corpuscles are diminished in amount, and often deformed; the white corpuscles are increased; and excrementitious products--urea, leucin, tyrosin, and cholesterin--are found in greater or less quantity.

COURSE, DURATION, AND TERMINATION.--Although, as a rule, the course of acute atrophy is rapid, it is not invariably so. In some instances the prodromic symptoms have continued through several months, but, according to Thierfelder, one-half of the cases terminate in from three to five weeks, and in only 10 per cent. is the duration continued into eight weeks. The course of the disease is extremely rapid in pregnant females, rarely extending beyond the second week. An extended course of the disease is due to delay in the prodromic stage, the toxæmic period being always absolutely and relatively shorter. In the condition of pregnancy the danger is increased by the hemorrhages, and the early termination is due chiefly to this factor. When the duration of the disease is protracted and its evolution normal, the accumulation of hepatic excrementitious matters sets up cerebral disturbance, which becomes a pronounced feature of the case.

The termination cannot probably be otherwise than fatal. As in the course of the disease the hepatic cells undergo solution and disintegration, their restoration can hardly be regarded as possible, certainly not probable. Any curative result must, then, be wrought in the prodromic period, when the diagnosis must be viewed with some mistrust.

DIAGNOSIS.--George Harley[132] maintains the singular doctrine that acute yellow atrophy is only the "sporadic form of the contagious jaundice of the tropics," or yellow fever. He bases his opinion on the identity of their symptoms, pathological anatomy, mortality, and contagious character; for he affirms that acute yellow atrophy may exhibit contagious power in temperate climates.

[Footnote 132: Diseases of the Liver, Amer. ed., 1882, p. 255.]

As acute yellow atrophy comes on as an ordinary catarrhal jaundice, it is impossible to distinguish it from the latter affection during the prodromal period. When cerebral symptoms, black vomit, and tarry stools appear, the area of hepatic dulness very decidedly diminishes, and leucin and tyrosin replace urea in the urine, acute atrophy may be suspected.

Acute phosphorus-poisoning, as regards its symptomatology and morbid anatomy, does not differ from acute yellow atrophy, and many cases of the latter have been mistaken, it is supposed, for the former. To distinguish between them the history of the case must be carefully ascertained.

When, after the prodromal symptoms, which may not be accurately diagnosticated, there occurs a rapid decline in the area of hepatic dulness, hemorrhages take place from the mucous surfaces, stupor and delirium {1030} supervene, and urea disappears from the urine, being replaced by leucin and tyrosin, there can be no difficulty in coming to a conclusion: the case must be one of acute yellow atrophy.

TREATMENT.--It was formerly supposed that a case of acute yellow atrophy must necessarily prove fatal, but this opinion must now be modified, since examples of cure of supposed cases have been reported from Oppolzer's clinic,[133] by Lebert,[134] by Harley,[135] and others. As at the onset the symptoms cannot be distinguished from a bilious attack or from catarrhal jaundice, the treatment must be appropriate to these states. When the serious symptoms begin, a large dose (scruple j) of quinine should be at once administered, and half the quantity at regular intervals to keep up the cinchonism. Phosphate of soda, with some arseniate and such mild hepatic stimulants as euonymin, iridin, etc., should be given to maintain a gentle aperient action. Experience has proved that active or drastic cathartics do harm rather than good; on the other hand, mild laxatives, especially those having cholagogue action, seem to do good.

[Footnote 133: Thierfelder, op. cit.]

[Footnote 134: Ibid.]

[Footnote 135: Diseases of the Liver, Amer. ed., supra.]

Important symptoms arising during the toxæmic period require remedies to combat them. Nausea and vomiting, and also diarrhoea, are best relieved by carbolic acid and bismuth in combination. Hemorrhage requires, when intestinal, the chloride and perchloride of iron; when from other mucous surfaces, ergotin, gallic acid, and other hæmostatics. The depression of the vital forces should be treated by small and frequently-repeated doses of alcohol, by quinine, by iron, and, under some conditions, by digitalis. After the disintegration of the hepatic cells has been produced no remedies can be of any service. Until this occurs, however, it seems to the author well worth while to attempt to stay the destruction by the administration of those remedies which, by their accumulation in that organ, indicate a special affinity for its tissue. These drugs are phosphorus, antimony, gold, silver, and mercuric chloride. By the timely administration of one or more of these would it not be possible to stay the progress of the atrophic degeneration?

The Liver in Phosphorus-Poisoning.

DEFINITION.--Poisoning by phosphorus may seem to be a toxicological question rather than a merely hepatic disease, but as the morbid complexus thus induced is so similar to acute yellow atrophy that the conditions are regarded as identical by many of our German colleagues, it is necessary to enter into some details regarding it.

PATHOGENY.--Phosphorus-poisoning occurs at any period from youth to old age, but is most common from twenty to thirty years of age. Women seem more inclined to effect self-destruction in this way than are men, probably because phosphorus matches are so readily obtained. Children may munch match-heads in a spirit of mischief. That form of chronic poisoning seen in workmen in match-factories, and consisting in necrosis of bone, etc., does not come within the scope of the present inquiry.

A body poisoned by phosphorus does not exhibit a tendency to putrefactive decomposition within the usual period. The tissues are more or less {1031} deeply stained by bile-pigment, and this coloration extends to pathological fluids as well. The serous and mucous membranes contain points of blood-extravasation, but they are especially numerous in the serous membranes. Hemorrhages of this kind are due to two causes--to the disorganization of the blood, and to fatty degeneration of the arterioles. The heart is also more or less advanced in fatty degeneration, the muscles granular, the striations obscure or obliterated, and the whole soft and easily torn. The spleen is usually enlarged--often, indeed, to twice its natural size. The liver presents highly-characteristic alterations. When death occurs early the organ is generally enlarged, infiltrated with fat, the connective tissue undergoing hyperplasia; but in more advanced cases atrophy has taken place, the cells have disappeared and are replaced by fat-granules, crystals of leucin and tyrosin, connective tissue, etc.--in fact, the changes characteristic of acute yellow atrophy. The jaundice has been variously interpreted. As the bile-ducts in advanced cases are found to contain no bile, but only a colorless mucus, the advocates of a hæmatogenic jaundice hold that the jaundice is due to a failure of the liver to excrete the biliary principles in the blood; whilst the opponents of this view maintain the existence of an obstruction in the ultimate ducts. Harley[136] has recently brought forward some strong facts and arguments--which we believe can be successfully controverted--maintaining the former view. The jaundice of phosphorus-poisoning, if Harley's opinion prove to be correct, must be regarded as a hæmatogenic jaundice.

[Footnote 136: Diseases of the Liver, loc. cit.]

The mucous membrane of the stomach, as might be supposed, is more or less ulcerated or in an advanced state of catarrh, and the gastric glands are affected by fatty degeneration.

The kidneys are affected in a similar manner to the liver; the epithelium is fatty and sometimes detached, and the same process is found to occur in the vessels and epithelium of the cortex.

SYMPTOMS.--Not only in the morbid anatomy, but in the symptoms, do we find that a very remarkable resemblance exists between acute yellow atrophy and phosphorus-poisoning. As phosphorus is usually swallowed in bulk, some hours may elapse before the local symptoms begin, for the contents of the stomach and the tough mucus lining the mucous membrane may, and usually do, prevent immediate contact of the poison with the mucous membrane. When the stomach is entirely empty the symptoms may begin in an hour or two. The symptoms produced may be arranged in two groups--those due to the local irritation excited by the poison; those due to its systemic impression. In the first group belong burning in the gullet, pain, nausea, and vomiting. According to Lewin,[137] who has collected a number of cases for analysis, vomiting occurs in 26 out of 32 instances of poisoning. Some hours--often, indeed, three or four days--then elapse before the systemic symptoms begin. Vomiting, which was for the time being suspended, occurs again, and instead of the mere contents of the stomach, containing more or less phosphorus, blood, somewhat changed by the gastric juice--chocolate-colored or as coffee-grounds--appears in the vomited matters. The evacuations from the bowels may at first, as the contents of the stomach, appear phosphorescent, and afterward exhibit the appearances due to the presence in them {1032} of altered blood. At this time, if the liver be examined it will be found somewhat enlarged and tender to pressure, and on or about the third day jaundice appears; but it should not be overlooked that jaundice, as Bamberger[138] has shown, may be postponed to the second or third week after the phosphorus has been taken.

[Footnote 137: Virchow's Archiv für path. Anat., etc., Band xxi. p. 514 et seq.]

[Footnote 138: Legg, On the Bile, Jaundice, and Bilious Diseases, loc. cit.]

In favorable cases the area of hepatic dulness decreases and the jaundice declines. In the fatal cases certain nervous phenomena become prominent. There occur drowsiness, developing into coma, with intercurrent attacks of delirium which may be of a maniacal character; convulsions, spasmodic attacks, dilated pupils, and involuntary evacuations. The disorganization of the blood and the fatty change in the vessels are exhibited in the hemorrhages from the gastro-intestinal mucous membrane. The nervous phenomena are due chiefly to the retention in the blood of various excrementitious matters which it is the function of the liver to separate from the blood. Flint's theory of cholesteræmia has been so abundantly disproved that no one upholds it at the present time, but the cerebral symptoms are properly referred to the retention of all hepatic excrement.

The temperature in phosphorus-poisoning rises from 99° to 102° F., but it may reach in severe cases to 103° to 105° F., and at death or immediately afterward to 105°, even to 107° F. The same fact is true of acute yellow atrophy. With the jaundice the pulse declines, but in the further progress of the case, especially toward the close, the pulse becomes rapid and small.

The changes occurring in the urine are highly significant. The amount of urea decreases as the symptoms increase in severity, and leucin and tyrosin take its place. If the case tends to recovery the urea again increases in amount, but if the tendency is in the opposite direction the quantity of urea steadily diminishes. Bile acids and bile-pigment are found in quantity, and albumen is present in small amount.

COURSE, DURATION, AND TERMINATION.--Phosphorus-poisoning is necessarily an acute affection, but the duration of cases is much influenced by the form in which the poison is taken. If in a liquid and diffusible form, as oleum phosphoratum, the local and systemic symptoms will develop in a few hours, but if in solid masses, as particles of match-heads, many hours (six to ten) may elapse before the local irritation begins. The proportion of cures in phosphorus-poisoning varies from one-fourth to one-half of the cases. Much depends, however, on the promptness and efficiency of the treatment. The prognosis is the more favorable the earlier proper measures of relief have been instituted. If the case has proceeded to jaundice, hemorrhages, black vomit, etc. without the administration of suitable antidotes, little can be expected from any kind of treatment.

DIAGNOSIS.--The history of any case involved in doubt is indispensable to a correct conclusion. The phosphorescent appearance of the matters vomited or passed by stool may make the differentiation comparatively easy; but if the case has passed beyond this stage, phosphorus-poisoning can be separated from acute yellow atrophy only by the history of the case. If the fact of the administration of phosphorus is successfully concealed, no differentiation can be made, since {1033} even the best authorities hold to the identity of the toxic symptoms produced by this poison and of the morbid anatomy, with the symptoms and lesions of acute yellow atrophy.

TREATMENT.--The poison should be evacuated as quickly as possible by emetics and proper diluents. The best emetics are sulphate of copper, apomorphia, and ipecacuanha, the antimonial and mercurial emetics being unsuited, since their effects are similar to those of phosphorus. Oleaginous protectives do not prevent, but really favor, the absorption of phosphorus. Decoctions of flaxseed, slippery elm, acacia, etc. are suitable demulcents and protectives. The fatty matter in food, eggs, etc. will have an injurious effect by promoting the solution and absorption of the phosphorus, and should hence be excluded from the diet. The most effective antidote is oleum terebinthinæ, and the most suitable preparation is the French acid oil. Freshly-distilled turpentine appears to be almost if not entirely useless. It is probable that the American oil which is old and has been exposed to the air for many months will answer the purpose, but it cannot be too strongly insisted on that the turpentine which has proved to be efficient in phosphorus-poisoning is the French acid oil. Turpentine when exposed to the air absorbs oxygen as ozone, and to this principle are probably due the curative effects of old turpentine. Phosphorus when acted on by this agent is converted into a spermaceti-like substance entirely devoid of toxic power. As rapidly as possible the poison should be acted on by the antidote, and then the stomach should be evacuated, using, cæteris paribus, the sulphate of copper, since this forms an insoluble phosphide with any portion of free phosphorus, whilst at the same time it empties the stomach of its contents. Although the immediate results of the poison may be thus removed, the damage to the red corpuscles and to the whole mass of the blood requires special management. The success of transfusion, as practised by Jürgensen,[139] proves that the substitution of fresh blood may save life when the existing blood-supply is inadequate to the performance of its proper functions. It follows that if the toxic effects of phosphorus have continued for several days, blood-transfusion will be necessary in those cases characterized by an inability to recuperate notwithstanding the successful removal of the poison.

[Footnote 139: Berliner klinische Wochenschrift, No. 21, 1871.]

For the inflammatory symptoms produced by the local action of phosphorus, opium in some form is indispensable. This remedy is equally valuable as a means of maintaining the vital resources and to prevent the evil results of shock and inflammation.

Carcinoma of the Liver.

DEFINITION.--Under the term carcinoma of the liver are included primary and secondary cancer of the liver. The malady with which we are now concerned is the primary affection, occurring in the organ proper or in some pathological new formation connected with it.

ETIOLOGY.--Heredity is the most important factor. A careful investigation of the reported examples demonstrates that from 15 to 20 per cent. owe their origin to hereditary influence clearly, and probably {1034} considerably more are indirectly derived in this way when the immediate connection may not be demonstrable. Next to heredity, age must be regarded as the most important pathogenetic influence, much the largest number occurring at from forty to sixty years of age. It is a malady of advanced life, therefore, rather than of youth or middle age. Excluding the female organs from consideration, it is quite certain that sex has little special influence, and that males and females are affected about equally.

Primary cancer of the liver is comparatively infrequent, occurring in not more than one-fourth of the cases. Frerichs collected 91 cases, and of these 46 were secondary to cancer in organs having vascular communication with the liver.

PATHOLOGICAL ANATOMY.--Under the term cancer of the liver are included several distinct forms of morbid growth, but united in the characteristic of malignancy. From the merely clinical standpoint this characteristic is the most decisive bond of union between them, and serves as the point of departure in the study of this affection. Primary cancer of the liver is divisible into two forms: 1, as a single, defined tumor; 2, as an infiltration through the whole mass of the organ.[140] Secondary cancer occurs in nodular masses, and with extreme rarity as an infiltration. The form of cancer is really the same; the differences in structure are only apparent, the variations being due to the relative proportion of cells, fibres, and vessels. If the fibrous stroma is abundant and the cells small in quantity, the form of structure approaches scirrhus; on the other hand, if the cells largely preponderate, the type is encephaloid; if vessels predominate, it is called telangiectatic. The usual form in cancer of the liver is the soft, cellular variety, encephaloid or medullary. When the cancerous new formation is nodular, the masses vary in size from a pea to a child's head,[141] and are numerous inversely as their size. When the cancer occurs as a solitary tumor, it may attain to enormous dimensions. It has a spherical shape usually, protrudes from the surface of the organ somewhat irregularly, and the overlying peritoneum is thickened, cloudy, and adherent from a local inflammation. The central portion, whether there be one, several, or many nodules, is depressed, giving an umbilicated appearance to the tumor; and this central depression is found to be soft, almost diffluent, and full of juice. The fibrous stroma which extends through this central soft material has a reticulated arrangement and a shining, fibrous appearance. The cancerous masses are not confined to these nodules, but extend into the surrounding hepatic structure, push their way into the portal (especially the hepatic) veins, block the ducts, and invade the lymphatic glands in the fissure of the liver.

[Footnote 140: Virchow, Krankhaften Geschwülste, loc. cit.; Perls, Virchow's Archiv für path. Anat., etc., Band lvi. p. 448 et seq.; Frerichs, A Clinical Treatise, etc., Syd. Soc. ed., loc. cit., vol. ii. p. 281 et seq.]

[Footnote 141: Förster, Lehrbuch der Pathologischen Anatomie, by Seibert, Jena, 1873.]

When the cancerous new formation takes the form of an infiltration of the organ instead of distinct nodules, the liver is usually uniformly enlarged and its outlines preserved.[142] The peritoneum is opaque, thickened, and adherent. The organ is traversed by fibrous bands, and the {1035} intervening portion is a soft, juicy pulp, stained by the imbibition of bile. In extreme cases hardly any portion of the proper hepatic tissue remains, but is replaced by a cancerous new formation having the same shape.

[Footnote 142: Perls, Virchow's Archiv, Band lvi. p. 448 et seq.]

As regards the minute structure of cancer of the liver, it may be regarded as a degeneration (cancerous) of the proper gland-cells and of the epithelium of the bile-ducts. As cancer develops in the liver it is to be noted that the cellular elements preponderate over the fibrous or the stroma, and hence the new formation presents the characteristics of softness, rapid growth, and a multitudinous cellular hyperplasia. As regards the form of the new cells, it cannot now be doubted that they are descendants of the secretory gland-cells and of the epithelial lining of the ducts. According to some observers, it is to the proliferation of the proper gland-cells that the new formations owe their origin; according to others, to the hyperplasia of the cells lining the ducts. As the growth of the new formation can take place only through an adequate blood-supply, it becomes very important to ascertain its source. There can be little doubt that primary cancer of the liver receives its nutrient supply through the hepatic artery, in connection with which new capillaries form in the pathological tissue.

Secondary cancer of the liver is the usual form of the specific manifestation. From the merely clinical standpoint the primary affection is the more important. From the pathological point of view the secondary implication of the liver may be a true metastasis or a mere communication by contiguity of tissue. The most usual metastasis occurs from epithelial cancer of the face (Schüppel), but the ordinary communication of the new formation is from primary cancer of the stomach, intestine, pancreas, mesentery, etc. The cancer elements, as the author has several times verified, crowd the lymphatics and veins, and through these channels reach the liver and other parts. As the cancer elements in the case of secondary implication of the liver are distributed chiefly by the portal vein, it follows that there must be numerous secondary foci and multiple nodes. Cancerous infiltration under these circumstances is the rarest possible form for the new growth to take. The size and number of nodes forming in these cases of secondary implication of the organ vary greatly--from two or three to twenty, or a hundred, or even more. As regards the form, structure, and ultimate behavior of the secondary formation, they do not differ from the primary. As respects the relative proportion of stroma and cellular elements--fibres and cells--they vary greatly, some presenting the firm texture of a predominating fibrous stroma, others the softness and ready diffluence of the excessive cellular production. The latter is undoubtedly the usual condition, and when the nodular masses are incised an abundant creamy juice exudes. With the development of these nodules an increase in the size of the liver takes place and the organ has an uneven and indurated feel. As the cancerous masses develop the proper hepatic structure undergoes atrophy, and finally little is left of the organ but the cancerous new formation. The blood-vessels, lymphatics, and peritoneal investment are invaded, the first mentioned most decidedly; and especially are organized exudations the favorite seats of cancer new formations, those, for example, about the gall-bladder and cystic duct resulting from repeated attacks of passage of calculi.

{1036} Secondary changes take place in the cancerous nodes. As the cells develop pressure is brought to bear on the vessels supplying them and on each other, with the result of fatty degeneration of the central portion, which effects the change in the form of the nodules and in their consistence, already mentioned. The blood-supply to the cancerous nodes in the liver is derived from the hepatic artery, as Frerichs has determined by carefully-made injections; they also are new formations of exceedingly delicate structure, and form a network about the periphery of each mass or node. By reference to these anatomical considerations it is easy to understand the failure of nutrition of the central portions of the nodes.

Pigment cancers of the liver are rare as secondary formations, and excessively infrequent as primary formations. They are, properly speaking, melano-sarcomas (Schüppel). They are more often metastatic than merely secondary--that is, transferred from different parts, as in the case of melanotic sarcoma of the choroid--than due to neighboring disease transferred by contiguity of tissue. This variety of cancer, so called, takes the form of multiple nodes or of diffused infiltration, the former more frequently; but both modes of development may go on at the same time. The nodes vary in size from a pea to a child's head, have a grayish, brownish, or blackish tint, and exude on section a fluid not creamy like true cancer-juice, but rather watery and containing black particles floating in it. In the case of diffuse infiltration the pigment masses are thoroughly distributed through the original hepatic tissue. In both forms the size and weight of the organ are enormously increased. In the case of the melanotic infiltration the whole organ is uniformly enlarged, reaching in a few months the enormous size of twelve to twenty pounds.

Sarcomas also occur very rarely as primary growths in the liver, but secondary sarcomas are more frequent. There are fibro-sarcoma, lympho-sarcoma, and osteo-sarcoma as secondary deposits, the first being very firm in consistence, the second soft and medullary, and the last of hard, bony consistence.

SYMPTOMS.--We are especially concerned here with primary cancer of the liver. The secondary disease is so obscured by the main and primary lesion that a diagnosis may be impossible. Furthermore, the progress of the original disease is that which demands immediate consideration. As, therefore, the secondary implication of the liver is of relatively trifling importance, and only an incident in the course of the main disease, the matter for consideration now is primary cancer of the liver.

It is the fact that in some, even a considerable proportion, of the cases the onset and progress of cancer of the liver are very obscure. For some time the symptoms may be of the vaguest description. The usual history is this: A person of forty to sixty years begins to fail in flesh and strength, becomes sallow, has disorders of digestion, pain and uneasiness in the right hypochondrium, and the bowels are now confined, now relaxed. The abdomen, notwithstanding the general loss of flesh, increases in size, and the superficial veins are enlarged; very considerable pain is experienced in the right hypochondrium, and often extreme tenderness to pressure is a pronounced symptom. The pains are not limited to the hepatic region, out extend widely from this point in all directions. On palpation the {1037} liver is found to be enlarged, its texture indurated, and its outline irregular and nodular, and pain--often, indeed, quite severe--is developed by pressure.

The condition of the liver on palpation is best ascertained by suddenly depressing the abdominal wall with the tips of the fingers arranged in a line. Displacing thus the movable bodies in the cavity, the liver is quickly reached, and nodules, if they exist, are readily felt. If the new formation has developed from exudations about the gall-bladder and cystic duct, it may be felt by suddenly depressing the walls of the abdomen over this organ in the usual position of the fissure.

In the case of general cancerous infiltration of the organ, with the remarkable enlargement which occurs in such cases, there will be present an obvious distension of the right hypochondrium; the intercostal spaces will be forced outward and the arches of the ribs rendered more prominent; the area of hepatic dulness, both vertical and transverse, will be increased; and the limits of dulness will move with a full inspiration downward, and with a full expiration upward. This mobility of cancer-nodules of the liver with the inspiratory and expiratory changes serves to distinguish them from tumors of the abdominal walls. Seen early, the changes in the size of a nodule or of the liver itself may be noted from week to week,[143] especially in cases of rapidly-growing cancer.

[Footnote 143: Murchison, Clinical Lectures, p. 187.]

As the cancerous new formations extend into the portal system within the liver, obstruction to the portal circulation results from the blocking of the blood-current. Also, interference in the portal circulation arises by compression of the vessels from without, either through the accumulation of cancer-products in the liver or by the enlargement of the lymphatics in the fissure of the organ. In what way soever it may be produced, the practical fact remains that ascites is a frequent symptom, occurring in somewhat more than one-half of the cases. The character of the fluid varies. It may be a clear serum containing a small proportion of albumen; it may be colored by bile or be of a deeper greenish or reddish hue; it may contain flocculi of lymph and numerous leucocytes floating in it; and the ordinary serum may be rendered cloudy and be filled with shreds of exudation in consequence of peritonitis, or bloody because of hemorrhage from a softening nodule. When the fluid is considerable in amount the difficulty of ascertaining the condition of the liver is greatly enhanced, and symptoms due to the interference of the fluid with the action of various organs are introduced into the complexus of morbid signs. Especially is the upward pressure of the ascitic fluid, and the consequent interference in the movements of the lungs and heart, a source of considerable distress. First, a local and afterward a general peritonitis ensues as a consequence of the extension outwardly of the new formations to the peritoneal layer, and its implication by contiguity of tissue or the rupture of a spreading fungous growth and hemorrhagic extravasation into the cavity. The peritoneal complication is not only a serious addition to the sufferings experienced by the patient, but it adds to the difficulties of a diagnosis. In the case of a celebrated savant who died of cancer of the liver (seen by the writer) there was such a pronounced peritonitis that the diagnosis made by the attending physician was chronic peritonitis. When this complication occurs, there takes place {1038} a decided increase in the local tenderness, and this increased sensibility to pressure quickly extends over the abdomen, causing a general exquisite tenderness. Besides this tenderness characteristic of most cases of peritonitis, distension of the abdomen and the decubitus peculiar to this state are obvious symptoms. It is therefore clear that the occurrence of peritonitis not only contributes to the severity and painfulness of the case, but seriously complicates the diagnosis.

It has been already stated that pain in the right hypochondrium is a nearly constant symptom in cancer of the liver. With the initial symptoms, uneasiness, heaviness, a sense of pressure in the hepatic region are experienced, and as the case progresses more or less acute pain develops as a rule. But there are exceptions. In cases of cancer involving the deeper portion of the liver there may be little pain, and in some rare cases of cancer involving the external part of the liver--the capsule and peritoneum--but little pain is experienced. In much the largest proportion of cases the pain is severe, and the production of any considerable pain means the implication of the hepatic plexus of nerves or the hepatic peritoneum. It follows, then, that the pain in the former case is not limited to the locality of the disease, but is more or less widely distributed through the anatomical relations of the hepatic plexus, being felt in the epigastrium, the walls of the chest, the shoulders, etc.

In secondary cancer of the liver, following cancer of the stomach, vomiting is a constant symptom, but also in those cases of primary disease in which the left lobe is especially enlarged, relatively, are nausea and vomiting pronounced symptoms. At the onset of the malady the appetite fails and a gastro-intestinal catarrh is set up. More or less catarrh of the bile-ducts also ensues. The interference with nutrition thus occasioned is enhanced in those cases in which the obstruction of the ducts is sufficient to prevent the escape of bile into the intestine. Jaundice is not a constant symptom, occurring in little more than one-third of the cases. When it occurs, the peculiar stools are present and the intestinal digestion is deranged, as in cases of ordinary obstruction to the ducts. In two cases of cancer of the liver occurring in the writer's practice, and examined by post-mortem, there were calculi present in the gall-bladder; in one case the principal calculus was egg-shaped and the size of a pullet's egg.

The nutrition rapidly fails from the beginning of cancer of the liver. The downward pace is accelerated when the gastro-intestinal digestion fails and vomiting occurs after taking food. The skin becomes dry and wrinkled, and if not jaundiced has a peculiar tint, varying in depth of color from an earthy or fawn-like hue to a deep bronze. Failure of strength is a pronounced symptom from the beginning, and is out of proportion to the loss of flesh. As the wasting advances the decline of strength is accounted for, but the feeling of weakness and the distaste for exertion which occur so early are very significant signs of internal cancer, although they do not indicate the position of the neoplasm. Emaciation finally becomes extreme.

The urine declines in amount as the case progresses. It is usually very high-colored, contains bile-pigment when jaundice is present, and other forms of pigment produced by conditions not at present known. Sometimes albumen is present, and leucin and tyrosin rarely.

{1039} COURSE, DURATION, AND TERMINATION.--As has been already set forth, cancer of the liver may present so few really distinctive symptoms as to escape recognition. Under favorable circumstances the diagnosis may be comparatively easy. In forming an opinion it is useful to review the whole course of the malady and draw conclusions not only from the characteristic signs, but from the development of the symptoms as a whole.

A case of cancer of the liver occurs usually after the middle period of life. The person so affected begins to decline in flesh and strength, has uneasiness in the right hypochondrium, disorders of digestion, and begins to have a pallid or earthy hue of the countenance. Presently, much pain is felt in the hepatic region, the organ distinctly enlarges, and some effusion of fluid and much flatus increase the dimensions of the abdomen. Much tenderness, often exquisite sensibility, is produced by pressure over the liver, and often over the whole abdomen. By careful palpation nodules can be made out and their growth noted in those cases free from peritoneal inflammation. The abdominal swelling and tenderness incommodes the lungs, and a semi-erect decubitus is assumed to relieve the pressure on them; the breathing becomes short, catching, hurried, and painful, and sometimes a most distressing hiccough is superadded to the other sufferings. Great wasting and weakness ensue. Jaundice appears, or the earthy hue of the skin deepens into a bronze discoloration. The case may be terminated by some intercurrent disease--by an attack of pleuritis, pneumonia, by peritonitis from rupture or perforation, by intra-peritoneal hemorrhage, by an exhausting diarrhoea. The natural termination is by gradual failure of the powers, by marasmus, the immediate cause of death being due to cerebral anæmia, to failure of the heart from fatty degeneration of the cardiac muscle, from thrombosis of the portal vein, from the development of a hemorrhagic state, and hemorrhages from the various mucous surfaces, etc. The duration is much influenced also by the character of the cancer, whether scirrhous or medullary. The latter are not only more rapidly growing, more destructive of the hepatic tissue, and more rapidly distributed to neighboring organs, but more quickly perforate the capsule and excite a fatal result by hemorrhage or by peritonitis. The average duration of cancer of the liver is variously stated. Having reference to my own personal observation, controlled by the experience of other observers, the duration is from three to nine months, one year being exceptional. There are cases in which the symptoms are very acute, the progress rapid, the whole course from the initial symptoms to the termination being completed in from two to three months. It need hardly be observed that no case of cancer of the liver has been cured. The invariable termination is in death. If any case has seemed to be cured, it may be asserted with confidence that cancer of the liver did not exist.

DIAGNOSIS.--The differential diagnosis is concerned, first, with the existence of cancer; second, with its form. As cancer causes enlargement of the liver in two textural conditions--namely, uniformly smooth, and nodular--it must be differentiated from other diseases producing similar results. Amyloid disease and echinococcus cysts present us types of the former; cirrhosis and syphilis, of the latter. The history of the amyloid disease and of the echinococcus cyst is very different, and both {1040} develop much more slowly. Amyloid disease of the liver arises simultaneously with the same form of degeneration in other organs, and is connected with suppurative disease of some kind, with syphilis, with chronic malarial poisoning, etc., and may occur at any age. Echinococcus cysts enlarge painlessly and do not impair the vital forces; the liver is elastic, and under favorable circumstances presents by palpation the purring-tremor symptom. Cirrhosis may have to be differentiated at two periods--during the time of enlargement, which, however, is rather brief; and during the stage of contraction and nodulation. The history in cancer and in cirrhosis is different: the age, the habits of life, the rate of hepatic change, are opposed in the two diseases; the diminution in size with nodulation is characteristic of cirrhosis; enlargement with nodulation belongs to cancer. The rapid progress of cancer, the wasting, the debility, the cachexia, serve to distinguish it from all other affections of the liver except acute yellow atrophy and phosphorus-poisoning; both, however, are so different in history and development as not to require differentiation. It may be quite impossible in latent cases to distinguish primary cancer of the liver from secondary, but in those examples of the disease occurring in the stomach, intestines, and pancreas there is usually an antecedent history of the primary malady which distinctly separates it in point of time and the character of the symptoms from the secondary implication of the liver. Cancer of the gall-bladder, and especially of the organized exudation about it, may not be readily separated from cancer of the pancreas or of the duodenum. In doubtful cases the history of attacks of hepatic colic becomes an important element in making the differentiation.

TREATMENT.--As we are not in possession of a cure for cancer, the treatment of cancer of the liver must be palliative. Anodynes to relieve pain, paracentesis of the abdomen to remove accumulation of fluid which causes distress, carbolic acid to check nausea and vomiting, and the usual hæmostatics for hemorrhage, are the measures most necessary. In fact, the treatment must be throughout symptomatic--for the relief of symptoms as they arise.

Amyloid Liver.

DEFINITION.--By amyloid liver is meant a deposit in the cells of the organ, in its vessels and interstitial tissue, of a peculiar albuminoid matter called amyloid because of a superficial resemblance to starch-granules. Various designations have been applied to this condition of the organ; thus it has been entitled waxy liver and lardaceous liver, because of the apparent resemblance to wax and lard respectively.

CAUSES.--There exists in the blood a peculiar material, albuminoid in form, applied in the normal state to the structure of tissue--dystropodextrin, as it is called by Seegen--which, when precipitated under certain conditions not now known, assumes the peculiar appearance with which we are now familiar under the term amyloid. The character of the amyloid matter was first distinctly set forth in 1858 by Virchow, who also discovered the characteristic reaction by which it can always be detected. The reaction to iodine gave to the material the designation amyloid, or starch-like, by which it is chiefly known. The {1041} circumstances inducing the deposit of this material are by no means clearly understood. It has long been known that suppuration, especially in connection with bone, has had a distinct influence. Syphilis, especially the tertiary lesions accompanied by pus-formation, has an evident causative relation. Chronic malarial infection has a more distant and doubtful, but still recognized, power to develop this morbid state. Of the various causes above mentioned, the most frequent is the suppuration of pulmonary cavities. In regard to the influence of this, however, it must be remembered that no form of suppurative disease is so common. The relative frequency of the association between suppurating cavities and amyloid disease is not greater than long-standing necrosis with an extensive sequestrum is with the same state; but the actual number of the former is greater. Amyloid disease of the liver is most frequent between the ages of ten and thirty, but it may occur at any age, the period in life being determined by the operation of the causes. Thus, Frerichs' statistics are: under ten there were 3 cases, from ten to twenty there were 19, and from twenty to fifty there were 37 cases. Men are, relatively to sex, more frequently attacked, and in the proportion of three-fourths, but this difference means, of course, the character of men's occupations and their greater liability thereby to the accidents and diseases incident to such employments.

Besides the pathogenetic factors above mentioned, it may be well to refer in this connection to the effect of long-standing neoplasms. It has been found that amyloid disease is produced in some subjects by the cachexia resulting from the slow development and persistence of such a new formation. The special character of the neoplasm is of less importance in respect to this condition than the constitutional condition--the cachexia--induced by its slow growth and interference with nutrition. Although long-standing disease, especially of a suppurative kind, is known to be necessary to cause amyloid disease, Cohnheim[144] has lately published some facts which seem to prove that the degeneration may occur more speedily than has been heretofore supposed. He has shown, contrary to the previously-accepted view, that amyloid degeneration may follow in three months after the reception of a gunshot wound. He records three cases in which the amyloid deposits ensued in six, five, and three months, respectively.

[Footnote 144: Virchow's Archiv, vol. liv. p. 271 et seq., "Zur Kentniss der Amyloidentartung."]

According to the author's observation, a peculiar somatic type is either necessary to, or at least is greatly promotive of, the amyloid degeneration. If, for example, the same suppurative process occurs in a person of a blond and lymphatic type and in another of brunette and nervo-muscular type, the former will be much more likely to suffer from amyloid change than the latter. "The gelatinous progeny of albuminous parents" is the mode of expression used to designate this particular type.

PATHOLOGICAL ANATOMY.--To use the term amyloid liver is rather misleading, since this indicates the restriction of the morbid process to the liver, whereas it is perfectly well known to be rather widely distributed through various organs and tissues of the body. The term amyloid is itself confusing, since the albuminoid material so designated is not really starch-like. The corpora amylacea, so called, differ materially from starch-granules, and still more from the amyloid matter. According to {1042} Wagner,[145] these substances "have nothing in common." In the study of the amyloid deposit it has not been possible to separate it from the tissue in which it is imbedded; hence the published analyses of this peculiar material are probably far from correct. However, it has been rendered probable that the amyloid deposit has close affinities with fibrin. One of the theories--that of Dickinson of London--assumes that this material is fibrin deprived of the potash associated intimately with it. According to Seegen, dystropodextrin, a material existing in normal blood, agrees with amyloid matter in its most essential characteristics. Although Dickinson's theory is not tenable, it has served a useful purpose in showing the close affinity of fibrin with this pathological product. What view soever may be entertained of its nature, it is certain that the material to which we apply the term amyloid is of albuminous origin. Under circumstances with which we are now unacquainted this material is deposited from the vessels, and, instead of undergoing organization and contributing to the structure of tissues, remains unorganized and unappropriated. It is known that this deposition of the amyloid material is related to the process of suppuration and to certain cachexiæ, but the intermediate steps remain unknown and inexplicable.

[Footnote 145: A Manual of General Pathology, by Prof. Dr. E. Wagner, p. 325 et seq.]

The amyloid matter is first exuded into the coats of the finest ramifications of the hepatic artery, and therefore the first appearance of the disease is in the middle zone of the lobules. In this respect pathologists are agreed: that the amyloid deposits first appear in the walls of the vessels. Wagner maintained, in opposition to Virchow, that the exudation is limited to the vessels and does not extend to the hepatic cells, which perish by pressure and consequent atrophy. This point has not yet been decided. It seems most probable, however, that the ramifications of the hepatic artery and all the capillaries of the lobule are affected, and that the deposits in them lead to atrophic degeneration of the cells.

In consequence of this extensive implication of the vascular system of the liver important changes occur in the size, density, and appearance of the liver. The organ is greatly enlarged in all its diameters. When felt through the walls of the abdomen its outline is distinct, it is firm, even hard, to the sense of touch, and it projects from a finger's breadth to a hand's breadth below the margin of the ribs. The increase of size of the amyloid liver is very great, attaining in weight, on the average, twice that of the normal organ; but this size may be largely exceeded in exceptional instances. In respect to shape and outline the amyloid liver does not differ from the normal organ; for although its dimensions are increased, its relations to the parts adjacent are not altered. The weight of the amyloid liver may reach ten, twelve, even sixteen pounds avoirdupois. The color of the amyloid liver is very different from that of the normal organ: instead of having the reddish-brown tint, it becomes grayish, yellowish, or reddish-gray. In consistence the amyloid liver is firm and rather elastic and doughy, and on section the margins of the incision are well defined, even sharp. A very characteristic feature of the cut surface is its paleness, anæmia, or bloodlessness, and scarcely any blood is exuded, even from the large vessels. The appearance of the incised surface of the liver has been described by comparison with various substances: according to one, it is waxy; according to another, it is lardaceous. A thin {1043} section of a part of the liver far advanced in the amyloid change is distinctly translucent, almost transparent; but a marked difference is observable between the amyloid matter and the lobules proper, even in the cases of extreme deposit. The lobules are separated by an opaque yellow border, and the centre of each is marked by a spot of a similar yellow color.

The amyloid material is remarkable for its power to resist the action of chemical agents and putrefactive decomposition. The test originally proposed by Virchow--iodine--continues to be the most characteristic. Orth[146] suggests a method of applying it which is very excellent in respect to the clearness with which the reaction is shown: A large, thin section of the affected liver is placed in a saucer of water containing some iodine, and after the reaction has taken place is laid on a white plate. Iodine tincture, diluted or the compound solution, is brushed over the affected region, when the amyloid matter assumes a deep mahogany tint and the normal tissues a merely yellowish hue. The distinctness of the reaction may be increased by brushing over the iodized surface some dilute sulphuric acid, when the amyloid matter takes a deep violet, almost black, color.

[Footnote 146: Diagnosis in Pathological Anatomy, Riverside Press, 1878, p. 321.]

Only a part of the organ--namely, the smaller vessels--may be involved in the degeneration, and this may be restricted to patches or parts of the organ. With the amyloid change there may be associated syphilitic gummata, or the liver may be more or less advanced in fatty degeneration or in cirrhosis. Those parts of the organ not invaded by the disease are not often entirely normal; they are more or less darkened in color by venous congestion, distinctly softer, etc. The amyloid change is not limited to the liver, but extends to the kidneys, lymphatic glands, the intestinal mucous membrane, etc.

SYMPTOMS.--As the amyloid change in the liver is usually coincident with a simultaneous alteration of other organs, and as the deposits characteristic of the affection are dependent on long-previous disease of an exhausting kind, it is not surprising that the subjects of this affection present the evidences of a cachexia. To the effects of a chronic malady we have added the complications growing out of the amyloid change in the liver, associated, as it usually is, with amyloid degeneration of other important organs.

The symptomatic expression of amyloid liver is therefore mixed up with various derangements that occur simultaneously, but especially with the causes inducing the existing cachexia, with chronic suppuration of pulmonary cavities, or in connection with diseased bone, with the syphilitic cachexia, or with chronic malarial toxæmia. With what cause soever the cachexia may be associated, the symptomatology of amyloid liver is secondary to, or ingrafted on, the conditions produced by the cachexia. The liver is enlarged in all well-marked cases from a finger's breadth to a hand's breadth or more below the inferior margin of the ribs; it is also firm to the touch, well defined, elastic, and its margin rounded, but yet well defined. There is usually no tenderness nor pain, and, without any uneasy sensations to indicate the change taking place, the organ is found to have slowly enlarged, sometimes to an extraordinary extent. Careful palpation may also demonstrate an enlargement of the spleen. When the abdominal muscles are relaxed and there is no swelling of the abdomen by flatus or peritoneal effusion, the very considerable enlargement of {1044} the liver can be readily ascertained. If the effusion is not so great as to distend the abdomen unduly, the increased consistence and dimensions of the liver can still be made out with comparative ease. The hepatic functions are not always sufficiently disturbed to produce characteristic symptoms. In a small proportion--scarcely one-tenth--of the cases does jaundice appear, and when present it is due, usually, to enlargement of the lymphatics in the hilus of the organ, and thus directly compressing the hepatic duct. In the writer's experience, although jaundice has not occurred, there was present a peculiar dark earthy or bronzed tint of the skin, significant of chronic hepatic troubles. Obstruction of the portal circulation is rather unusual, and the explanation is to be found in the fact that the amyloid degeneration occurs first in the radicles of the hepatic artery. In about one-fourth of the cases ascites is present, but in a somewhat larger proportion hemorrhoids, blackish, tarry stools, and other evidences of portal congestion. When the intestinal arterioles are attacked, an intractable colliquative diarrhoea comes on; the stools are offensive, sometimes light from the absence of bile, sometimes dark from decomposition or the presence of blood. When the stomach arterioles are also involved, which is usual under these circumstances, the blandest and simplest articles of diet will pass unchanged or simply decomposed. Blood may be vomited sometimes in large quantity from thrombic ulcers, but the matter ejected from the stomach when the case is well advanced is a thin, watery fluid, faintly acid or neutral, and greenish or brownish in color.

An enlarged spleen is often present, produced by the same conditions--by amyloid degeneration. The same change taking place in the kidney, the urine becomes pale, abundant, of low specific gravity, and albuminous. General dropsy supervenes in a majority of the cases finally, due largely to the hydræmia; and of this condition ascites is a part. In some cases enlargement of the abdomen is the first step in the dropsical effusion, and may throughout be the most prominent, as the author has seen. In other cases oedema of the feet and legs is the first evidence of dropsy; in still others the dropsy is general from the beginning.

Amyloid liver may coexist with a fairly good state of the bodily nutrition, but if digestion and assimilation be interfered with by any of the causes above mentioned, the strength rapidly declines and emaciation reaches an extreme degree.

COURSE, DURATION, AND TERMINATION.--As amyloid liver is never a substantive affection, but secondary to some constitutional malady or to long-continued suppuration, its course must be considered in relation to the agency producing it. It is very silent in its origin and progress, and causes no pronounced symptoms until it attains considerable size and its functions are interfered with by the extent of the deposits. The history of the affection to which it is secondary therefore precedes the onset of the amyloid change and accompanies it throughout. The enlarged organ, with the results of its enlargement in altered functions of the abdominal organs, is a symptom superadded to existing disturbances. The period elapsing in the course of a chronic suppurative disease before the amyloid change occurs differs greatly in different cases, and may be stated as from three months (Cohnheim's case) to many years. Many of the cases terminate by an intercurrent disease; others by uræmic {1045} convulsions; a very few by hemorrhage from the stomach or intestines; and those pursuing their course uninterruptedly, by exhaustion.

The prognosis is very unfavorable. By some a cure at the beginning of the morbid deposits is regarded as possible, and examples of cures have been reported. The writer has seen supposed cases of amyloid liver terminate in recovery. There must always remain an impression that in such instances an error of diagnosis was committed. Those of syphilitic origin are probably more curable, but syphiloma of the liver may be confounded with amyloid disease, and hence the cure may be referred to the latter.

DIAGNOSIS.--Amyloid degeneration of the liver may be confounded with the various non-febrile enlargements of the organ. An important element in making the differentiation is the history of suppuration in connection with bone, with lung cavities, with constitutional syphilis, with chronic malarial toxæmia, etc. From fatty liver, amyloid degeneration is distinguished by the history as just sketched; by the fatty tendencies of the body in the former, emaciation in the latter; by the concomitant changes in the spleen, kidneys, and elsewhere; and by the subsequent history, fatty liver terminating by a weak heart usually, whilst the amyloid disease ends in the modes described in the preceding paragraph. From hydatid disease, amyloid liver is differentiated by the history, by the difference in the physical characteristics of the enlargement, by the presence of the purring tremor in the one, its absence in the other, and especially by the subsequent course. In all doubtful cases the use of an aspirator-needle and the withdrawal of some fluid containing the characteristic hooklets of the echinococcus will serve to determine the nature of the growth. From cancer, amyloid liver is separated by the previous history, by the nodular character of the enlargement, by the pain, and by the cachexia and associated derangements. Whilst amyloid liver is secondary to suppurative diseases, cancer is usually secondary to cancer of the stomach or other organ within the limits of the portal circulation.

TREATMENT.--As amyloid disease owes its origin to syphilis, to chronic malarial toxæmia, to suppuration, these, so far as they are remediable conditions, should be cured as speedily as may be, to prevent the development of the amyloid disease or to arrest it if begun. Unfortunately, the condition of the liver is not recognized until the morbid change is effected, and therefore practically irremediable.

The treatment necessarily involves that of the morbid state to which the amyloid deposits are owing. The syphilitic disease requires iodine and mercury; the malarial, quinine, iodine and the iodides, eucalyptus, iron, etc., according to the state of each case; and surgical diseases, especially necrosis of bone, should be effectively treated by suitable surgical expedients. The cause being removed if possible, what means, if any, can be resorted to to cause the absorption of the amyloid matter? The only specific plan of treatment hitherto proposed is that of Dickinson,[147] based on his theory of the constitution of amyloid matter; according to which the amyloid deposits consist of fibrin altered by the separation of the potash and soda salts, which have been eliminated in the pus. If this theory be admitted, the obvious indication is to supply the alkaline materials. The cases reported by Dickinson in which this theory was {1046} practically demonstrated were not sufficiently improved to lend any empirical support to this method.

[Footnote 147: The Pathology and Treatment of Albuminuria, p. 214 et seq.]

The medicinal remedies which do any good are the iodides--notably the iodides of ammonium, of iron, of manganese, etc., the compound solution of iodine, and the double iodide of iron and manganese. As the officinal ointment of the red iodide of mercury, rubbed in over the splenic region, does so much good in chronic enlargement of the spleen, it is probable that it will prove effective in this form of enlargement of the liver. The writer has observed results from it in such cases that justify him in strongly urging its employment. The method of its application consists in rubbing perseveringly a piece of the ointment, a large pea in size, over the whole hepatic area, and repeating it daily until some irritation and desquamation of the skin is produced, when it should be suspended until the parts will bear renewed applications. Besides the topical application of the red iodide, this remedy may be given internally with advantage without reference to syphilitic infection. It seems to the writer probable that bichloride of mercury may be as useful, as it is certainly more manageable. The chloride of gold and sodium, arsenic in small doses, and the metallic tonics, so called, may be useful carefully administered, especially the first mentioned, which the writer believes has some real power over the disease.

Dietetic rules are of great importance. As the hepatic functions are much disturbed, if not entirely suspended, it is necessary to give those foods which are converted into peptones in the stomach. As a rule, fats, starches, and sweets are mischievous, and milk, meats, oysters, and the nitrogenous foods best adapted to nourish the patient. If the diarrhoea should prove exhausting, the mineral acids, with opium, are the best remedies. Nausea and vomiting are best relieved by carbolic acid mixture, and hemorrhages by the solution of the chloride or subsulphate of iron.

Fatty Liver; Fatty Degeneration of the Liver (Hepar Adiposum).

DEFINITION.--By the term fatty liver is meant a change in the organ characterized by the excessive quantity of fat- or oil-globules contained in the cells of the parenchyma.

CAUSES.--The liver acts, under normal conditions, as a reservoir for the surplus fat, which it gives out as the demand is made. It is not only the fat brought to the liver by the blood which accumulates in the organ, but it apparently possesses the power to transform certain substances--albumen, for example--into fat. An important causative element, therefore, is the quantity of fat present in the food habitually consumed. This has been proved by the investigations of Radziejewsky[148] and others, who have shown that the fat in the food is stored up in the normal places of deposit, one of which, of course, is the liver. Another causative element is the formation of fat from the albumen of the hepatic cells in consequence of diminished oxidation. In respect to both causes the consumption of oxygen is an important factor. The insufficient supply of oxygen {1047} which is a necessary result of a sedentary life leads thus, directly, to the accumulation of fat in the liver-cells. A constitutional predisposition is also an important factor. There are those who under certain conditions of daily life store up large supplies of fat, and others who under the same conditions continue lean. Women more than men are subject to such inherited predispositions.

[Footnote 148: Virchow's Archiv für path. Anat., etc., Band lvi. p. 211.]

Again, fatty liver occurs in the course of certain cachexiæ, notably phthisis. In this case the obstructive pulmonary lesions interfere with the process of oxidation, and also maintain a constant hyperæmia of the portal system. This condition of the liver also occurs in the cancerous cachexia, in anæmia and chlorosis of long standing, in chronic suppurative diseases, etc. The dyscrasia of chronic alcoholism is a very common cause of fatty liver. At the same time that hyperplasia of the connective tissue is taking place the fat is accumulating in the hepatic cells. So great is the accumulation of fat in the blood that the serum presents a milky appearance. This excess in the quantity of fat is rather due to diminished oxidation, to lessened combustion, than to increased production. Another causative element of the fat-production in cases of alcoholism is the interference of alcohol with the process of digestion and assimilation.

Poisoning by phosphorus, antimony, arsenic, and other metals sets up an acute fatty degeneration of the liver. Pregnancy, lactation, and suppuration also have the same effect, but to a slighter and less permanent extent.

PATHOLOGICAL ANATOMY.--Fatty liver agrees with amyloid liver in that the fatty deposits increase the size and weight of the organ. The surface is smooth, the peritoneal investment unaltered, and the margins rounded. Sometimes the organ is merely increased in thickness, sometimes in diameter. It has a greasy feel and cuts like a mass of fatty tissue. Examined at a low temperature--below freezing--it seems like a mass of suet, the proper structure being almost extinguished in the fatty metamorphosis. The outline of the lobules remains distinct even in cases far advanced in the fatty degeneration, but in the extreme cases it is obliterated, the cut surface presenting a uniformly yellowish or grayish-yellow tint. The fatty liver is also wanting in blood; it is dry, and on section only the largest vessels contain any blood. When cardiac disease of a kind to produce congestion of the venous system exists--for example, mitral or tricuspid lesions--the same relative decrease in the quantity of blood in the liver is observable after death, although during the life of the subject the opposite condition may have been present. The cause of this bloodlessness of the fatty liver is to be sought in the pressure exerted by the growing fat-cells.

Not all cases of fatty liver are advanced to the degree indicated in the above description. From the normal size up to the maximum attained by the most advanced fatty liver there are numerous gradations in the quantity of fat and in the dimensions of the organ. Fatty degeneration may accompany cirrhosis, in which the liver is contracted. The deposits of fat may take place in particular areas. In cases of fatty liver per se the deposit occurs within the liver-cells, as may be demonstrated on microscopic examination, the initial change consisting in the formation of granules in the protoplasm which ultimately coalesce, thus producing {1048} fat-globules or cells. The fatty change in the hepatic cells proceeds in a certain methodical manner from the cells at the periphery of each lobule to the centre. The quantity of fat deposited in the liver in cases of fatty change is very great. In the normal condition of the organ fat exists, according to Perls,[149] in the proportion of 3 per cent. of the weight of the liver. When the condition of fatty liver exists the quantity of fat rises to 40, even 45, per cent.--almost one-half. It is important to note, as was pointed out by Frerichs, that in an inverse ratio with the increase of fat was the quantity of water.

[Footnote 149: Virchow's Archiv, supra.]

That more or less fatty change in the liver is not incompatible with a normal functional activity is quite certain, but the boundary between health and disease is by no means well defined in respect to the quantity of fatty change in the liver-cells. The liver, within certain limits, is a mere reservoir of the surplus fat of the body, and hence a variable, but not excessive, amount of accumulation of fat is not incompatible with a normal functional performance of the organ. The limits of a merely functional state and of a diseased state are not, therefore, very clearly defined. In certain inferior animals, as Frerichs has shown, a fatty condition of the liver is normal.

SYMPTOMS.--The signs and symptoms of fatty liver are by no means well defined. This state of the organ, as a rule, accompanies the general tendency to fatty metamorphosis and deposit in the body. It is a symptom in the course of phthisis, of chronic alcoholism, and of various forms of metallic poisoning, but under these circumstances there is no material change in the course of the symptoms produced by this complication. As an independent affection it rarely, if ever, exists alone. So far as its symptoms can be defined, they are referable to the organs of digestion and assimilation and to the liver itself.

The appetite is generally good, but distress after eating, acidity and heartburn, eructations of acid liquid and of certain articles of diet, are experienced. The stools are usually rather soft or liquid, wanting in color, whitish or pasty, and occasionally dark, almost black, owing to the presence of blood. Hemorrhoids are usually present. The discharges are often offensive from the decomposition of certain constituents of the food, acid and burning because of the presence of acetic, butyric, and other fat acids, or merely offensive because of the formation of hydrogen compounds with sulphur and phosphorus. Notwithstanding the derangement of the stomachal and intestinal digestion, the deposition of fat continues in an abnormal ratio. With the increase in body-weight a decline in muscular power takes place. The respiration is hurried on the slightest exertion, and dyspnoea is produced by any prolonged muscular effort. The circulation is feeble and the pulse slow in the state of repose, but on active exertion the pulse becomes rapid and at the same time feeble. The sleep is disturbed by horrifying dreams, and only on assuming a nearly sitting posture can the patient sleep with any degree of quietude.

In these cases of fatty liver a very considerable mental inquietude, despondency, even hypochondria and melancholia, result. The relation of insufficient hepatic excretion to the mental state is yet sub judice, but there can be no doubt that some connection exists. From the earliest {1049} period hepatic derangements--as the term hypochondria denotes--have been associated with certain disorders of the mind. This relation certainly holds good in respect to the mental perturbation occurring in cases of fatty liver. With a rotund countenance and a well-nourished body there is associated very considerable mental despondency.

Without distinct jaundice the skin has an earthen or tallow-like hue, the conjunctiva is muddy or distinctly yellow, and now and then well-defined jaundice appears.

The urine is rather scanty, high-colored because of the presence of bile-pigments, and deposits urates abundantly. When jaundice accompanies fatty liver the urine will be very dark, muddy, thick, and will react to the usual tests for bile, urates, etc.

The area of hepatic dulness is, as a rule, enlarged in cases of fatty liver. The deposition of fat in the cells adds to the gross size of the organ, and hence the inferior margin extends below the border of the ribs to a degree determined by the amount of increase in its substance. If the liver can be felt, it is smooth, not hard and resisting, and is free from nodules. Usually, however, owing to deposits of fat in the omentum and in the abdominal walls, the outlines and condition of the liver cannot be ascertained, and must remain merely conjectural. Rather, therefore, by implication than by direct examination can the condition of the liver be ascertained.

COURSE, DURATION, AND TERMINATION.--The course of fatty liver, as an element in a general change not of a toxic character, is essentially of a chronic character. The fatty liver of acute phosphorus, antimonial, and other forms of poisoning is acute and fatal, but it is not these forms with which we are here concerned. Acting the part of a reservoir of the surplus fat stored up in the body, which may be disposed of under normal and physiological conditions, the fatty liver becomes by careful management a normal organ again. The course, duration, and termination will therefore largely depend on the nature of the management pursued. A fatty liver cannot, then, be regarded as fatal, or even as dangerous to life per se. The course and termination will therefore be those of the associated condition.

DIAGNOSIS.--The determination of the existence of fatty liver will not be difficult in all those cases in which this condition may properly be suspected; for example, in phthisis, in chronic alcoholismus, in obesity, and in cases of habitual indulgence in eating and drinking. If in these cases the organ is distinctly enlarged, is smooth, and is flabby in outline; if at the same time the digestion is deranged, the stools are light in color, there are hemorrhoids, flatulence, acid indigestion, and torpid bowels,--a fatty liver may be reasonably suspected. The subjects of fatty liver are usually obese, and present the characteristics typical of that condition, or they are the victims of alcoholismus or present the evidence of habitual indulgence in the pleasures of the table. The differentiation of fatty liver from amyloid degeneration, from cystic disease, and from other maladies causing enlargement of the organ is made by reference to these points in the etiological history--by a careful study of the condition of the organ itself and of the organs associated with it in function. As the amyloid liver is more likely to be confounded with the fatty liver, it should be noted that the former is an outgrowth of the process of suppuration, that the organ {1050} is hard in texture, and that amyloid change occurs at the same time in other organs--conditions opposed to those characteristic of the fatty liver. Cancer of the liver is accompanied by a peculiar cachexia; the body wastes, and the enlarged liver is hard and nodular instead of being smooth and flabby.

TREATMENT.--When fatty liver is a symptom merely, its treatment is merged into that of the primary condition. Thus, in phthisis and in the various forms of metallic and phosphorus-poisoning the condition of the liver is quite secondary. There are cases of obesity, however, in which the fatty change in the liver is a part of the general morbid process, and must be treated accordingly. There are still other cases in which, without a decided tendency to obesity, the food habitually consumed is of a fatty or fat-forming nature. The first requisite in the treatment of fatty liver is to amend the diet. From the time of Hippocrates down to Mr. Banting it has been recognized that the starchy and saccharine constituents of the food, as well as the fatty, contribute to the formation of fat. In arranging a dietary in cases of fatty liver this fact should be regarded. Besides excluding the fats, saccharine and starchy substances should be cut off. The diet should be composed of fresh animal foods, game, fish, oysters, and such succulent vegetables as lettuce, celery, spinach, raw cabbage (cole-slaw), etc. Amongst the articles excluded should be bread, but the greatest difficulty is experienced in its withdrawal, many patients declaring themselves unable to live without it. In such instances a small biscuit (water-cracker) may be allowed, but, as far as may be accomplished, bread should be cut off from the diet.

If there are acidity, heartburn, pyrosis, and regurgitation of acid liquid, much good may be expected from the administration of diluted nitric acid before meals, especially if there be considerable uric acid in the urine. The simultaneous administration of tincture of nux vomica will prove useful if the appetite is poor and the digestion feeble. When the complexion is muddy, the conjunctivæ yellow, and the tongue coated, excellent results are had from the persistent use of phosphate of sodium. Under these circumstances also arsenic is very beneficial. Even better results may be had from a combination of the two agents, a teaspoonful of the pulverized phosphate being given with one-fortieth of a grain of the arseniate of sodium. Alkalies, as lithium citrate, solution of potassa, etc., are unquestionably useful as remedies for obesity and fatty liver, but they must be administered with a proper caution. Also, the permanganate of potassium has seemed to the author to be especially valuable as a remedy for these states.

Remedies to increase the activity of the portal circulation and diminish congestion of the hepatic vessels are useful at the outset, but the anæmia which succeeds renders their use improper at a later period. Amongst the hepatic stimulants of great use in those cases characterized by whitish, pasty stools, yellow conjunctivæ, etc., are resin of podophyllin, euonymin, baptisin, and others having the same powers. Saline laxatives are also useful, but to a less extent. It must be remembered, however, that these subjects are wanting in bodily vigor, often suffer from weak heart, and always have flabby muscles, so that they bear all depleting measures badly. The hepatic stimulant of greatest utility in these cases is sulphate of manganese. The writer has had excellent results from a {1051} combination of quinine and manganese. For the general state, which denotes insufficient oxidation according to the chemical pathologists, permanganate of potassium is a remedy of value, as above mentioned. The best form in which to administer this is the compressed tablet, and the dose usually is two grains. As chalybeate tonics are indicated, the oxidizing power of the succinate of the ferric peroxide, the remedy so warmly advocated by Buckler, may be utilized with advantage. The combination of quinine, iron, and manganese in pill form, or the syrup of the iodides of iron and manganese, or the phosphate of iron, quinine, and strychnine, are tonics adapted to the relief of the depression accompanying this malady.

III. AFFECTIONS OF THE BILIARY PASSAGES.

Catarrh of the Bile-Ducts.

HISTORY AND DEFINITION.--Although catarrh of the bile-ducts had been incidentally referred to by some previous writers, notably by Stokes of Dublin, Virchow[150] was the first to treat of this condition systematically. Amongst recent writers, Harley[151] appears to be the only one disposed to question the importance of catarrh of the bile-ducts as a factor in the production of jaundice. Even in phosphorus-poisoning the appearance of jaundice, at one time supposed to be hæmatogenic in source, has been referred to a catarrh of the bile-ducts.[152] It seems probable that opinions have too decidedly veered toward the importance of this condition as a factor in the production of jaundice.

[Footnote 150: Archiv für path. Anat., Band xxxii. p. 117 et seq.]

[Footnote 151: Diseases of the Liver, supra.]

[Footnote 152: Wyss, Archiv der Heilkunde, 1867, p. 469 (Legg).]

CAUSES.--Catarrh of the bile-ducts has been referred to all those causes which can excite a catarrhal process in any situation. These are systemic and local. Amongst the systemic may be placed peculiarities of constitution or idiosyncrasy. A tendency to hepatic disorders is a feature in certain types of constitution, and, as such types are transmitted, the hepatic disorders seem to be inherited. In such persons, possessing the so-called bilious nature, catarrh of the biliary passages is not uncommon, and a special susceptibility to it apparently exists. The atmospherical and other causes which in some subjects will set up a catarrh of the bronchi will in the bilious type induce a catarrh of the duodenum and bile-ducts. The malady is not inherited; only the character of bodily structure which favors it under the necessary conditions.

Climatic changes and certain seasons, especially the autumn, are influential causes. Exposure to cold and dampness, the body warm and perspiring, will set up a catarrhal process in the bile-ducts and intestine, especially in those having the special susceptibility which belongs to certain bodily types. Malarial miasm is an especially active cause in malarial regions. The writer has seen many examples in various parts of the United States within the malaria-breeding zone. Other miasmatic agencies are not without importance. The exhalations from the {1052} freshly-upturned soil of some cities, the gases from cesspools and sewers, and illuminating gas exert a causative influence. The bad air thus made up has been happily called civic malaria.

The most influential causes of catarrh of the biliary passages are local in origin and in action: they are the agencies which induce catarrh of the duodenum. Disturbances of the portal circulation should be first named. Whenever obstructive lesions of the cardiac orifices exist, whenever the pulmonary circulation is impeded by disease of the lungs, the portal vein is kept abnormally full, and as a necessary result of the stasis a catarrh of the mucous membrane follows. Congestion of the portal system may be a result of vaso-motor paresis. The abdominal sympathetic may be the seat of various reflex disturbances: those of a depressing kind induce stasis in the portal system. Certain medicinal agents have this effect, and prolonged and severe cutaneous irritation, it is probable, may act on the portal circulation in the same way. The action of cold on the peripheral nerves may be similarly explained.

Catarrh by contiguity of tissue is the most frequent factor. Catarrh of the duodenal mucous membrane is the initial condition, and from thence the process extends to the bile-ducts. Although the duodenum may be alone affected, the usual state of things is a gastro-intestinal catarrh, the stomach and the whole length of the small intestine being simultaneously diseased. When the catarrhal process is thus diffused the duodenal mucous membrane is most deranged, probably because the acid and fermenting chyme is first received here, and what acridity soever it may possess attacks this part in its greatest strength. It must be remembered that the secretion of the duodenal glands and of the pancreas and liver must also have an abnormal character; hence those foods which in the healthy condition of things are digested in this part of the canal undergo ordinary putrefactive decomposition and furnish very irritating products. This observation is especially true of the fats: the fat acids are in the highest degree irritating. The digestive fluid of the duodenum has a more or less pathological character, because the catarrhal process not only interferes with the habitually easy flow of the gland secretions, but, extending to the gland elements themselves, gradually alter their structure.

Gastro-intestinal catarrh results from the misuse of foods and the abuse of certain condiments and of spirits. Excess in the quantity of starchy, saccharine, and fatty foods which undergo conversion and absorption in the intestine, habitually consumed, decomposition of such portions as escape proper digestion ensues, and the products of this decomposition exercise an irritant influence on the mucous membrane. The daily consumption of sauces and condiments and of highly-seasoned foods has a constant irritating action; but more influential than any other causative agency is the abuse of malt liquors and spirit. Whilst the latter acts more on the stomach and the liver proper, the former affect more the duodenal mucous membrane and the bile-ducts.

To these causative agencies must be added a pathological state of the bile itself. Under conditions not now known the bile seems to acquire acrid properties and set up a catarrh in passing along the ducts.

PATHOLOGICAL ANATOMY.--The area affected by the catarrhal process varies greatly. The termination of the common duct for a short space may be the only part affected, but with this there is always more or less, {1053} sometimes most extensive and severe, duodenal catarrh, followed by jaundice. The extent to which the common duct is affected may be exactly indicated by the staining with bile, which extends down to the point of obstruction. The catarrhal process may invade the whole extent of the common duct, the cystic duct, gall-bladder, and the ramifications of the tube throughout the organ. The resulting appearances will vary accordingly.

The first change observable is a more or less considerable hyperæmia of the mucous membrane; but this is rarely seen, because the examination cannot be made at the time when this condition is present. The epithelial layer is swollen, sodden, the cells cloudy, undergoing rapid multiplication and desquamating. The cast-off cylindrical epithelium, mucous cells, and serum make up a turbid mixture, which, with bile, fills the smaller ducts, and may in places, especially at the orifice of the common duct, form an obstruction sufficient to prevent the passage of the bile; which may, however, be readily pressed out with a little force. Especially near the end of the common duct the mucus is apt to accumulate, and a plug of it, often tenacious and somewhat consistent, obstructs the orifice. It is probable that whilst catarrh is the chief cause of jaundice, it may also, by a merely intermittent activity, cause the condition of biliousness--now so far relieved as to permit the bile to descend into the intestine, now so much obstruction as to prevent the escape of any considerable part of that formed. When the common duct is the seat of the catarrhal process, and the outflow of bile thus prevented, it accumulates in the gall-bladder, which may be so far distended as to present a recognizable tumor of pyriform shape through the abdominal parietes.

When the catarrhal process invades the finer ducts the appearances are somewhat different. There are no bile-stains along the course of the common and cystic ducts, and the gall-bladder is empty, or at most contains only some mucus, with altered bile. The tubes at or near their ultimate ramifications contain a turbid mucus composed of cylindrical epithelium and lymphoid cells, and tenacious enough to close them firmly. More or less hyperæmia of the liver-structures proper, and consequent increased dimensions of the organ, a more or less active catarrhal condition of the duodenal mucous membrane, accompany the changes in the finer ducts.

SYMPTOMS.--There are marked differences in the behavior of the more acute cases of catarrh of the bile-ducts and the chronic examples of the same disorder. The former is held to be the most frequent cause of jaundice, whilst the latter is an important element in the so-called bilious state, in lithæmia, and as a secondary condition in some cardiac and pulmonary diseases. Also, the morbid complexus of catarrh of the bile-ducts includes the symptoms of duodenal and gastro-duodenal catarrh.

The acute form of this disease sets in with the symptoms of gastro-duodenal catarrh. Usually, after indulgence in too highly stimulating food or in some article having a specially irritating character, an attack of acute indigestion supervenes. The tongue is more or less heavily coated, the breath heavy, the taste bitter, pasty, or sourish, the appetite poor or actual repugnance to food, especially to the offending articles, is experienced, and nausea, not unfrequently vomiting, ensues. The epigastrium and the hypochondriac regions have a heavy, overloaded, distressed, {1054} and sore feeling; there is some tenderness to pressure; sometimes the gall-bladder, abnormally full, may be detected by careful palpation; and the area of hepatic dulness will usually be increased. The abdomen is more or less distended by gases, and eructations of offensive gases (hydrogen and sulphur compounds, volatile fat acids, etc.) occur. Constipation exists when the catarrhal process is limited to the duodenum, and the stools consist of hard lumps having a light yellow, clay-colored, or whitish appearance. When the whole extent of the small intestine is affected, the stools will be soft, liquid, or watery, and will vary in color from yellow to gray or white. In some cases the fecal matters will have an offensive odor--the odor of decomposition--and considerable discharges of very foul-smelling gas will attend the evacuations. This symptom will occur when the intestinal digestion is suspended and the contents of the bowel in consequence undergo putrefactive decomposition.

During the initial period of the disorder the urine will simply be high-colored and loaded with urates and uric acid, but when jaundice supervenes the pigment will convert the urine into a dark, coffee-colored, and somewhat thick liquid.

With the onset of the malady symptoms referable to the nervous system appear. Headache, dizziness, and hebetude of mind are present, and now and then an attack of catarrh of the bile-ducts will have the objective signs of an ordinary migraine or sick headache. Usually, however, as the intestinal and hepatic troubles develop, headache and some mental hebetude come on, but when jaundice supervenes the headache becomes more severe, and very considerable mental depression, irritability of temper, and moroseness are experienced. Chilly sensations, with flashes of heat, are felt at the outset, but with the appearance of jaundice the sensation of coldness predominates. In some cases, the intestinal catarrh being extensive, there will be, after some preliminary chilliness, a febrile movement, but this is never of a pronounced character, and in the slighter cases of the disease or when the catarrhal process is limited to the bile-ducts, there is no elevation of temperature. With the first symptoms the pulse is somewhat quickened, but as the bile acids accumulate in the blood they effect a decided slowing of the heart's action, the pulse falling as low, it may be, as 50 per minute. This lessened activity of the circulation is accompanied by corresponding reduction of temperature, the body-heat falling a degree or more.

The most distinctive symptom of catarrh of the bile-ducts is jaundice. In the acute or quickly-developing form above described of catarrhal icterus the symptoms of gastro-intestinal disturbance precede the first indication of jaundice from five to eight days. Yellowness of the conjunctiva and of those parts of the body exposed to the air is the first manifestation; afterward the jaundice hue becomes general. The tint varies in depth from a faint gamboge-yellow, only discernible in a favorable light, to a deep greenish- or brownish-yellow.

In the more chronic cases of catarrh of the bile-ducts the symptoms are simply those of a gastro-duodenal catarrh, to which some hepatic disturbances are superadded. Some abdominal uneasiness felt in the epigastrium and in the right hypochondrium, especially in two to three hours after meals; flatulence, sometimes accompanied by colic; {1055} constipation, persistent or alternating with diarrhoea--in the one case in hard lumps with more or less mucus adherent, in the other soft or liquid, and in both cases having a rather golden-yellow color, grayish or black and tar-like appearance,--such are the symptoms referable to the intestinal canal. The disturbances in the hepatic functions produced by the catarrhal swelling of the mucous membrane of the ducts are further exhibited in a somewhat sallow, earthy, or muddy complexion, yellowish tint of the conjunctiva, high-colored, acid urine loaded with urates and phosphates. Such subjects, although having, it may be, a keen appetite, rather lose than gain in weight: they experience lassitude, headache, much depression of spirits, and the mental symptoms are most pronounced during the time intestinal digestion is going on. In fact, the morbid complexus is rather that of intestinal catarrh; nevertheless, the slight degree of obstruction to the outflow of bile occurring in these cases has an influence both in the intestinal digestion and in the nutritive functions. Any degree of obstruction, as has already been pointed out, leads to serious structural change of the liver, and this in turn produces well-defined symptoms.

Disturbances of the hepatic functions, even jaundice, accompany the paroxysms of malarial fever. Without the occurrence of fever, catarrhal jaundice may come on during the course of chronic malarial poisoning. Catarrh of the bile-ducts is the pathogenetic factor in these cases. More especially in malarial regions, but also in temperate and warm climates, paroxysmal attacks, with or without jaundice, are comparatively frequent. These acute seizures occur in those having the chronic form of the malady, and are excited by sudden climatic changes, by excesses in eating, especially by the use of improper articles of diet. Considerable nausea, flatulence, and constipation or diarrhoea, weight, tension, and soreness in the right hypochondrium and sometimes in the shoulder, chilliness, general malaise, headache, and an increasing icterode tint of the skin, constitute the complexus of symptoms belonging to these cases.

COURSE, DURATION, AND TERMINATION.--Acute catarrh of the bile-ducts with jaundice has a well-defined course--in its mildest form, with little gastric or gastro-intestinal disturbance--lasting ten days or two weeks; in the ordinary form, with the accompanying gastro-duodenal catarrh, running its course in a month to six weeks. In the chronic form, with acute exacerbations due to indiscretions in diet or to climatic influences, the course of the disease is chequered by vicissitudes, the result of the causes just mentioned, and its duration must therefore be indefinite and, as a rule, protracted. Catarrh of the bile-ducts, or catarrhal jaundice, usually terminates in health after a period of functional derangement of the intestines and liver. Without exhibiting any features of a special character, some cases do not pass through this benign course: the intestinal catarrh sets up an ulcerative process at one or more points in the duodenum; but more especially the obstruction to the free course of the bile caused by the catarrhal swelling of the mucous lining of the ducts induces structural changes in the liver--an hypertrophy of the connective-tissue elements, a sclerosis.

DIAGNOSIS.--There are but two signs which indicate the nature of the disorder, and only one that is really distinctive. Intestinal indigestion with slight coincident biliary derangement is one, and jaundice is the {1056} other. When, after the signs and symptoms of gastro-duodenal catarrh have declared themselves, jaundice appears, there can be no question as to the nature of the case. The diagnosis is more difficult in the chronic cases with exacerbations due to the exciting causes above mentioned, for the persistence of the jaundice will suggest the occurrence of some permanent organic lesion. The differentiation of the various kinds of jaundice has already been made.

TREATMENT.--Regulation of the diet is of the first importance. Those foods requiring the intestinal juices for their solution and absorption, and which cannot be properly digested when a duodenal catarrh exists or when bile is absent, should of course be excluded from the diet. These articles are the fats, starches, and sweets. The mucus playing the part of a ferment, these substances are converted into various secondary products of an irritating character. Flatulence is caused by the evolution of carbonic acid gas and the hydrogen compounds of sulphur and phosphorus; and acetic, butyric, and other acids not only change the reaction of the intestinal juices, but are directly irritating to the mucous membrane. In the acute cases a diet of skimmed milk, taken hot and at three hours' interval, and after the acute symptoms have subsided, in conjunction with some other aliment, is the most appropriate mode of alimentation. Meats, fish, eggs, and oysters are the chief articles of diet, besides the milk, during the whole course of the more chronic cases; and to these may be added the succulent vegetables, as lettuce, spinach, celery, raw cabbage, and tomatoes. If, in consequence of irritability of the mucous membrane or of idiosyncrasy, any article occasions distress, it should be omitted from the diet.

The medicinal management includes the administration of remedies for gastro-intestinal catarrh. The treatment of catarrhal jaundice has been discussed. When constipation exists, saline laxatives, especially phosphate of sodium and Rochelle salt, are useful. If there be diarrhoea, the most appropriate remedies are bismuth, with or without carbolic acid, Hope's mixture, oxides of zinc and silver, and other mineral tonic astringents.

The propriety of the administration of special hepatic stimulants--cholagogues--has been much disputed. When the disorder consists merely in an obstruction to the outflow of bile, the utility of stimulating the production of this secretion seems more than doubtful. Much harm has been done by the indiscriminate use of mercury. Its power to increase the production of bile having been assumed, and the quantity of bile present in the feces being manifestly less in cases of catarrhal jaundice, it followed that mercury should be employed in this disorder. Modern experience has quite demonstrated its inutility in the mode and for the purpose to which it was formerly devoted. Nevertheless, good effects are had from calomel in small doses as a sedative to the mucous membrane. When there are nausea, headache, vertigo, and constipation present, excellent results may be had from the 1/20 gr. to 1/10 gr. of calomel, exhibited at short intervals until the bowels are moved. If calomel possessed the property formerly ascribed to it, of stimulating the hepatic functions, it would be contraindicated in catarrh of the bile-ducts. This contraindication exists in respect to all hepatic stimulants.

If there be decided irritability of the stomach and constipation, {1057} Seidlitz powders may be given at regular intervals. Phosphate of sodium in drachm doses is highly useful for the double purpose of a laxative effect and to prevent the tendency to inspissation of the bile, which is one of the most important results of catarrh of the bile-ducts and gall-bladder. In the more chronic cases the persistent use of sodium phosphate is to be highly commended.

In this disease, especially as it occurs in gouty subjects, sulphate of manganese is often decidedly serviceable. If anæmia and debility coexist, this remedy can be combined with sulphate of iron and sulphate of quinine--a combination which the writer has found peculiarly effective under such circumstances. When oxidation is deficient and the urates are present in the urine in excessive quantity, good effects are had from the permanganate of potassium, a tablet containing two grains being given four times a day. In the more chronic cases the salts of silver, copper, and zinc are really very useful, especially the oxides of silver and zinc; and of these the former is more efficient. Better than any of those mentioned is arsenic, as arseniate of sodium or as Fowler's solution, but the best results are had from small or medium doses persistently used. If there be much intestinal catarrh and consequent diarrhoea, bismuth and aromatic powder, oxide of silver, Fowler's solution with a little opium, Hope's mixture, etc. are appropriate remedies.

It is in catarrh of the bile-ducts that nitric and nitro-muriatic acids have proved useful, rather than in cirrhosis and other diseases of the liver-tissues. They prevent fermentation, promote oxidation, and increase the activity of the assimilative functions. When there occurs active fermentation of certain foods, and consequently considerable flatulence, excellent results are obtained from the members of the antiseptic group--from creasote or carbolic acid, salicylic acid, biborate of sodium, the benzoates, etc. To these may be added quinine, the dose of which will be determined by the purpose for which it is prescribed. So often is catarrhal jaundice of malarial origin that quinine becomes a remedy of high importance in the cases occurring in the malarial-forming zone.

Certain special plans of treatment have been proposed for the cure of catarrhal jaundice. One of the most effective of these is enemata of cold water. By means of an irrigating apparatus the large intestine is well distended with water once a day for several days. The first enema has a temperature of 60° F., and subsequent injections are a little warmer. The increased peristalsis of the bowels and the reflex contractions of the gall-bladder dislodge the mucus lining and obstructing the gall-ducts. When the bile flows into the intestine, digestion is resumed and the catarrhal inflammation subsides. But with the irrigation method may be employed other remedies, as above indicated.

Faradization of the gall-bladder has been used successfully for the expulsion of the stored-up bile and the removal of the mucus obstructing the ducts. It is applied by means of one moistened sponge electrode placed directly over the gall-bladder, and the other on the opposite side of the body and posteriorly. A slowly-interrupted faradic current is then passed. This expedient is not suitable when the case is acute in character.

{1058} Biliary Concretions; Gall-Stones; Hepatic Calculi; Hepatic Colic.

DEFINITION.--There are two classes of concretions which may occasion symptoms: inspissated bile and regularly-formed gall-stones. Slowly-developing symptoms of jaundice from obstruction may arise from the deposit of particles of inspissated bile in the hepatic ducts, or sudden attacks of hepatic colic be due to the passage of concretions. When biliary calculi reach the intestines, certain kinds of disturbance may be caused by their presence there. Under the term biliary concretions must be considered, therefore, the mechanism of their production, their composition, the symptoms caused by their passage through the ducts (hepatic colic), and the intestinal disturbance due to their retention in the bowel.

Formation: Inspissated Bile.--Those concretions consisting of inspissated bile are irregularly-shaped masses of a brownish, greenish-brown, or reddish-brown color, friable and crumbling into a gritty dust with slight pressure of the fingers. When recent and before drying, they are softer, almost pultaceous, and may take the form of the canal through which pressed. But as seen after drying they present the appearance of a dark vegetable extract, dried and partly pulverized. When examined as found in the gall-bladder or lodged in the larger hepatic ducts or distributed in irregular fragments (gall-sand) in the various hepatic passages, they present the shape, color, and general characteristics of a partly-dried vegetable extract roughly broken up, but still soft enough to take any shape from pressure. The writer has seen them thus in situ accompanying regularly-formed gall-stones in a case of gunshot wound of the liver. These masses of inspissated bile differ from gall-stones in composition; they consist of bile, but with a preponderance of the coloring matter. According to Harley,[153] who has given a more correct account of these bodies than any other systematic writer, their composition is as follows:

Water 5.4 Solids 94.6

The contents of the solids are--

Bile-pigment 84.2 Cholesterin 0.6 Salts (iron, potash, soda) 15.2

[Footnote 153: The Diseases of the Liver, with and without Jaundice, etc., by George Harley, M.D., F.R.S., Philada., 1883, p. 349.]

Some years ago, before I was aware of the nature of such concretions. I detected a number in examining the stools of a patient who had in quick succession many attacks of hepatic colic, but as the usual form of concretion was looked for and not found, the relation of these bodies to the symptoms in the case was not understood. I now recognize the value of Harley's observations on these bodies.

The biliary concretion which is properly a gall-stone has a definite form and a more or less well-defined crystalline structure. The forms taken are various. The most usual form is octagonal or hexagonal or polyangular, with smooth facets, corresponding to points of contact of other calculi. Instead of smooth facets and sharp angles, the concretion may be studded with irregularly-shaped masses. When there are numerous {1059} calculi present, they have smooth surfaces and rather sharp angles, made, not by attrition, as has been supposed, but by deposition of the new material under pressure. When they have this form there are many present, but the number of facets does not indicate the number of calculi, and the absence of facets is not proof of the absence of other calculi. The smooth opposing surfaces are not always plane, but may be convex or concave to fit the shape of the adjacent bodies.

Calculi may be globular, ovoid, cylindrical, and truncated cones. The largest in my collection is egg-shaped, and nearly filled the gall-bladder which contained it, a little mucus free from bile-elements only being present. If a concretion forms in a duct or a single one is present in the gall-bladder, the shape is determined by the pressure of the walls of the duct or of the gall-bladder, respectively. As found in the stools, and still somewhat soft, the shape will represent the form of the common duct through which it has been pressed. Such a soft, recently-formed gall-stone will have the crystalline structure and chemical constitution of these bodies, and will therefore differ from, apparently, similar masses of inspissated bile. Although a round, ovoid, or cylindrical calculus indicates the absence of others because there are no evidences of mutual pressure and adaptation, a positive conclusion cannot be reached in that way, for the gall-bladder may contain numerous calculi of long-standing, and a recent concretion formed in a duct be discharged with the usual symptoms.

The number of calculi which may be present at any time or be produced in the course of years ranges from one to several thousand. The number is in inverse ratio to the size. One case[154] is reported in which 7802 calculi were found in the gall-bladder, but they must have been very minute in size. Of the specimens now in my collection, there are 230 obtained from one gall-bladder, which they entirely filled; they are nearly uniform in size, have an average weight of two grains, and contain four, five, and six smooth facets. Another collection of calculi removed from a closed gall-bladder contains 45, of large size, distending the organ and forming a tumor which projected beyond the margin of the liver. Hepatic calculi are rarely solitary; hence if one attack of hepatic colic occur, others may be expected.

[Footnote 154: Frerichs, op. cit., vol. ii. p. 499.]

In color gall-stones vary from a clear white to a dark-brown, almost black, tint. The most usual tint of the mature calculi in the gall-bladder is that of the ripe chestnut. Long stay in the intestines increases the depth of the color, until it becomes almost black; on the other hand, detention in the gall-bladder has a slightly bleaching action; but the real cause of difference of color is the presence or absence of pigment. If composed of pure cholesterin, the color will be whitish, opaque, or glistening and almost translucent.

In size gall-stones vary from the smallest pea up to a hen's egg. When several hundreds are contained in the gall-bladder, they will usually be of the dimension of a medium-sized pea. Two large solitary concretions in my possession are respectively 2 inches and 1½ inches in long diameter, and 1 inch and ¾ of an inch transversely. Very much larger calculi have, however, been recorded; thus, one mentioned by Frerichs is 5 inches in length and 4 inches in circumference. The most frequently {1060} encountered calculus, at least in this country, is polyangular in shape and of the size of a large pea. Globular or ovoid seems to be the prevailing form, and the dimensions that of a small pea, in Germany, according to Frerichs and Von Schüppel, but this statement must refer to the initial shape of these bodies.

Not all hepatic calculi have defined mathematical forms, but may consist of branching cylinders composed of irregular nodular masses, not unlike the concretions of inspissated bile. As a rule, in each case where the calculi are multiple there is uniformity of color, shape, and composition. This feature is well exhibited in my collection. The calculi obtained from each subject are in one case white, polyangular, rather unctuous, and nearly equal in size; in another, chestnut-brown in color, polyangular in shape, and varying slightly in size, but uniformly characteristic in shape; and in a third, singular in number, ovoid in shape, dark-brown in color.

In composition gall-stones vary somewhat. When fresh they contain considerable water, and at all times are hygroscopic. Dried in the air, they are composed of--

Water 4 Solids 96 --- 100

The solids consist of--

Cholesterin 98 Pigment 1 Inorganic or mineral matter 1 --- 100

Such are the constituents, according to Harley, of the usual concretion, the cholesterin calculus. But as other varieties are encountered occasionally, it may be well to give the composition of these. The following table by Ritter, to be found in Robin's Journal for 1872 (p. 60), is a correct representation of the contents of different specimens:

---------------+------+------+------+------+------+------+------+----- Composition | | | | | | | | of Different | | | | | | | | Kinds. | 1st. | 2d. | 3d. | 4th. | 5th. | 6th. | 7th. | 8th. ---------------+------+------+------+------+------+------+------+----- Cholesterin | 98.1 | 97.4 | 70.6 | 64.2 | 81.4 | 84.3 |trace.| 0 Organic | | | | | | | | matter | 1.5 | 2.1 | 22.9 | 27.4 | 15.4 | 12.4 | 75.2 | 18.1 Inorganic | | | | | | | | matter | 0.4 | 0.5 | 6.5 | 8.4 | 3.2 | 3.3 | 24.8 | 91.9 Number of | | | | | | | | specimens | 28 | 16 | 580 | 94 | 220 | 16 | 3 | 1 ---------------+------+------+------+------+------+------+------+-----

The above may be regarded as the average composition, expressed in round numbers. The variations from these figures will be comprehended in two parts.

A calculus consists of three several parts: the nucleus, the body, the rind. A calculus of small or medium size may be a nucleus for the formation of a large one. Usually the nucleus consists of a bit of mucus, casts of the biliary ducts (Thudicum), inspissated bile, a blood-clot, a liver-fluke or other parasite, as a desiccated round-worm, or some foreign body, as a seed, or, as in one reported example, a globule of mercury.[155] {1061} The central mass of mucus may contain a large proportion of pigment or crystals of cholesterin or lime-salts, giving it special characteristics.[156] There may be several nuclei. Fauconneau-Dufresne reports an instance in which a pyramidal concretion contained four, and Guilbert a globular stone with five, distinct nuclei. Such examples of calculi having multiple nuclei are produced by the adhesion whilst in a soft state of two or more, and the subsequent addition of material to the conjoint mass, welding it into a single stone. A few calculi are homogeneous throughout, composed of nearly pure cholesterin, mixed intimately with a little coloring matter and lime salts. The cholesterin calculus will have a somewhat translucent appearance, will be a dead white or a yellowish-white, or present a greenish- or brownish-yellow tint through the white. Even the white calculus, apparently composed of nearly pure cholesterin, will be found on section to contain traces of a nucleus. By long detention in a gall-bladder whose duct is permanently occluded, and is therefore free of fluid, the mucus nucleus may so shrivel as to leave a cavity which is merely stained. One of my specimens--a solitary calculus of large size--exhibits this peculiarity.

[Footnote 155: Thudicum, J. L., On Gall-stones, London, 1863; also Frerichs, op. cit., vol. ii. p. 503.]

[Footnote 156: Cyr, Jules, Traité de l'Affection calculeuse du Foie, Paris, 1884, p. 11 et seq.]

The body consists of cholesterin, nacreous or darkened by pigment, deposited in radiating lines or in concentric layers, or in both together. Pigment may be intimately incorporated with the cholesterin or deposited between the layers of this substance, pure or nearly pure, forming an alternating arrangement.

The crust or rind usually is smooth, unctuous to the touch, firm, but when broken with the finger-nail readily crumbles. When composed of lime salts, or when the cholesterin is mixed with varying proportions of these salts and of pigment, the surface is still smooth, but thicker, firmer, and darker in color. The rind may not be smooth, but studded with wart-like projections, or it may consist of several layers of earthy matter separated by pigment. These layers may be very friable, and readily crumble and fall off. In some instances the crust, several lines in thickness, is the body of the calculus, and the cavity contains only a light honeycomb of mucus and pigment.

The specific gravity of gall-stones composed of crystallized cholesterin is nearly that of water. Air-dried calculi will float on water, but the recent ones, full of moisture, sink. The relation of the weight of the calculus to that of the bile is more important. As the specific gravity of bile ranges from 1020 to 1026, it is obvious that on this fluid air-dried calculi will float, but, holding in the recent state much water, ordinary gall-stones will sink. Those containing much mineral matter will have a correspondingly high specific gravity--much higher than bile.

ORIGIN AND FORMATION OF HEPATIC CALCULI.--Certain conditions are necessary to the formation of these bodies on the part of the bile and on the part of the gall-bladder and ducts. Constituted for the most part of cholesterin, which exists in such small quantity in normal bile, there must be some change in the composition of this fluid to increase the quantity or to diminish the solubility of that constituent. It will conduce to a better understanding of the subject to premise the composition of the bile: {1062}

Bile contains, in 1000 parts, Water 860 Solids 140

The solids of bile are, Glycocholate and Taurocholate of soda 90.8 Fat 9.2 Cholesterin 2.6 Mucus 1.4 Pigment and extractive 28. Salts 8. ----- 140.

Normal bile is neutral or slightly alkaline in reaction. If the reaction become acid from any cause, the constituent cholesterin is precipitated; and this occurs the more readily the larger the proportion of this substance held in solution. Cholesterin is an excrementitious material found in the blood and excreted by the liver. It represents in part, probably, the waste of nervous matter, but more certainly of the fatty tissues in general. Conditions of the system in which the metamorphosis of the fatty elements occurs more freely--as obesity, advancing life, etc.--are accompanied by an increased production and excretion of cholesterin.

So long as the neutral state or the alkalinity of the bile is maintained, the cholesterin will be kept in solution, although its relative proportion may be in excess of the normal. A lack of the soda constituent of the system is one factor, but the most important is a catarrhal state of the mucous membrane of the bile-ducts and gall-bladder. The mucus formed plays a double rôle: it furnishes a nucleus about which cholesterin crystallizes; it acts as a ferment and inaugurates a process of acid fermentation which results in the precipitation of cholesterin. When all the conditions favorable to the separation and crystallization of cholesterin are present, any foreign body may serve the purpose of a nucleus. The articles which have thus served have been enumerated.

A by no means infrequent combination is that of bilirubin with calcium; and this may constitute the nucleus or form a part of the body or the crust of a calculus. The mechanism of its formation is not unlike that of the cholesterin concretion. Bilirubin is soluble in alkalies, and is precipitated from its solution by acids. It follows that when acid fermentation takes places under the influence of mucus, bilirubin may be precipitated in combination with calcium. The salts of sodium and potassium are much more abundant in bile than those of lime, but the latter much more often enter into the formation of calculi because of their slighter solubility. Other combinations of bile-pigments, mucus, and the salts of the bile take place, but they are relatively less frequent. The principal lime salt is the carbonate, and this combines in varying proportions with the bile acids, the fat acids, and bile-pigment.

Certain physical conditions are not less important than the chemical in the production of hepatic calculi. Accumulation of bile in the gall-bladder, stasis, and concentration are essential conditions. If bile remains long in the gall-bladder, it becomes darker in color and more viscid, its specific gravity rises, and the relative proportion of solids increases, doubtless because of the absorption of a part of the water. The reaction--which, as has been stated, is in the fresh state neutral or {1063} alkaline--becomes acid in consequence of a fermentative change (Von Gorup-Besanez) set up by the mucus. If a catarrhal state of the mucous membrane exist, the mucus, epithelium, and lymphoid cells cast off play the part of a ferment. The lime which is so important a constituent of biliary concretions is not present even in concentrated bile in sufficient amount to account for its agency in the formation of these bodies, is furnished by the diseased mucous membrane (Frerichs). Indeed, numerous crystals of carbonate of lime have been seen in situ in contact with the mucous membrane in cases of chronic catarrh. It follows, then, that catarrh of the biliary passages has an important causative relation to that pathological condition of the bile which precedes the formation of calculi. In this connection we must not lose sight of the researches made by Ord[157] on the action exerted by colloids on the formation of concretions. The mucus is the colloid; cholesterin, lime, and soda salts are the crystalloids. These latter diffusing through the colloid medium, the resulting combinations assume spheroidal forms. The union of bilirubin and lime salts illustrates the same principle.

[Footnote 157: On the Influence of Colloids upon Crystalline Forms and Cohesion, with Observations on the Structure and Mode of Formation of Urinary and other Calculi, by W. Miller Ord, M.D., F.R.C.P. Lond., etc., London, 1879.]

CAUSES.--We have here to consider the external conditions and the general somatic influences which lead to the formation of biliary concretions. Age has an important causative action. Besides other agencies due to advancing life, the increase of cholesterin is an influential factor. The less active state of the functions in general, diminished oxidation, loss of water, and concentration of the bile are influential factors in determining the formation of hepatic calculi in advancing life, as the opposite conditions oppose their production in early life. Although not unknown in infancy, at this period in life and until twenty years of age they occur but rarely. Fauconneau-Dufresne,[158] of 91 cases, had 4 in infants; Wolff[159] had 1 in a collection of 45 cases; and Cyr,[160] 2 cases under ten in a group of 558 cases. The following table illustrates the influence of age on the productivity of gall-stones:

AUTHORS.

HEIN. Whole No. 395 From infancy to 30 18 From 30-70 377

FAUCONNEAU-DUFRESNE. Whole No. 91 Before 20 10 From 20-40 13 From 40-90 68

WOLFF. Whole No. 45 Before 20 3 From 30-60 42

DURAND-FARDEL. Whole No. 230 Before 20 2 From 20-30 28 From 30-60 162 From 60-90 38

CYR. Whole No. 558 Before 20 20 From 21-30 208 From 31-40 185 From 41-50 91 From 51-60 48 Above 60 6

[Footnote 158: Traité de l'Affection calculeuse du Foie, Paris, 1851.]

[Footnote 159: Virchow's Archiv f. path. Anat., etc., Band xx., 1861, p. 1.]

[Footnote 160: Traité de l'Affection calculeuse du Foie, Paris, 1884, p. 53.]

Although there is a general correspondence in the results of the observations on the age most liable, there are differences. Thus, Cyr, whose figures represent the experiences at Vichy, makes the age of maximum liability from twenty to forty years--distinctly earlier than any other observer; and hence it is necessary to bear in mind the extreme latitude of his diagnosis. Of my own collection, 30 in number, all doubtful cases {1064} excluded, there were 20 between thirty and fifty years, and 10 between fifty and seventy. Of these, 22 occurred in subjects between forty and sixty. The period of maximum liability is about fifty years of age. Cyr refers the difference of his statistics from those of other observers to the character of the patients. The preponderance in the number of cases of hepatic calculi at or about the fiftieth year is referable to the lessened activity of the nutritive functions at this period, and to the increase in the relative proportion of cholesterin in the blood in advanced life (Luton[161]). Charcot[162] maintains that after sixty biliary calculi are more frequent, but owing to the physiological conditions then existing the migration of these bodies is effected without notable inconvenience.

[Footnote 161: Jaccoud's Dictionnaire encyclopéd., art. "Voies Biliaires;" idem., Bull. gén. de Thérap., March 15, 1866.]

[Footnote 162: Leçons sur les Maladies du Foie, etc., p. 145.]

According to most authorities, females are more liable to the formation of gall-stones than are men. Thudicum, after an analysis of the statistics given by the most experienced and celebrated authorities, places the proportion at 3 to 2. Von Schüppel gives the same figures. Cyr, whilst recognizing this estimate as true of the great mass of observations on this point, finds that in his own cases the preponderance of females over males was even greater, being 4 to 1--inversely to the liability of the sexes to gout; but this excess is to be explained by the character of the subjects falling under his observation. Women are subjected to influences which favor the formation of these concretions, such as pregnancy, sedentary habits, diet of a restricted character, the use of corsets, and the somatic changes at the climacteric period.

The social state, by reason of the conditions associated with a good position in life, has an influence in the production of calculi. Luxurious habits and indulgence in the pleasures of the table are important factors, and hence this malady is encountered amongst the better class of patients in private practice rather than amongst laboring people in the hospitals.

As the somatic conditions which exert a predisposing action, and the social circumstances also favoring the formation of hepatic calculi, are transmitted, heredity is by some classed among the etiological factors, but it can only be regarded as indirect.

Malarial influences unquestionably exert a very powerful influence as this malady occurs in this country. Paroxysms of intermittent either induce or accompany the seizures of hepatic colic, and chronic malarial poisoning exerts a direct causative influence through the hepatic disturbances and the gastro-duodenal catarrh which are associated with it. Attacks of hepatic colic are extremely frequent in the malarial regions of the West and South. It may be, however, that this malady is frequent rather in consequence of the diet of pork than of climatic causes, for it is probable that indulgence in such food plays an important part in the formation of biliary concretions (Harley). Due allowance made for diet, climate is yet, no doubt, an influential factor. In warm, especially in malarial, regions the functions of the liver are taxed to compensate for the increased action of the skin and lungs; but this organ is, besides, affected by the poison of malaria, and to the congestion caused by it is superadded a catarrhal state of the bile-ducts and of the duodenum. A {1065} pathological condition of the bile itself is first induced; then the fermentative changes set up by the mucus cause the separation and crystallization of pigment and cholesterin.

Certain seasons favor the formation of biliary concretions, because then the special influences which operate at all times are more active and persistent. These seasons are fall, winter, and early spring, and gall-stones are more numerous then in consequence of the activity of the malarial poison, the character of the diet then employed, and the lessened oxidation due to the more sedentary life. Climate is a factor of some consequence, but not in the direction that might have been supposed. Gall-stones are more common in temperate than in tropical climates--a statement confirmed by the observation of the physicians of India. They are, according to Harley, quite common in Russia, where also they attain to extraordinary dimensions; but these circumstances are not due to the climatic peculiarities of that country, so much as to the diet habitually consumed, consisting so largely of fatty substances.

Of all the conditions which favor the production of gall-stones, none are so influential as the bodily state and the associated dietetic peculiarities. Those troubled with these concretions, as they have occurred under my observation, have been either obese or have had a manifest tendency in that direction. They have had a strong inclination for the fat-forming foods, also for starchy, saccharine, and fatty articles, such as bread and butter, potatoes, beans and peas, pork, bacon, and fat poultry, etc. Harley thinks indulgence in bacon (p. 367) is a prime factor. Thudicum rejects this notion on chemical grounds, for obesity and the free consumption of fat cannot be concerned in the production of these bodies, because cholesterin is an alcohol.[163] The agency of a fatty diet has been so strongly indicated in clinical observations, and the relation of cholesterin to the fats so obvious, that it can hardly be doubted the free consumption of fat in food contributes directly to the formation of calculi. An indirect relation may also be traced. A catarrhal state of the duodenal mucous membrane existing, and the bile excluded by swelling and obstruction of the bile-ducts, fats are decomposed, and the fat acids, absorbed into the portal blood, contribute to those chemical changes in the bile which result in the precipitation of cholesterin. Beneke[164] traces a connection between atheromatous degeneration of the vessels and the formation of biliary concretions. A general increase in the amount of fat in the body is usually coincident with the atheromatous change, and at the same time the relative proportion of cholesterin in the bile becomes greater.

[Footnote 163: A Treatise on Gall-stones, p. 214.]

[Footnote 164: Deut. Archiv für klin. Med., Band xviii.]

Indulgence in the starchy and saccharine foods plays a part in the formation of gall-stones not less, if not more, important than the consumption of fats. A diet of such materials is highly fattening, and if the necessary local conditions exist they readily undergo fermentation, and thus cause or keep up a catarrh of the mucous membrane.

Too long intervals between meals, Frerichs[165] thinks, is more influential than errors of diet in causing concretions. The bile accumulates in the gall-bladder, and the condition of repose favors the occurrence of those changes which induce the separation and crystallization of cholesterin. {1066} Obstacles to outflow of every kind have the same effect. The largest calculus in my possession was obtained from a case of cancer of the gall-bladder which compressed, and finally closed, the cystic duct. Sedentary habits have the same mechanical effect, but, as already pointed out, insufficient air and exercise act by lessening oxidation. Corpulent persons indulging in rich food and avoiding all physical exertion, those of such habits confined to bed by illness or injury, the literary, the well-to-do, self-indulgent, lazy, are usual subjects of this malady. Any condition of things which causes a considerable retardation in the outflow of bile will have a pathogenetic importance, especially if the causes of chemical change, the lessened quantity of taurocholic and glycocholic acid, and an increased quantity of cholesterin, coexist. Moral causes, as fear, anxiety, chagrin, anger, etc., have seemed to exercise a causative influence in some instances (Cyr).

[Footnote 165: A Clinical Treatise on Disease of the Liver, Syd. Soc. ed., vol. ii. p. 511.]

To the causes of retardation of the bile-flow mentioned above must be added catarrh of the bile-ducts. This acts in a twofold way--as an obstruction; a plug of mucus forming the nucleus. It has already been shown that fermentative changes may be set up by the mucus, which plays the part of a ferment, an acid state of the bile resulting.

Situation of Gall-stones, and their Destiny.--The gall-bladder is, of course, the chief site for these bodies, but biliary concretions and masses of inspissated bile may be found at any point in the course of the ducts. Single stones may be impacted at any point in the cystic, hepatic, or common duct, or masses composed of numerous small calculi may take the form of a duct and branches, making a branching calculus of the shape and size of the mould in which it is cast. Such casts may be hollow, thus permitting an outlet to the bile, or they may completely close the tube, and a cyst form, the walls of which grow thicker with connective-tissue deposits. Stones of very large size may be thus enclosed, Frerichs having seen one the size of a hen's egg formed about a plum-seed, which was the nucleus. In some rare instances the major part of the larger tubes have been filled with inspissated bile, through which the fluid bile could only be slowly filtered.

Calculi are not often found in the hepatic duct, since they can only lodge there in descending from the smaller tubes, and hence are too small to become wedged in. The usual site, as has been sufficiently explained, is the gall-bladder. At the entrance to the cystic duct and at the terminus of the common duct in the duodenum are the points where migrating calculi are most apt to be arrested.

Spontaneous disintegration of gall-stones sometimes occurs. Cholesterin being dissolved off of the corners and edges, the cohesion of the mass is impaired and it falls apart in several fragments. By very slight mechanical injury air-dried calculi will be broken up. In the gall-bladder two factors are in operation to effect the disintegration of the contained calculi: the movements of the body, by which the corners and the borders are crumbled; the solvent action of the alkaline bile on the cholesterin. When, however, these concretions are made up of lime and pigment, their integrity can be impaired only by the process of cleavage; no solvent action can take place.

Various changes occur in the ducts or in the gall-bladder in consequence of the presence of these concretions. Whilst a catarrhal state of the mucous {1067} membrane of the ducts is an element of much importance in the process by which concretions are formed, on the other hand the presence of these bodies excites catarrh, ulceration, perforation, and, it may be, abscess of the liver. When concretions form or are deposited in the ducts, they cause inflammatory reaction, the walls yield, and the neighboring hepatic structures may also be affected by contiguity. The dilatation of the tube is usually cylindrical, much more rarely sacciform. The neighboring connective tissue may undergo hyperplasia and a more or less extensive sclerosis occur. More frequently the calculus ulcerates through, and an abscess is produced which will take the usual course of that malady. Very rarely a calculus is found enclosed in a separate sac and surrounded by healthy hepatic tissue (Roller).[166]

[Footnote 166: Berliner klin. Wochensch., No. 42, 1879; ibid., Nos. 16, 17, and 19 for 1877, Fargstein.]

As the gall-bladder is the usual place for the formation and storage of gall-stones, the changes in connection with this organ are the most important. The calculi may be so numerous or so large as to distend the gall-bladder and cause it to project from under the inferior border of the liver, so as to be felt by palpation of the abdominal wall. The stones may be few in number and float in healthy bile, or they may fill the bladder to the exclusion of fluid, the cystic duct being closed permanently; or there may be, with one or more concretions, a fluid composed of mucus, muco-pus, serum, and bilious matter. The mucous membrane may be in a normal state, but this is rare; usually it is affected by the catarrhal process, and atrophic degeneration has taken place to a less or greater extent; the rugæ are obliterated, the muscular layer hypertrophied. When attacks of hepatic colic have occurred, more or less inflammation of the peritoneal layer of the gall-bladder and cystic duct is lighted up, and organized exudations form, changing the shape and position of the organs concerned. It is usual in old cases of hepatic colic to find the gall-bladder bound down by strong adhesions, the cavity much contracted or even obliterated, the cystic duct closed, and the neighboring portion of the liver the seat of sclerosis. Such inflammatory exudations about the gall-bladder may become the seat of malignant disease--of scirrhus. Several examples of this have been reported, and one has occurred in my own practice.

The contact of a gall-stone, especially of a polyangular stone, may cause ulceration of the mucous membrane. This is the more apt to occur if the muscular layer of the gall-bladder is hypertrophied, especially if certain fasciculi are thickened and overacting, leaving intervening parts weak and yielding to the pressure of the stone forced in by the spasmodically contracting muscles. Finally yielding, the stone and other contents of the gall-bladder escape into the cavity of the abdomen. Adhesions to neighboring parts may prevent rupture. Such adhesions are contracted with the colon, the duodenum, the stomach, and other organs. In some rare instances the closed gall-bladder has undergone a gradual process of calcification, the mucous membrane losing its proper structure, the muscular layer degenerating, and a slow deposit of lime salts taking place, the ultimate result being that the biliary concretions are enclosed in a permanent shell.

As above indicated, biliary concretions may remain where deposited for an indefinite period. Very often they migrate from the point of formation, the gall-bladder, into the duodenum, producing characteristic {1068} symptoms called hepatic colic. As the size of the ducts increases from above downward, obviously but little vis a tergo is needed to propel the concretions onward. The chief agency in the migration of these bodies is the discharge of bile. Common observation shows that the symptoms of hepatic colic usually declare themselves in two or three hours after a meal--at that time when the presence of the chyme in the duodenum solicits the flow of bile. The gall-bladder contracts on its contents with an energy in direct ratio to the amount of bile present, and with the gush of fluid the concretion is whirled into the duct. Once there, the cystic duct being unprovided with muscular fibres, the onward progress of the stone must depend on the flow of bile; and, as the canal is devious, this may not always carry the concretion into the common duct. Just behind the neck of the gall-bladder the duct makes an angle somewhat abrupt, and here also its folds project into the canal, so that at this point the stone is apt to lodge; but much depends on the size and shape of the calculus. If it pass through the cystic duct, the inflammation resulting may close the canal, several instances of which have fallen under my observation. The next point where stoppage of the migrating calculus may, and frequently does, occur is the orifice of the common duct in the duodenum. This orifice has a funnel shape, the smaller extremity toward the intestine, the object of this being to prevent the entrance into the duct of foreign bodies from the intestine. A diverticulum is thereby made (Vater's) in which a concretion may lodge, partly or wholly preventing the escape of bile into the bowel. The various forces concerned in the propulsion of the concretion onward from the common duct into the intestine are the discharges of bile, the contraction of the few muscular fibres in the walls of the duct, the respiratory movements, especially forced expiration, coughing, sneezing, vomiting, defecation--in fact, all of those acts in which the abdominal muscles, the diaphragm, and the sphincters are simultaneously brought into strong contraction. The symptoms produced by the migration and stoppage of a concretion will vary according to the size and shape of the stone, and the consequent diminution in the amount of bile discharged or its complete arrest. In other words, the stone may be firmly wedged in, completely closing the canal against the passage of bile, or it may lie loosely in the diverticulum Vateri, acting as a sort of ball valve, now permitting a gush of bile, and now stopping the passage-way more or less tightly.

The migration of calculi may take place by ulcerating through into neighboring hollow organs. Usually the first step consists in stoppage of the bile. To the accumulating bile mucus is added, and the gall-bladder or the duct--usually the common or cystic duct--dilates, often to a considerable extent, and, adhesions forming, discharge ultimately takes place through some neighboring hollow organ. The routes pursued by such fistulous communications are various. The organs most frequently penetrated are the stomach, duodenum, and colon, less often the urinary passages, and very rarely the portal vein. Numerous examples of external discharge of calculi have been reported. The most usual, as it is the most direct, is the fistulous connection of the gall-bladder or common duct with the duodenum. Solitary stones of immense size have been thus discharged. Murchison[167] gives references to many interesting {1069} examples, and the various volumes of Transactions of the Pathological Society are rich in illustrative cases. The symptoms produced by the migration of calculi by the natural route and by ulceration into other organs will be hereafter considered.

[Footnote 167: Clinical Lectures on the Diseases of the Liver, 2d ed., p. 487 et seq.]

SYMPTOMS DUE TO THE PRESENCE OF GALL-STONES AT THEIR ORIGINAL SITE.--Very large calculi or numerous small ones may be present in the biliary passages without causing any recognizable symptoms. The migration of these bodies by the natural channel and by ulceration into the duodenum may also be accomplished without any local or systemic disturbance.[168] That the retention of calculi may not induce any characteristic reaction by which they may be recognized is probably due to the fact that the gall-bladder, in which they chiefly form, possesses but slight sensibility, and as it is in a constantly changing state of distension or emptiness according to the amount of bile present, it is obvious that a foreign body made up of the biliary constituents, and having nearly the same specific gravity as the bile, is not likely to cause any uneasiness or recognizable functional disturbances. Furthermore, the slowness with which biliary concretions form enables the organ to accommodate itself to the new conditions. The lack of sensibility which is a feature of the gall-bladder, and which I have had the opportunity to ascertain by actual puncture in an individual not anæsthetized, is in some instances supported by a general state of lowered acuteness of perception. There are great differences in respect to readiness of appreciation and promptness of response to all kinds of excitation in different individuals. To what cause soever we may ascribe the lack of sensibility, the fact remains that in not a few cases of gall-stones in the gall-bladder there are no symptoms to indicate their presence. On the other hand, there are some disturbances that have a certain significance.

[Footnote 168: Amongst the numerous examples of this kind to be found recorded may be mentioned the case reported by M. L. Garnier, Agrégé à la Faculté de Médecine de Nancy (Archives de Physiologie normale et pathologique, No. 6, 1884, p. 176): An hepatic calculus, weighing 24.5 grammes, was discharged without any symptoms or even consciousness on the part of the patient, a man of sixty years. He had had colic and jaundice, but these subsided entirely, and there was no further disturbance. As has happened in so many instances, this stone must have ulcerated through into the bowel without causing any recognizable symptoms.]

The subjective signs are uneasiness--a deep-seated sensation of soreness--felt in the right hypochondrium, increased by taking a full inspiration and by decubitus on the left side. Pain or soreness, sometimes an acute pain, is experienced under the scapula near the angle, at or about the acromion process, and sometimes at the nape of the neck. In one case under my observation within the past year a patient who had had several attacks of hepatic colic, the usual polyangular stones having been recovered, had from time to time severe pain over the right side of the neck, shoulder, and scapula, accompanied by a severe herpes zoster in the district affected by the pain. This is of course an extreme example, but it is very suggestive of the relation which may exist between hepatic disturbances and shingles. Attacks of gastric pain coming on some time after food, and not soon after, as is the case in true gastralgia, are usual in the early stage of the disease--are constant, according to Cyr,[169] who quotes approvingly an observation of Leared on this point. Migraine {1070} or sick headache and vertigo occur in many cases, but it may well be doubted whether these symptoms are not due to the accompanying gastro-duodenal catarrh, which is a nearly constant symptom. Acidity, flatulence, epigastric oppression, a bitter taste, a muddy rather bilious complexion, and constipation are symptoms belonging to catarrh of the gastro-duodenal mucous membrane. Most of these symptoms are rather indefinite. Some additional information may be supplied by palpation. When the gall-bladder is distended with gall-stones, or is in the enlarged state which occurs when the common duct is obstructed, it may project beneath the inferior border of the liver far enough to be felt. In thin persons a grating sound, produced by the friction of the calculi, may be heard, the stethoscope being applied as palpation is made over the hypochondrium. It is rare that these symptoms can be elicited, since the calculous affection of the liver occurs for the most part in persons of full habit, in whom the abdominal walls are too thick to allow of the necessary manipulation. There may be also some tenderness on pressure along the inferior margin of the ribs, especially in the region of the gall-bladder.

[Footnote 169: Traité de l'Affection calculeuse du Foie, p. 71.]

SYMPTOMS DUE TO THE MIGRATION OF GALL-STONES BY THE NATURAL CHANNELS.--A calculus passing into the cystic duct from the gall-bladder causes the disturbance known as hepatic colic or bilious colic, because of the jaundice which accompanies the major part of these seizures. But jaundice is not a necessary element in these cases; it is not until the concretion reaches the common duct that the passage of bile into the intestine is interfered with. The gall-bladder has a function rather conservative than essential, for its duct may be permanently closed without apparently affecting the health.

The time when an attack of hepatic colic is most likely to occur would seem to be determined by the flow of bile; for this, as has been stated, is the chief factor in moving calculi along the ducts. As, no doubt, the presence of the chyme in the duodenum is the stimulus for the production of bile and also for the contractions of the gall-bladder, it follows that a few hours after meals is the time when the attacks of hepatic colic would a priori be expected. This is in accord with experience, but there are exceptions. In one of the most formidable cases with which the writer has had to deal--the diagnosis confirmed by the recovery of the calculi--the most severe attacks occurred in the early morning. According to Harley,[170] colic from the passage of inspissated bile occurs when the stomach and duodenum are most nearly empty--from ten at night until ten in the morning--and this he relies on as a means of diagnosis, but the exceptions are too numerous to assign much importance to this circumstance.

[Footnote 170: On Diseases of the Liver, p. 354.]

The onset of pain is usually sudden, but it may develop slowly from a vague uneasiness in the region of the gall-bladder; or after some pain and soreness at this point, accompanied by nausea, even vomiting, the paroxysm will begin with very acute pain. The situation of the pain is by no means constant, and usually varies in position in the same case. The point of maximum intensity is near the ensiform cartilage, outward and downward two or three inches, about the point of junction of the cystic and common duct. From or about this region the pain radiates through the epigastrium, the right hypochondrium, upward into the chest, {1071} backward under the scapula, and downward and inward toward the umbilicus. In some instances under my observation the most acute suffering was located in the right iliac region, in others in the lumbar region, and in still others in the epigastrium. The position of the pain may be such as to draw attention from the liver, and thus greatly confuse the diagnosis. In a well-defined attack the pain is intense, shooting, and boring, irregularly paroxysmal; the patient writhes in agony, screams and groans, rolls from side to side, or walks partly bent, holding the part with a gentle pressure or rubbing with an agonized tension of feeling. Meanwhile the countenance is expressive of the intensest suffering, is pallid and drawn, and the body is covered with a cold sweat. Nausea presently supervenes, and with the efforts to vomit a keen thrust of pain and a sense of cramp dart through the epigastrium and side. Very considerable depression of the vital powers occurs; the pulse becomes small, feeble, and slow, or very rapid and feeble. The patient may pass into a condition of collapse, and, indeed, the pain of hepatic colic may cause death by sudden arrest of the heart's action. The cases which prove fatal in this way are doubtless examples of fatty heart, the degeneration of the cardiac muscle being a result of the action of the same factors as those which cause gall-stones to form, if the relation of general steatosis to these bodies which I have set forth prove to be true. The pain is not continuously so violent as above expressed: it remits from time to time, and seems about to cease altogether when a sudden access of anguish is experienced and the former suffering is renewed, and, it may be, more savagely than before. The pain of an attack of hepatic colic has no fixed duration. It will depend on the size of the calculus, on the point where impacted, and on the impressionability of the subject. The severity of the seizures varies within very wide limits. The attack may consist in a transient colic-like pain, in a mere sense of soreness, in epigastric uneasiness with nausea, or it may be an agony sufficient to cause profound depression of the powers of life--to destroy life, indeed. The usual attack of hepatic colic is one in which severe suffering is experienced until relief is obtained by the exhibition of anodynes. Under these circumstances the subsidence of the pain may be rather gradual or it may be sudden: in the former case, as the effects of the anodyne are produced, we may suppose that the spasm subsides and the stone moves onward, at last dropping into the intestine: an enchanting sense of relief is at once experienced. Very serious nervous disturbances may accompany the pain. Paroxysms of hysteria may be excited in the hysterical; convulsions occur in those having the predisposition to them from any cause, and in the epileptic.

The onset of a severe seizure is announced by chilliness, sometimes by a severe chill. Now and then the paroxysms commence with the chill, and the pain follows. It occasionally happens that the attacks in respect to the order in which the symptoms occur, and in their regularity as to time, behave like an ordinary ague. In fact, there appear to be two modes or manifestations of the attacks of hepatic colic in malarious localities: those in which the phenomena are merely an outcome of the passage of the calculi; those in which an attack of intermittent fever is excited by the pain and disturbance of hepatic colic. To the first Charcot[171] {1072} has applied the phrase fièvre intermittente hépatique. It is supposed to correspond pathogenetically to urethral fever produced by the passage of a catheter. On the other hand, the second form of intermittent can occur only under the conditions producing ague. A calculus passing in a subject affected with chronic malarial poisoning, the latent malarial influence is aroused into full activity, and the resulting seizure is compounded of the two factors. The truly malarial form of calculus fever differs from the traumatic in its regular periodicity and the methodical sequence of the attacks, which occur in the order of an intermittent quotidian or tertian. During the attacks of hepatic colic, when protracted and severe, a sense of chilliness or distinct chills occur, sometimes with the regularity of an intermittent; but these differ from the seizures which the chill inaugurates at distinct times, the intervening period being free from disturbance.

[Footnote 171: Leçons sur la Maladies du Foie, p. 178.]

The fever which accompanies some severe paroxysms of hepatic colic has a distinctly intermittent character, hence the name applied to it by Charcot. There are two forms of this calculus fever as it occurs in malarious localities: one intermittent, coming on during a protracted case, and immediately connected with and dependent on the passage of the stone; the other a regular intermittent quotidian or tertian, which determines and accompanies the paroxysm of colic. A case occurring under my observation very recently, in which these phenomena were exhibited and the calculi recovered, proves the existence of such a form of the malady. In this case with the onset of the pain a severe chill occurred; then the fever rose, followed by the sweat, during which the pain ceased, but much soreness and tenderness about the region of the gall-bladder, and jaundice, followed in the usual way. At the so-called septenary periods also attacks come on in accordance with the usual laws of recurrence of malarial fevers.

Not all cases are accompanied by fever. In many instances, probably a majority, the pulse is not accelerated, rather slowed, and the temperature does not rise above normal. The inflammation which follows an attack of hepatic colic will be accompanied by some elevation of the body-heat, and fever will occur when ulceration of the duct and perforation cause a local peritonitis; but these conditions are quite apart from those which obtain in the migration of calculi by the natural channel.

Nausea and vomiting are invariable symptoms of hepatic colic. First the contents of the stomach are brought up, then some glairy mucus only, with repeated and exhausting straining efforts; and with the sudden cessation of the pain there may appear in the vomit a quantity of bilious matter, the contents of the gall-bladder liberated by the passage of the stone into the intestine. If bile is present in the vomit from the beginning, it may be concluded that the obstruction is not complete.

Constipation is the rule. The abdomen may be distended with gas--is usually, indeed, when constipation exists. Free purgation gives great relief. The stools are composed of scybalæ chiefly at first, afterward of a brownish offensive liquid, and when jaundice supervenes they become whitish in color, pasty, and semi-solid. Now and then it happens that a copious movement of the bowels takes place as the attack is impending, but during the paroxysm no action occurs.

Jaundice is an important, but not an invariable, symptom. It comes on within the first twenty-four hours succeeding the paroxysm, and appears {1073} first in the conjunctiva, thence spreading over the body generally. The intensity of the jaundice depends on the amount of the obstruction: if complete, the body is intensely yellow; and if partial, the tint may be very light. The very slight degree of obstruction which suffices to determine the flow of bile backward has been already stated. There may be no jaundice, although all the other symptoms of the passage of gall-stones may be present. Such is the state of the case when a calculus enters and is arrested in the cystic duct. Under these circumstances the natural history differs from that which obtains when the obstruction is in the common duct and ends abruptly by the discharge of the calculus into the intestine. After the persistence of the symptoms of hepatic colic for a variable period without jaundice, this sign of obstruction may appear, indicating the removal of the stone from the cystic into the common duct. The symptoms accompanying the jaundice--the hebetude of mind, the slow pulse, the itching of the skin, the dark-colored urine--have been sufficiently detailed in the section on that topic in another part of this article.

The duration of the jaundice is different in different cases, and is influenced by the degree and persistence of the obstruction. When the obstruction is partial and the stone is soon removed, the jaundice will be slight and will disappear in a day or two; on the other hand, when the stone completely blocks the passage and is slowly dislodged, the jaundice will be intense and will persist for ten days to two weeks.

After the paroxysm has passed, if severe, the liver will be swollen, more or less tenderness will be developed by pressure, and in some instances, a local peritonitis coming on, there will occur the usual symptoms of that condition.

Although all the symptoms produced by the passage of biliary calculi may be present, some uncertainty will always be felt unless the body causing the disturbance is recovered from the feces. A properly-conducted search is therefore necessary. As this is so often done inefficiently and the calculus not found, an error of diagnosis may seem to have occurred. Every stool should be examined in the mode hereinafter described for a number of days after the attack until the calculus is found. It should be remembered that only air-dried calculi float on water. The stool, as soon as passed, should be slowly stirred up in water sufficient to make a thin mixture, and all solid particles removed for further examination, the thinner portion poured off, and more water added from time to time until only solids remain at last. It should not be forgotten that masses of inspissated bile, biliary sand, may produce symptoms not unlike those due to gall-stones proper, and hence all particles having the appearance of this material should be examined chemically. Place some of the supposed bile on a white plate and pour over it some drops of strong sulphuric acid, when the biliverdin will take on a brilliant scarlet color.

The discharge of particles of inspissated bile causes symptoms not unlike those due to the migration of biliary calculi, but there are points of difference. A strongly-marked case diagnosticated biliary calculi, and in which masses of inspissated bile were discharged in great quantity, will furnish the symptomatology to be now described. The onset of the paroxysms of pain is less abrupt than is the case with gall-stones, and the attacks may occur at any time; the pain also subsides more gradually, and hardly {1074} ceases at any time, but revives every now and then, so that several days, even weeks, may be occupied with one seizure. Jaundice is less apt to follow, and indeed well-defined jaundice rarely occurs in this affection. There is much swelling of the liver, also considerable tenderness, and relief is most certainly afforded by free purgation, anodynes seeming rather to keep up the disturbance, probably by checking the hepatic secretions.

Attacks of hepatic colic may be expected to recur when a calculus with multiple facets migrates, but the time when its associates may be expected to move cannot be predicated on any data now available. Single attacks may happen at intervals of weeks, months, or years. The migration of one large stone may so dilate the ducts as to facilitate the passage of those that remain behind, thus ensuring a recurrence of the seizures at an early period.

IMPACTION OF CALCULI AND MIGRATION BY ARTIFICIAL ROUTES.--The point at which impaction takes place is an element of great importance. The size of the calculus is far from being decisive as to the certainty of impaction or as to the untoward results. A not unfrequent accident is the blocking of the cystic duct at its opening, thus preventing the influx or outgo of bile from the gall-bladder. If the stone does not ulcerate through, in this position it does no damage, for the gall-bladder, as has been stated, may be closed without any apparent detriment. Just at the bend of the cystic duct, near its origin, is the point where arrest of a calculus is most likely to take place. The next most likely point is the duodenal end of the common duct. When impaction occurs a local inflammation comes on, an exudation is poured out, ulceration begins, and presently the peritoneum is reached. Adhesions usually form with the neighboring organs, but now and then perforation takes place, and bile, pus, and the calculus are precipitated into the peritoneal cavity. A fatal peritonitis follows, as a rule; but rarely the inflammation is localized, and an abscess forms which pursues the usual course of such accumulations; or adhesions may take place about the site of the perforation and prevent a general inflammation of the peritoneum. In this way a very large sac may be produced, with the ultimate result of rupture into the general cavity, although a fistulous communication may be established with some neighboring organ, permitting safe discharge in this direction.

A gall-stone impacted in one of the hepatic ducts or in the main duct, ulcerating through, may form an abscess not distinguishable from other solitary hepatic abscesses except by the presence of the concretion causing the mischief and the absence of the usual conditions giving rise to these accumulations of pus. It is probable that fatal abscesses of the liver not infrequently are caused in this way in extra-tropical countries. Adhesions forming to neighboring hollow organs or to the external integument, such abscesses discharge, carrying out the calculus with them. In this way may be explained the discharge by the intestine of calculi much too large to have passed by the natural route and unattended by the usual symptoms of hepatic colic. These gastro-intestinal biliary fistulæ extend from the gall-bladder and the larger ducts to the stomach, to the duodenum, and to the transverse colon; but of these the communication with the stomach is the least common. The adhesion of the gall-bladder or common duct to the duodenum or colon may be direct, exudations uniting {1075} the two parts without the intervention of an abscess cavity, or such a sac or cavity may be interposed. In some cases the discharge of biliary calculi is effected through these routes with so little disturbance as to escape notice, or the symptoms may be only vague indications of a local inflammation in the neighborhood of the liver.

Biliary fistulæ communicating externally, caused by the migration of calculi, are comparatively common. They have the clinical history, and are usually treated as cases, of hepatic abscess. Sometimes hundreds of calculi are thus discharged. In such instances it may be assumed that communication has been established with the gall-bladder. Hepatic abscess thus due to the migration of calculi may discharge into the pelvis of the kidney, into the ascending vena cava, or through the lung, but these places of outlet are comparatively uncommon.

COURSES AND COMPLICATIONS.--Although symptoms cease for the time being when the calculus passes into the duodenum, and although in most instances no after unpleasant effects are experienced, there are cases in which the presence of the concretion in the intestine proves to be fruitful of mischief. Calculi of very large size--from a pigeon's to a hen's egg--are also found in the intestine, without the occurrence of symptoms indicative of their migration. It has been shown that this silent migration of calculi from the liver-passages to the intestinal is not uncommon. Hepatic concretions are distinguishable from the intestinal by their crystalline form and by their composition. The former are usually polyangular, and are composed of cholesterin crystallized about a nucleus of bile-pigment, inspissated bile, or mucus. After entrance into the intestine, lime salts and mucus are deposited in successive layers, so that the form of the calculus is modified and its size increased. The solitary ovoid concretion is most frequently found in the intestine, without previous symptoms of hepatic source, and, although increased in size in the intestine, it retains its original shape. A specimen of this kind now in my possession illustrates these points. It is composed of cholesterin crystallized in radiating lines and concentric rings about a central nucleus of inspissated bile. Around the hepatic concretion there have formed layers of lime and mucus since it has reached the intestine, and after drying this rind became brittle and was readily detached. The polyangular calculus is apt to form the nucleus of a scybala-like mass of feces; hence in the search for these bodies every such mass should be broken up. An example of this has recently come under my own observation. Concretions of all sizes, having reached the intestines, as a rule pass down without creating any commotion, and are silently discharged. But various disturbances occur in some instances. Obstruction of the bowels is one of the results. A great may cases have been collected by Murchison,[172] as many more by Leichtenstern,[173] of impaction of the intestine produced by an accumulation of feces about a biliary concretion. A calculus may be retained in a fold or diverticulum of the small intestine, and may indeed cause a loop to be formed which in turn readily twists, becoming an immovable obstruction. This mode of obstructing the bowels is less common than the simple impaction. It is affirmed by some authorities, especially by Von Schüppel, that obstruction of the bowels--impaction--is more often caused by stones that have ulcerated through into the {1076} intestines than by those that have descended by the common duct; and this conclusion must be reached if jaundice has not been present. It is not only the size of the calculus which determines impaction, as has been stated: several may be agglutinated in one mass, and reflex spasm of the muscular layer may be induced by their presence in the bowel. Nevertheless, some enormous concretions have been found in the canal, and others have been discharged without special trouble. Hilton Fagge exhibited to the Pathological Society[174] of London two gall-stones passed with the stools, measuring 2½ by 1-1/5 inches in long and short diameter, and Fauconneau-Dufresne[175] refers to concretions of the size of a hen's egg. Mention has been made of one in the writer's possession of the size of a pullet's egg, which, until its discharge, caused a train of characteristic symptoms. These immense bodies may have ulcerated through from the gall-bladder or may have grown by successive deposits of carbonate and phosphate of lime after reaching the intestine.

[Footnote 172: Lectures on Diseases of the Liver, p. 573.]

[Footnote 173: Ziemssen's Cyclopædia, vol. vii.]

[Footnote 174: Transactions of the London Pathological Society, vol. xix. p. 254.]

[Footnote 175: Op. cit.]

The symptoms caused by the presence of concretions in the intestines are, when pronounced, sufficiently characteristic. At a variable period after an attack or attacks of hepatic colic the disturbance begins. The condition of impaction above referred to does not differ from ordinary fecal accumulation. It is true that occasionally the intestinal irritation due to the presence of these bodies in some instances preceded the symptoms of impaction, but usually there is no evidence to indicate that the stoppage of the bowel is due to anything else than feces. The irritability manifested by the intestinal mucous membrane when gall-stones are present varies remarkably. There may be only some ill-defined pain which, as a rule, indicates the position of the calculus, or it may be pain with a feeling of soreness, or it may take the form of violent colic, with nausea, vomiting, and depression. In my own cases pain was experienced at or near the ileo-cæcal valve, where one was lodged, and along the descending colon, where the others were; the pain and soreness ceased when these bodies were discharged.

In a few instances gall-stones are brought up by vomiting. The most remarkable example of this is a case to be found in the Transactions of the Pathological Society (vol. xii. p. 129): A woman ninety-four years of age vomited a stone the size of a nutmeg. In the reported examples violent pain, nausea, and much vomiting preceded the discharge of the calculus.

Like other foreign bodies, a gall-stone may ulcerate through the intestine, producing fatal peritonitis.

Many conditions due to the presence of biliary concretions, and which arise during their migrations, may be viewed as complications. Many of those produced directly have been described as a part of the proper course of the malady; others are local and reflex, and these may with propriety be considered as complications. First in importance are those due to obstruction and the local inflammation.

The passage of a calculus along the duct excites an inflammation of the mucous membrane, which by contiguity of tissue invades the peritoneal layer if the stone is retained for a sufficient time, and especially if it is immovably lodged. The stoppage in the flow of bile leads to dilatation of the ducts, and a change takes place in the character of that fluid, {1077} owing to the admixture of mucus with the bile and to the pouring out of a pathological secretion: it loses the bilious appearance and becomes a merely sero-purulent fluid. Serious changes ensue in the structure of the liver, as was first suggested by O. Wyss and Leyden, and afterward more especially by Wickham Legg[176] and Charcot.[177] A ligature to the common duct in animals is followed in so short a time as two weeks by hyperplasia of the connective tissue and atrophy of the gland-elements. It has been ascertained that similar changes ensue in man from the impaction of a calculus in the common duct. Under these circumstances the size of the liver, as indicated by the area of hepatic dulness, at first enlarges, and subsequently more or less contraction, coincident with the atrophy, ensues. When the cystic duct is obstructed the contents of the gall-bladder increase, and become ultimately sero-purulent (dropsy). In some instances, the walls of the abdomen being thin, a globular elastic tumor may be felt projecting from beneath the liver.

[Footnote 176: St. Bartholomew's Hospital Reports for 1873. See also Treatise on Diseases of the Liver, by the same author, loc. cit.]

[Footnote 177: Leçons.]

Angiocholitis, or inflammation of the duct, is caused by the passage, especially by the impaction, of a calculus. The inflammation may extend by contiguity of tissue and involve the surrounding parts. Several cases have been examined by the writer in which the gall-bladder and the cystic and common duct were imbedded in a mass of organized exudation. An extension of inflammation may take place, and be confined to the hepatic peritoneum. Heavy organized exudations will form, adhesions be contracted to the diaphragm, to the parietal peritoneum, and to the neighboring organs, and the capsule, thickened and contracting, will ultimately induce changes in the structure of the adjacent part of the liver. When the inflammation extends to the peritoneum there are the usual systemic symptoms, and locally acute pain, increased by the respiratory movements and by pressure, and assuming a constrictive character; nausea and frequent vomiting, and often a very troublesome hiccough, caused, doubtless, by implication of some branches of the phrenic nerve; constipation, etc.

The relation of biliary colic to cancer of the biliary passages was first noted by Frerichs, who ascertained the occurrence of gall-stones in 9 out of 11 cases of cancer of these parts. Hilton Fagge[178] reports a case of the kind, and the writer can add another from his own observations.

[Footnote 178: Guy's Hosp. Rep., 1875.]

The most important of the reflex symptoms are those pertaining to the circulatory system. The action of the heart becomes irregular in rhythm and diminishes in force. The circulation of the bile acids in the blood causes slowing of the heart's action, as has been set forth in the section on jaundice; but that is a direct consequence, and is not a reflex impression. Potain was the first to show that the structure of the heart is affected. A mitral murmur is a recognized symptom in the icterus of gall-stones, but Potain[179] has shown that the real seat of this murmur is the tricuspid, and that the affection of the heart is a dilatation of the right cavities. The physiological reason for this condition of the heart is the rise of tension in the pulmonary artery, which is secondary to irritation of the splanchnic nerves; and to this factor is also due the reduplication of the first sound and the accentuation of the second sound--characteristic signs of the cardiac change in these cases.

[Footnote 179: Cyr, Traité de l'Affec. calc. de Foie, loc. cit.]

{1078} There are certain reflex nervous troubles in cases of hepatic colic, some of them of great importance. One of the lesser troubles is herpes zoster. A very violent attack in the course of the distribution of the first, second, and third cervical nerves has happened in a case under the writer's observation. There have been reported from time to time cases of sudden death during the paroxysms of hepatic colic, in which a calculus lodged in Vater's diverticulum, at the intestinal extremity of the common duct, was the cause of the accident. An explanation of this result is to be found in the intimate nervous communications between the liver and the heart through the solar plexus and the large number of ganglia contained in Vater's diverticulum. The most severe pain is felt as the calculus is passing through the orifice of the common duct into the intestine, and here also the spasm of the muscular fibre is most tense. The so-called crushing-blow experiment of Goltz illustrates how intense suffering, such as the passage of a gall-stone, can paralyze the heart through the solar plexus. The depression of the heart's action does not always occur on the instant, but it may be gradual--several hours, even a day or two, being occupied in the suspension of activity. Leigh of Liverpool[180] has reported an example of death in six hours in a female of thirty, previously in good health; Cornillon,[181] another in a female of fifty-three, who died in twelve hours from the beginning of the paroxysm; Williamson,[182] a female of fifty-one years, who expired on the fourth day; Habershon,[183] two, who died during the paroxysms at a period not stated; and Brouardel, one which was the subject of a medico-legal investigation. In the first case the calculus was yet in the gall-bladder, the appearances indicating that persistent spasms had occurred to force the calculus into the cystic duct; in the others in which the position of the stone is mentioned, it was engaged in the orifice of the common duct or had reached the intestine.

[Footnote 180: Medical Times and Gazette, 1867, vol. i. p. 248.]

[Footnote 181: Cyr, op. cit., p. 185.]

[Footnote 182: The Lancet (London), vol. ii. p. 780.]

[Footnote 183: Lectures on the Pneumogastric, 3d Lecture.]

In several instances sudden death has resulted from uncontrollable vomiting induced by the paroxysms of hepatic colic. Trousseau[184] mentions a case in which strangulated hernia and death ensued in consequence of the violent vomiting brought on by the passage of a calculus.

[Footnote 184: Clinique médicale.]

DIAGNOSIS.--Unless the distension of the gall-bladder is sufficient to cause a recognizable tumor, gall-stones in that organ do not produce symptoms by which they can be diagnosticated. If sudden attacks of violent pain in the right hypochondrium, accompanied by nausea and vomiting and followed by jaundice, have occurred from time to time, then the presence of biliary concretions may be suspected if the symptoms belonging to them are present in the intervals between the seizures. The migrations of calculi produce symptoms so characteristic that error is hardly possible. The only disorders with which an attack of hepatic colic may be confounded are gastralgia and hepatalgia. As regards the first, the distinction is made by the seat of pain, by the absence of after jaundice, and by the lack of a concretion passed by stool. As the diagnosis may depend on the finding a concretion, the writer must again affirm the importance of a properly-conducted search of all the stools passed for several days after the paroxysm.

{1079} Hepatalgia is diagnosticated with great difficulty, for the pain has the same seat, the same character, but as a rule it does not terminate so abruptly, is not accompanied by such severe vomiting and depression, jaundice is absent, and no stone can be found in the evacuations. Both gastralgia and hepatalgia occur in the subjects of neurotic disturbances--in the pale, delicate, and hysterical--whereas, as a rule, hepatic colic happens to the obese, to the persons of active digestion addicted to the pleasures of the table.

The passage of calculi may be confounded with flatulent colic, with the pain caused by lead and other mineral poisons, with impaction, internal strangulation, local peritonitis, and similar causes of sudden and violent pain. The differentiation is made by attention to the seat and character of the pain, by the previous history, and especially by the absence of jaundice and of a concretion. From renal colic the hepatic is separated by the position of the pain, by the direction taken by it, and by the retraction of the testicle, the irritability of the bladder, and the appearance of blood in the urine--all characteristic symptoms of the renal affection.

TREATMENT.--The treatment of biliary concretions includes the remedial management for the calculi in position, for the paroxysms of hepatic colic caused by the migration of these bodies, and for the results and complications.

Treatment of the Calculus State: Of Inspissated Bile.--As the particles of inspissated bile are deposited along the larger hepatic ducts, and form in consequence of a deficiency in the amount of glycocholate and taurocholate of soda, two methods of treatment are to be carried out: free purgation by an active cholagogue to wash out the offending substance, and the exhibition of a soda salt to promote the alkalinity of the bile and the consequent solution of the bile-pigment. Harley's method, which he strongly urges, consists in the administration of "one or two drachms of sulphate of soda in a bitter infusion every morning before breakfast, or from twenty to thirty grains of bicarbonate of soda, along with a drachm of taraxacum-juice in a bitter infusion, every night at bedtime at regulated intervals for a month or so, according to the constitution of the patient and the severity of the symptoms."

As persons who suffer from inspissation of the bile are naturally bilious, it is of the first importance in the prophylactic treatment to regulate the diet. Indulgence in malt liquors, in fatty and saccharine articles of food, must be forbidden. Acid fermentation in the course of duodenal digestion should be prevented by withholding the starches and sugars. Peptonized foods, given with an alkali, are highly useful. Milk, fresh meat, and the succulent vegetables are the proper constituents of a diet for these subjects. Bread is one of the most offending articles, and should be restricted in amount as much as possible.

Next to a suitable diet, systematic exercise is a measure of the highest utility in these cases. A daily morning sponge bath of a weak alkaline water not only maintains the skin in a healthy state, but also promotes the oxidation processes of the body. The alkaline mineral waters of Wisconsin, Michigan, Virginia, and other States, especially of the Bethesda Spring of Wisconsin, may be drunk with great advantage to accomplish the same purpose.

{1080} We possess direct means for preventing inspissation of the bile--remedies which act in the physiological way by increasing the proportion of glycocholate and taurocholate of soda. Harley prefers the sulphate and bicarbonate for this purpose, but my experience is in favor of the cholate and phosphate of sodium, especially the latter; for, whilst it plays the part of a soda salt, it exerts a decided cholagogue action, thus effecting the results achieved by the combined use of sulphate of soda and taraxacum. A cure may be confidently looked for in this malady by the persistent use of sodium phosphate--drachm j ter in die. It seems to act more efficiently when given dissolved in hot water.

The paroxysms of hepatic colic due to the passage of inspissated bile are to be treated in the same way as when this condition of things is caused by the migration of formed calculi. The action of cholagogue purgatives is more decidedly beneficial in the attacks due to the passage of inspissated bile.

Biliary Calculi in Situ.--Notwithstanding their crystalline form and firmness of texture, it is possible to effect the gradual solution of biliary calculi. Outside of the body it is easy to dissolve a calculus in chloroform, in Durande's remedy, etc., if time enough be given, but the problem is a far more difficult one when the calculus is in position in the gall-bladder or in a hepatic duct. As Trousseau[185] has wisely observed, it is not safe to apply to conditions within the body conclusions reached by experiments in the laboratory. Nevertheless, facts are known which justify the belief that an impression may be made on concretions in the gall-bladder. The motion of respiration and the voluntary actions of the abdominal muscles cause more or less attrition and breaking off of the angles and margins of the crystals, thus permitting the solvent action of the bile. If, however, the bile continues in the state in which it was at the time of the crystallization of the cholesterin, it will make no impression on this substance. We have now the means of restoring its power to dissolve crystallized cholesterin. As a necessary preliminary, fracture of the crystals must be effected. This may be accomplished, when the natural forces have failed to effect it, by manipulation of the gall-bladder through the walls of the abdomen, but especially by faradization. Excellent results have been achieved by this last-mentioned expedient, but no satisfactory explanation has been made of its methodus medendi, unless we accept the mechanical effect of the muscular movements. In applying the faradic current an electrode is introduced into the rectum, and the other, a sponge well moistened, is placed over the gall-bladder. An interrupted galvanic current is indicated, the electrodes in the position just mentioned, when a migrating calculus is stopped on its way. Such an application has rendered important service in a few cases.

[Footnote 185: Clinique médicale de l'Hôtel Dieu de Paris.]

Except that calculi have been found in a state of decay, their angles and edges broken, divided by cleavage, there is no evidence that they have undergone solution when in situ, except the clinical evidence which consists in a disappearance of the symptoms. The remedy of Durande, which consists in a mixture of ether and turpentine--three parts of the former and two of the latter--has been celebrated since the close of the last century, and is yet much employed in France, notably at Vichy. It {1081} is preferred by Cyr,[186] who advises its administration in capsules taken immediately before meals. Chloroform readily dissolves calculi out of the body, and hence it has been proposed, and indeed much used, for the purpose of effecting their solution in the gall-bladder; but, as Trousseau urges, there is no warrant for the belief. Corlieu,[187] who first proposed its use, and afterward Bouchut,[188] maintained that chloroform does exert this solvent action, and reported cases in confirmation; but there are so many sources of fallacy that such evidence must be viewed with suspicion. It has usually been administered in small doses (five minims) three times a day for a long period. That it is beneficial by stimulating the flow of pancreatic secretion and by allaying spasms is probably true, but that any quantity which can be administered in safety will act as a solvent of cholesterin concretions cannot be believed.

[Footnote 186: Traité de l'Affection calculeuse du Foie, p. 287.]

[Footnote 187: Gazette des Hôpitaux, 1856, June 19.]

[Footnote 188: Bullétin gén. de Thérap., vol. lxi. p. 49.]

If solution of hepatic calculi is possible under any circumstances, the most rational mode of effecting it would seem to be to restore that condition of the bile which in the normal state maintains cholesterin in the state of solution. Cholesterin is precipitated and crystallizes about a nucleus when the glycocholate and taurocholate of soda are deficient in amount. The agents most effective in restoring the solvent power of the bile are the salts of soda, of which the sulphate is preferred by Harley. In 1873 the cholate of soda was brought forward by Schiff, who prescribed it in doses of 50 centigrammes (8 grains nearly) three times a day, to be gradually increased until digestive or circulatory troubles arose. This remedy, which is eminently rational from the point of view above indicated, has apparently been of decided service in many published cases and in the writer's experience. It will be found, however, that five grains three times a day is as large a quantity as can be easily borne.

Another soda salt which in my own hands has proved in a high degree effective is the phosphate. As has been explained when referring to its use in cases of disorders due to inspissated bile, it has a distinct cholagogue action, but the chief sources of its utility in this affection are its chemical and resolvent powers. The usual quantity is one drachm three times a day, dissolved in sufficient warm water.

Bile itself, in the form of inspissated ox-gall, was formerly much used, a scruple to a drachm being given three times a day, and not without good results. It was also prescribed with chloride of ammonium. For the gastro-duodenal catarrh and the accompanying catarrh of the bile-ducts this combination is sometimes useful.

I have recently proposed a new expedient for effecting the solution of hepatic calculi. This method consists in puncture of the gall-bladder with a fine exploring-trocar, and the injection through the canula, after withdrawing the stylet, of a suitable solvent. Durande's remedy, chloroform, and other solvents can be introduced in this way without injury to the parts. I have punctured the gall-bladder, removed its contents, and explored its interior without damaging the organ in any way and without leaving after traces. The measure proposed offers no special difficulties in its execution.

The Paroxysms of Hepatic Colic.--The pain of hepatic colic being {1082} the most acute suffering known to man--in its severest form at least--the most powerful anodynes are required. The measures employed for relief of pain happen to be the most efficient for promoting the expulsion of the calculus and for limiting, if not preventing, the subsequent inflammation. As soon as the character of the seizure is manifest a hypodermatic injection of morphine and atropine--1/8 to 1/2 grain of the former and 1/200 to 1/80 grain of the latter--should be given; ether administered by inhalation if necessary; and by the stomach chloroform, chlorodyne, or chloral. As the stomach is usually exceedingly irritable, the subcutaneous injection of remedies is a precious resource: this failing or contraindicated, relief may be given by the rectal injection of laudanum or chlorodyne. As relief is often afforded by the act of vomiting, the attempts to empty the stomach should be encouraged, and to this end large draughts of warm water should be given. Hot fomentations and mustard plaster should be applied over the right hypochondrium, and an entire warm bath may be used if available.

Great relief is usually afforded by the action of purgatives. The irritability of the stomach forbids the employment of drastic purgatives, yet podophyllin resin is warmly commended by Dobell. It must be given in small doses, and preferably dissolved in spirit. Calomel in one-grain doses, every four hours until it purges, allays nausea and lessens the after-uneasiness in the right hypochondrium, but mercurial treatment given with a view to a supposed cholagogue effect only does evil by prolonged administration, especially if ptyalism is induced. If evidences of portal congestion are present, such remedies as euonymin, iridin, baptisin, and others of the cholagogue group give good results. The most effective of the remedies of this kind is ipecacuanha, given in purgative doses: the emesis induced by it favors the extrusion of the stone, and the powerful cholagogue effect relieves the portal congestion. Twenty grains at once, and repeated if need be in three hours, is a suitable quantity.

The various complications which may occur, and the results which follow the migration of the calculus, require treatment adapted to the conditions existing, and will be mentioned in the sections devoted to these topics.

Occlusion of the Biliary Passages; Stenosis of the Ductus Communis Choledochus.

DEFINITION.--By occlusion of the biliary passages is meant an obstruction, internal or external, of the hepatic, cystic, or common duct. The causes of the obstruction are various, but the results are quite uniform; hence the term includes a complexus of symptoms of a very distinctive type. Occlusion may be congenital or acquired: it is the latter with which we have especially to deal.

Stenosis signifies a narrowing which in its extremest form produces a nearly complete obstruction; when the canal is entirely closed the term occlusion is applied. Stenosis also may be congenital or acquired.

PATHOGENY.--The conditions producing narrowing of a hepatic duct or its complete obstruction are numerous, and some of them complex in their relations. As regards the ducts themselves, the interference may {1083} be entirely within the canal, or it may affect the walls, or it may be wholly extraneous; as, for example, when a cancer of the pancreas encroaches on the common duct. It will be convenient to consider the causes of stenosis and obstruction from these points of view: 1, internal; 2, of the duct walls; 3, extraneous.

The most usual situations for the occurrence of those changes that lead to occlusion by inflammatory adhesions are the beginning of the cystic duct, obstruction of which is of little moment, and the end of the common duct, which finally proves fatal.

The passage of a large polyangular calculus may cause such irritation, abrasion of the epithelium, and subsequent inflammatory exudation as to effect a direct union of the opposing sides of the canal. This takes place at the beginning of the cystic duct especially, since, owing to the spasm of the gall-bladder and the absence of muscular fibres in the walls of the duct, the stone crushes into, without passing through, the canal. The inflammatory exudation thus excited may close the duct. Not unfrequently the gall-bladder, full of calculi, is thus shut off from the liver permanently. In one instance the writer has seen a calculus wedged into the orifice of the cystic duct, whilst just beyond the lumen was permanently obstructed by an organized exudation. Permanent closure of the cystic duct is of far less consequence than of the common duct, and may, indeed, be a conservative condition, as in the case above mentioned, where numerous polyangular calculi may have migrated, except the closure of the passage.

The most usual point of obstruction in the course of the common duct is the intestinal end, but various processes are employed to effect it. The first in importance is catarrhal inflammation. This seems the more credible when it is remembered that to a simple catarrh of the mucous membrane is due the temporary stoppage of the duct, producing jaundice in much the largest proportion of cases. When the epithelium is detached and granulations spring up from the basement membrane, adhesions of the surfaces will readily take place, and the union may be so complete as that all traces of the duct will disappear. It is probable that in many, if not in most, of these cases the initial condition of the canal is that of simple catarrh, the more positive changes in the mucous membrane arising from peculiarities in the tissues of the individual affected, or from local injury caused by the passage of a concretion or irritation of pathological secretions of the duodenum.

Stenosis, and finally occlusion, of the common duct may arise from the cicatrization of an ulcer. Such ulcers may occur in several modes. They may result from catarrhal inflammation of a chronic type, much new connective-tissue material forming, and in the process of cicatrization, with the contraction belonging to it, the lumen of the canal is so far filled up that the passage of bile is effectually prevented. They may be produced in that state of the tissues which accompanies certain cachectic and profoundly adynamic conditions, as in severe typhoid fever. Such ulcers may also be due to the mechanical injury effected by the migration of a gall-stone. In cicatrizing, a tight stricture, impermeable to the passage of bile, may result, or the lumen of the canal be entirely obliterated. In the latter case the duct itself may disappear and leave no trace. An ulcer situated at the duodenal end of the common duct and extending into the {1084} duodenum may also in the process of healing so contract as to render the orifice impermeable to bile. The same effect may follow the cicatrization of an ulcer of the duodenum in the immediate vicinity of the orifice of the common duct.

Without the intervention of an ulcer as a means of explaining closure of the common duct, this accident may be caused by a catarrhal inflammation which effects denudation of the basement membrane, and thence union may be produced by the mere contact of the freshly-granulating surfaces. Congenital occlusion of the bile-ducts or obstruction occurring in a few days after birth, it is probable, is effected in this way, but no direct evidence of the process has thus far been offered. During intra-uterine life, as at any period in after-life, it seems necessary to the production of such changes that a peculiar constitutional state must exist; otherwise, such a result might happen to every case of catarrhal inflammation of the bile-ducts. The extent of the changes is further evidence in the same direction; for not only are the walls of the duct in permanent apposition and adhesion, but the duct degenerates into a mere fibrous cord, and in some instances is nearly, even entirely, obliterated.[189]

[Footnote 189: Ziemssen's Cyclopædia, p. 589.]

The cystic or common duct--the latter to be chiefly considered--may be occluded by the retention in its lumen of some foreign body. The impaction of a biliary calculus has already been repeatedly referred to, but there are some additional points demanding consideration. The larger concretions may be stopped in the neck of the gall-bladder; those small enough to enter the canal may be arrested at its bend behind the neck, and the very entrance of the cystic duct may be blocked, as in a case examined by the writer.

The hepatic duct is very rarely permanently occluded. As the calibre of this canal continuously enlarges downward, there is no point at which a stone is likely to be arrested; nevertheless, it occasionally happens that such an obstruction does occur. An example has occurred under the observation of the writer, but the cause was a gunshot wound of the liver.

The most usual, and for very obvious reasons the most important, of the sites where occlusion occurs is the common duct and at the termination of the duct in the small intestine, the intestinal orifice. Just behind and to the right of its orifice the duct is dilated into a fossa--the diverticulum Vateri; and here concretions of a size to pass along the common duct are stopped. It is not essential that the stone fit the canal: it may do so and prevent any bile passing into the duodenum; it may be a polyangular body, and, though wedged in, leave spaces through which more or less can slowly trickle. The symptoms will be modified accordingly. Again, the diverticulum may contain numerous concretions, which distend the canal greatly, but through the interstices of which some bile can flow.

Other foreign bodies very rarely close the intestinal end of the ductus communis; thus, for example, a cherry-seed, a plum-seed, a mass of raisin-seeds, may slip into the orifice after the passage of a gall-stone has stretched it sufficiently. A much more common cause of occlusion is an intestinal parasite, which crawls in and is fastened. The common round-worm is the most frequent offender, and much less often liver-flukes find a lodgment there.

{1085} The ductus communis choledochus may be closed by agencies acting from without. They are various, but the most common are the carcinomata. Primary cancer of the gall-bladder and gall-ducts, although not of frequent occurrence, is by no means rare. It develops in connection with the connective-tissue new formations produced by the inflammation following the migration of large calculi. A very instructive example has been examined by the writer. The patient, a woman aged forty-eight, had had numerous paroxysms of hepatic colic, and after death, which followed a protracted stage of jaundice by obstruction, a large ovoid calculus, filling the gall-bladder, was found, and an extensive organized exudation of inflammatory origin was the seat of carcinomatous disease involving the cystic and common ducts and closing the lumen of both. Cancer of the pylorus, of the duodenum, of the pancreas, of the right kidney, and of the liver itself, not unfrequently by exterior pressure permanently occlude the common duct. To this category of obstructing causes must be added enlarged lymphatic glands of the transverse fissure, large fecal accumulations, tumors of the ovaries and uterus, aneurisms of the abdominal aorta, and especially aneurism of the hepatic artery, several examples of which have been reported, and one has occurred in a case seen by the writer.

The effects of obstruction are much less important when the cystic duct is closed. The contents of the gall-bladder accumulate, constituting the condition known as dropsy of the gall-bladder. A catarrhal state of the mucous membrane is set up; the muco-pus formed mixes with the bile, and the mixture undergoes fermentative changes which further alter its character and impart to it irritating qualities, in consequence of which the mucous membrane becomes more decidedly inflamed, and a still more purulent fluid forms, so that ultimately the contents of the gall-bladder are entirely purulent, and that organ may attain to enormous size. Instead of a catarrhal inflammation leading to suppuration, the mucous membrane may pour out serum abundantly, the biliary contents and mucus disappear by absorption, and finally the gall-bladder will be moderately distended by a serous-like fluid. No further disturbance ensues, and the gall-bladder, thus shut off from participation in the hepatic functions, ceases to give trouble.

The results are far different when the obstruction occurs in the hepatic or common duct, for then the bile can no longer perform its double function of secretion and excretion--of contributing materials necessary to digestion and assimilation, and excreting substances whose removal is necessary to health. The liver continuing to functionate after closure of the duct is effected, obviously the secretion of bile continues to accumulate, and the irritation of the mucous membrane causes a catarrhal state; mucus is poured out, and serum escapes from the distended vessels. If the hepatic duct only is obstructed, the dilatation will not involve the cystic duct and gall-bladder, but as the common duct at its termination is occluded, usually the whole system of tubes will be affected by the ensuing changes. The alterations already described as occurring in the gall-bladder take place in all the hepatic ducts. The bile-elements are absorbed, and the fluid distending the whole system of hepatic tubes becomes finally a semi-transparent serum or a very thin sero-mucus, having in bulk a pale sea-green color. Although an intense jaundice {1086} coexists with the obstruction, no portion of the bile escapes into the ducts. At the beginning of the obstruction more or less bile is in the tubes, and then the fluid will have a distinct biliary character; but as it accumulates, first the bile-constituents disappear, then the mucus--which at the outset was formed freely--is absorbed, and at last only a colorless serum remains. This fluid, which has been examined chemically by Frerichs, is found to be slightly alkaline, to have only 2 per cent. of solids, and to present no trace of any biliary constituent. As the fluid accumulates the gall-bladder and ducts dilate, sometimes to an enormous extent, the fluid they contain amounting to several pints. The walls of the ducts grow thinner, and may finally give way with the pressure or from external violence, the fluid exciting an intense and quickly-fatal peritonitis. Important changes occur in the structure of the liver also. With the first retention of bile the liver conspicuously enlarges, and may indeed attain to twice its normal size, but it subsequently contracts, and may lessen in as great a degree as it had enlarged. Changes begin in the glandular structure as pressure is brought to bear on the cells by the enlarging ducts. The liver-cells become anæmic and the protoplasm cloudy, but granular and fatty degeneration does not take place. Even more important as an agency affecting the condition of the hepatic cells is the hyperplasia of the connective tissue, which ensues very promptly when an obstruction to the flow of bile arises from any cause, as has been shown by Legg[190] and Charcot.[191] The liver on section has a rather dark olive-green color, and is firmer in texture, owing to the increased development of the connective tissue; the cells are bile-stained and contain granules of coloring matter and crystals of bilirubin, and although they are at first not altered in outline, subsequently more or less atrophy is produced by the contraction of the newly-formed connective tissue and the pressure made by the dilated hepatic ducts.

[Footnote 190: On the Bile, Jaundice, and Bilious Diseases, p. 352 et seq.]

[Footnote 191: Leçons sur les Maladies du Foie, etc., p. 205 et seq.]

SYMPTOMS.--The symptoms produced by occlusion of the cystic duct are not sufficiently characteristic to be diagnosticated with any certainty. When an attack of hepatic colic has slowly subsided without jaundice, and an elastic tumor, globular or pyriform in shape, has appeared from under the inferior margin of the liver in the position of the gall-bladder, dropsy of that organ may then be suspected. As paracentesis of the gall-bladder may be performed with ease, safety, and little pain, the diagnosis may be rendered more certain by the use of the exploring-trocar.

Obstruction of the hepatic or common duct is accompanied by symptoms of a very pronounced and distinctly diagnostic character. Without referring now to the antecedent symptoms or to those belonging to the obstructing cause, the complexus of disturbances following the obstruction is the subject to which our attention must be directed. The great fact dominating all other considerations is the stoppage of the bile, whether this has occurred suddenly or slowly. Jaundice begins in a few hours after the canal is blocked. At first there is yellowness of the conjunctiva, then diffused jaundice, deepening into the intensest color in two or three weeks, or, when the obstruction is sudden and complete, in a few hours. At first the color is the vivid jaundice tint, a citron or salmon or yellow-saffron hue, but this gradually loses its bright appearance, grows darker, and passes successively into a brownish, bronze-like, and ultimately a {1087} dark olive-green, which becomes the permanent color. Under some moral emotional influences there may be a sudden change to a brighter tint, lasting a few minutes, but otherwise the general dark olive-green hue persists throughout. In a few instances, after some weeks of jaundice, the abnormal coloration entirely disappears, signifying that the liver is too much damaged in its proper glandular structure to be in a condition to produce bile. Such a cessation of the jaundice is therefore of evil omen.

Pruritus, sometimes of a very intense character, accompanies the jaundice, in most cases appears with it, and in the supposed curable cases it has persisted after the cessation of the discoloration. The irritation may become intolerable, destroying all comfort, rendering sleep impossible, and so aggravating as to induce a highly nervous, hysterical state. The scratching sets up an inflammation of the skin, and presently a troublesome eczema is superadded. In some of the cases a peculiar eruption occurs on the skin and mucous membranes, entitled by Wilson[192] xanthelasma. It has been carefully studied by Wickham Legg,[193] who has ascertained the character of the changes occurring in the affected tissues, and also by Mr. Hutchinson.[194] As a rule, this eruption appears after several months of jaundice, and manifests itself first on the eyelids, then on the palms of the hands, where it makes the most characteristic exhibit, and after a time on the lips and tongue. It occurs in irregular plaques of a yellowish tint slightly elevated above the general surface, and rarely assumes a tubercular form. As was shown by Hilton Fagge, xanthelasma occurs more especially in the milder cases of catarrhal icterus that had been protracted in duration, but it is also occasionally seen in the jaundice of obstruction.

[Footnote 192: Diseases of the Skin, 6th ed., Lond., p. 773.]

[Footnote 193: On the Bile, Jaundice, and Bilious Diseases, p. 317 et seq.]

[Footnote 194: Medico-Chirurgical Transactions, vol. liv. p. 171.]

According to the stage of the disease during which the examination is made the liver will be enlarged or contracted; more or less tenderness may be developed by pressure in the area occupied by the ducts, and a tumor in a position to effect compression may possibly be detected. The area of hepatic dulness will be increased in the beginning of all the cases in which the obstruction is complete, but will remain normal so long as the flow of bile persists despite the obstruction. When enlarged, the liver can be felt projecting below the inferior margin of the ribs, and with it, in most cases, the elastic globular body, the gall-bladder. The state of the hepatic secretion, and in consequence the duration of the obstruction, may be ascertained by puncture of the gall-bladder and withdrawal of some of its contents for examination. The presence of unaltered bile will indicate recent obstruction; of serum, will prove long-standing interruption of bile-production. The presence of concretions in the gall-bladder will indicate the character of the obstructing cause, and an increased amount of bile of a normal or nearly normal kind will be conclusive evidence that the obstruction is in the course of the common duct. In a fatal case of permanent occlusion examined by myself the cystic duct was closed by inflammatory adhesions and the common duct was stopped up by a calculus.

The enlarged area of hepatic dulness will, in a protracted case, not continue. The proper secreting structure, the hepatic cells, undergo atrophy, {1088} and the increased connective tissue--to the development of which enlargement of the organ is mainly due--contracts. The ultimate result is that the liver becomes sclerosed, and is distinctly smaller, the area of hepatic dulness diminishing to a greater relative extent than the area of dulness due to hypertrophic enlargement. The contraction of the liver goes on at the rate that several months are required to make the result evident on percussion and palpation. Not unfrequently, the contraction is too slight to affect the percussion note of the right hypochondrium, and then, to realize the condition of the organ, the history and rational signs must be closely studied.

Whilst the liver thus varies in size, the gall-bladder remains enlarged and projects from the under surface of the organ, elastic, globular, and distinctive. The shrinking of the liver from around it makes the impression of growing size; it may be increasing, indeed, but more frequently the enlargement is merely apparent.

Whether the liver be enlarging or diminishing in size, its functions are impaired, or indeed entirely suspended. As the digestive canal receives the bile immediately on its production, it will be best to begin with the gastro-intestinal disorders which accompany occlusion of the bile-ducts. The appetite is either wanting entirely and food is loathed, or an excessive or canine appetite is experienced. The latter belongs rather to an early stage of the disorder, and comes on after the first disturbance of the stomach belonging to the immediate effects of the occlusion. The former is the result of long-standing interference with the primary assimilation. The tongue is coated with a thick yellowish fur, which, drying, is detached in flakes, leaving the mucous membrane beneath red, raw, fissured, and easily bleeding. The taste is bitter, and the mouth has a pasty, greasy, and unclean feeling. There is much thirst, and as a rule the patient experiences a keen desire for acid drinks and for fresh fruits. The stomach is rather intolerant of food, and nausea comes on as soon as it enters the stomach. The mucus and stomach-juice accumulating over night, in the morning there is much retching and nausea until the acid and rather foul contents of the organ come up. When food is retained it causes much distress, gases of decomposition accumulate, distending the stomach and giving prominence to the epigastrium, and eructations of offensive gas, with some acid liquid, occur from time to time. Similarly, in the intestines the foods undergo decomposition instead of normal digestion; gases of putrefaction are evolved, the abdomen generally is swollen, and flatulent colic results. Very irritating fat acids are liberated by the decomposition of the fatty constituents of the food, which, with the acid products of the fermentation occurring in the starch and sugar of the diet, cause a sensation of heat and distress through the abdomen. Usually, the bowels are torpid, but in some cases the stools are relaxed, having the consistence and presenting somewhat the appearance of oatmeal porridge. They may be firm, moulded, even hard. The gas discharged and the stools are offensive, with a carrion-like odor. Sometimes decomposing articles of food can be detected in the stools by very casual inspection--always, indeed, when the examination is intimate. An excess of fat is also a characteristic of the condition induced by occlusion of the ducts, especially when the pancreatic duct is closed, as does happen in cancer of the head of the pancreas.

{1089} A significant change in the color of the stools takes place. They lose their normal brownish-red tint and become yellowish or clay-colored or white, pasty, or grayish. Sometimes the stools are very dark, tar-like in color and consistence, or more thin like prune-juice, or in black scybalæ. The most usual appearance of the stools in occlusion is grayish, mush-like, and coarsely granular. The very dark hue assumed at times or in some cases signifies the presence of blood. A dark tint of the evacuations may be caused by articles of food, as a greenish hue may be due to the use of spinach; a clay-colored tint to the almost exclusive use of milk; a grayish tint to the action of bismuth; a bilious appearance to the action of rhubarb; and many others. When the occlusion is partial, although it be permanent, sufficient bile may descend into the duodenum to color the stools to the normal tint, and yet all the other signs of obstruction be present.

The bile-pigment, not having an outlet by the natural route, by the intestine, passes into the blood; all the tissues of the body and the various secretions and excretions, notably the urine, are stained by it, constituting the appearance known as jaundice or icterus. This malady has been described (see anté), but it is necessary now to give a more specialized account of those conditions due more especially to the prolonged obstruction of the biliary flow. These are a morbid state of the blood; changes in the kidneys and in the composition of the urine; a peculiar form of fever known as hepatic intermittent fever; and a group of nervous symptoms to which has been applied the term cholæmia.

It has already been shown that but little pressure is required to divert the flow of bile from the ducts backward into the blood. Changes consequently ensue in the constitution of the blood and in the action of the heart and of the vessels. The bile acids lower the heart's movements and lessen the arterial tension; hence the pulse is slower, softer, and feebler than the normal. Should fever arise, this depressing action of the bile acids is maintained; and hence, although the temperature becomes elevated, the pulse-rate does not increase correspondingly. There are exceptions to this, however, in so far that the heart and arteries are in some instances little affected, but it is probable under these circumstances that there are conditions present which induce decomposition of the bile acids.

The most important result of the action of the bile on the constitution of the blood is the hemorrhagic diathesis. Soon after the occlusion occurs in very young subjects--at a later period in adults--the occlusion having existed for many months, in some cases only near the end, the disposition to hemorrhagic extravasations and to hemorrhages manifests itself. From the surface of the mucous membranes, under the serous, in the substance of muscles, the hemorrhages occur. Epistaxis, or nasal hemorrhage, is usually the first to appear, and may be the most difficult to arrest. The gums transude blood, and wherever pressure is brought to bear on the integument ecchymoses follow. The conjunctiva may be disfigured and the eyelids swollen and blackened by extravasations, and the skin of the cheeks and nose marked by stigmata. Hæmatemesis sometimes occurs, but the extravasations into the intestinal canal more frequently--indeed, very constantly--take place in a gradual manner, and impart to the stools a dark, almost black, tar-like appearance. In the same way the urine may contain fluid blood and coagula, or it may have a merely smoky {1090} appearance from intimate admixture with the blood at the moment of secretion.

Both the bile-pigment and bile acids exert an injurious action on the kidneys. In cases of prolonged obstruction not only are the tissues of the organ stained by pigment in common with the tissues of the body, but the epithelium of the tubules, of the straight and convoluted tubes, are, according to Moebius,[195] infiltrated with pigment. In consequence of the size and number of the masses of pigment, the tubes may become obstructed and the secretion of urine much diminished. Other changes occur, due chiefly to the action of the bile acids, according to the same authority. These alterations consist in parenchymatous degeneration. The urine contains traces of albumen in most cases, and, according to Nothnägel,[196] always casts of the hyaline and granular varieties stained with pigment. As the alterations in the structure of the kidneys progress, fatty epithelium is cast off, and thus the tubules come finally to be much obstructed and the function of the organ seriously impaired. To cholæmia then are superadded the peculiar disturbances belonging to retention of the urinary constituents.

[Footnote 195: Archiv der Heilkunde, vol. xviii. p. 83.]

[Footnote 196: Deutsches Archiv für klin. Med., vol. xii. p. 326; also, Harley, op. cit., p. 503.]

One of the most interesting complications which arises during the existence of obstruction of the bile-ducts is the form of fever entitled by Charcot[197] intermittent hepatic fever. Although its character was first indicated by Monneret,[198] we owe the present conception of its nature and its more accurate clinical history to Charcot. It does not occur in all cases. As has already been pointed out, the passage of a gall-stone may develop a latent malarial infection or a febrile movement comparable to that caused by the passage of a catheter, and known as urethral fever. Charcot supposes that true intermittent hepatic fever is septicæmic in character, and can therefore arise only in those cases accompanied by an angiocholitis of the suppurative variety--such, for example, as that which follows the passage of calculi. Illustrative cases of this fever, one of them confirmed by an autopsy, have been recently reported by E. Wagner,[199] who is rather inclined to accept Charcot's view of the pathogeny. A remarkable case has been published by Regnard,[200] in which the angiocholitis was induced by the extension of echinococcus cysts into the common duct. Whilst there are some objections to Charcot's theory, on the whole it is probably true that this intermittent hepatic fever is produced by the absorption from the inflamed surface of the ducts of a noxious material there produced. It may be likened to the fever which can be caused by the injection of putrid pus into the veins of animals.

[Footnote 197: Leçons sur les Maladies du Foie, etc., p. 178 et seq.]

[Footnote 198: Cyr, Traité de l'Affection calculeuse du Foie, p. 193.]

[Footnote 199: Deutsches Archiv für klin. Medicin, vol. xxxiv. p. 529.]

[Footnote 200: Gazette méd. de Paris, No. 49, 1873, quoted by Wagner, supra.]

Intermittent hepatic fever, as its name implies, is a paroxysmal fever, having a striking resemblance to malarial fever, but differs from it in less regularity of recurrence, in the fact that urea is below the normal amount instead of increased, and in the effect of quinine, which in the case of malarial fever is curative, but not curative in hepatic fever. The paroxysms are sometimes quotidian, rarely double quotidian, tertian, quartan, and even longer, and in the same case all of these varieties may occur; on {1091} the other hand, there may be entire regularity of the seizures. The severity of the chill, the maximum temperature, and the amount of sweating vary within considerable limits; there may be merely a slight sense of chilliness or a severe rigor; the temperature may rise to 101° or to 104° F., and there may be a gentle moisture or a profuse sweat. There does not seem to be any relation between the extent and severity of the local mischief and the systemic condition.

The period of onset of intermittent hepatic fever, and its duration and mode of termination, are by no means readily determined. Cyr fixes on the paroxysms of colic as the beginning, but he obviously confounds the chill and fever caused by the passage of a calculus with the true intermittent hepatic fever. In a carefully-observed case, the facts confirmed by an autopsy, E. Wagner[201] gives the clinical history of a typical example of this malady: Gall-stones were found in the duodenum, in the common and cystic ducts, but the most important one was a polyangular stone obstructing the hepatic duct. There was an ulcer with thickened margin at the entrance to the gall-bladder, and the mucous membrane of the common duct near the intestinal orifice had a smooth, cicatricial aspect of recent origin, indicating inflammatory ulceration. The conditions favorable to the production of a morbid material of a kind to induce septicæmic fever were therefore present. The onset of fever occurred ten days after the last seizure, time being thus afforded for the local changes necessary. The duration of the fever in this case was five months, but the existence of pulmonary phthisis with cavities will explain this apparently protracted hepatic intermittent fever. The duration of the disease in its usual form is uncertain, and ranges between a week and two months, or even three months, according to Charcot.[202]

[Footnote 201: Deutsches Archiv für klinische Medicin, Band xxxiv. p. 531, 1884.]

[Footnote 202: Leçons sur les Maladies du Foie, p. 180.]

Suspension of work by the liver necessarily involves retention in the blood of various excrementitious matters. The attempt of Flint[203] to establish the doctrine of cholesteræmia has not been supported by the evidence of contemporary or subsequent physiologists. This theory denies to the other constituents of the bile any morbific action, and concentrates those disturbances known as cholæmia on the effects of cholesterin. As uræmia signifies not merely the presence of urea in the blood, but of all of the toxic substances excreted by the kidneys, so the word cholæmia comprehends all the constituents of bile having power to derange the organism by their presence in the blood.

[Footnote 203: The American Journal of the Medical Sciences, 1862, p. 349 et seq.]

By cholæmia is meant those disturbances, chiefly nervous, which are due to the presence of biliary excrementitious matters in the blood, and not less to the effect on nutrition of the absence of bile from the process of digestion in the intestine. As the atrophic changes proceed in the liver, the quantity of urea and uric acid in the urine diminishes, and presently leucin and tyrosin appear. Amongst the means of differential diagnosis of hepatic intermittent fever from malarial fever Charcot mentions the quantity of urea present--in the former greatly lessened, in the latter much increased. There is, however, a source of fallacy here not mentioned by Charcot: that is, the variations in the amount of urea due to destruction of the hepatic secreting structure. It follows that as changes {1092} occur in the kidneys, to the condition of cholæmia is superadded the derangements belonging to uræmia.

When the occlusion has existed for some time--a variable period, partly due to peculiarities of individual structure--there come on certain characteristic symptoms of nervous origin: headache, hebetude of mind, dull hearing, obscure or hazy vision, xanthopsia; somnolence and greatly increasing stupor, leading into coma; rambling and incoherence of mind, passing into delirium; muscular twitching, subsultus; muscular weakness, deepening into paralysis; and finally, it may be, general convulsions. As these derangements of the nervous system develop, a light febrile movement supervenes, so that the whole complexus has the typhoid type, or, as it can be more definitely expressed, the patient thus affected lapses into the typhoid state.

COURSE, DURATION, AND TERMINATION.--Occlusion of the gall-ducts is an essentially chronic malady in the greatest number of cases. As a rule, the causes of obstruction operate slowly, but to this rule there are exceptions. Permanent occlusion may take place suddenly, as when a gall-stone is impacted immovably in the common duct, or when a round-worm makes its way into the duct and is firmly fixed there, incapable of further movement.

When occlusion is once effected the gradual changes occurring in the liver lead to slow decline of the nutrition; the bile-elements circulating in the blood poison it and set up alterations in the structure of the kidney, and ultimately, the brain becoming affected, the end is reached by convulsions and coma. Although permanent occlusion, if unrelieved, terminates in death, a small proportion of cases get well, either in consequence of giving way of the obstructing cause or from the opening of a new route to the intestine. Thus, a calculus lodged in the fossa of Vater may suffer such injury to its outer shell as to yield to the action of solvents, or, suppuration occurring around it, the stone may be loosened and forced onward, or ulceration may open a channel into the bowel. An incurable malady causing the occlusion, the termination in death is only a question of time. The duration of any case must be indefinite. There are several factors, however, whose value can be approximately estimated. When the obstructing cause is merely local--as, for example, a gall-stone or the cicatrix of a simple ulcer--the duration of the case is determined by the mere effect of the suspension of the hepatic functions. As the eliminating action of the liver and the part played by the bile in the intestinal digestion are necessary to life, it follows that the complete cessation of these functions must lead to death. The rate at which decline takes place under these circumstances varies somewhat in different subjects. Probably two years may be regarded as the maximum, and three months the minimum, period at which death ensues when no other pathogenetic factor intervenes.

DIAGNOSIS.--To determine the fact of occlusion is by no means difficult: the persistent jaundice, the absence of bile in the stools, and the appearance of the bile-elements in the urine are sufficient. It is far different when the cause of the occlusion is to be ascertained.

The ease and safety with which the exploring-trocar can be used in cases of supposed obstruction of the cystic duct enable the physician to decide with confidence points which before could only be matters of mere {1093} conjecture. The writer of these lines was the first to puncture the gall-bladder and to explore, by means of a flexible probe passed through the canula, the course of the duct.[204] It is possible in this way to ascertain the existence of gall-stones in the gall-bladder, to find an obstruction at the entrance of the cystic duct, to demonstrate the presence of echinococci cysts, and to remove for microscopical examination pathological fluids of various kinds. More recently, Whittaker and Ransohoff[205] of Cincinnati have attempted the detection of a gall-stone impacted at any point by the introduction of an exploring-needle; and this practice has been imitated by Harley[206] of London, but without any reference to the pioneer and prior investigation of his American colleagues. The case of Whittaker and Ransohoff survived the exploratory puncture, but Harley's case proved fatal from traumatic peritonitis. Notwithstanding this untoward result, Harley persists in the advocacy of this method. It must appear to any one familiar with the intricate arrangement of the parts composing the anatomy of this region a most hazardous proceeding, and hardly to be justified in view of the superior safety and certainty of my method. To explore the interior of the gall-bladder an aspirator-trocar is introduced; any fluid intended for microscopical examination is then withdrawn, and through the canula a flexible whalebone bougie is passed.

[Footnote 204: The Cincinnati Lancet and Clinic for 1878-79; also, W. W. Keen, M.D., "On Cholecystotomy," The Medical News, Sept., 1884.]

[Footnote 205: Lancet and Clinic, 1884.]

[Footnote 206: Lancet (London), July, 1884.]

When icterus comes on in a few days after birth and persists until death ensues by convulsions and coma, there can be no doubt regarding congenital absence or impermeability of the common duct. Permanent retention-jaundice, accompanied by the characteristic symptoms of that condition immediately succeeding an attack of hepatic colic, is probably due to impaction by a calculus. When, at or after middle life, in a patient with a history of former attacks due to gall-stones, there begins a fixed pain in the right hypochondrium, and subsequently retention-jaundice, the existence of a malignant growth in connection with the cicatricial tissue and ancient organized exudation should be suspected; and this suspicion will be confirmed if subsequently a tumor can be felt. If with a localized pain slowly-developing jaundice, intestinal indigestion, fats and oils appearing unchanged in the stools, and a condition of prostration more than is properly referable to the derangement of the hepatic functions, come on in a man or woman after thirty-five, cancer of the head of the pancreas should be suspected; and this suspicion will be confirmed if a tumor can be detected in that situation. It should not be forgotten, however, that in emaciated subjects the head of the pancreas may be so prominent as to be mistaken for a scirrhous growth.

A pulsating tumor of the right hypochondrium, accompanied by jaundice, may be an aneurism of the hepatic artery. Pulsation may be communicated to a bunch of enlarged portal lymphatic glands, which will compress the common duct, but in this case, as the increase in the size of the glands is due to caseous, amyloid, or cancerous deposits, there will be found a source whence these morbid products are derived, and will explain the nature of a tumor thus constituted.

The differentiation of hypertrophic cirrhosis from occlusion of a slowly-forming character is by no means easy. In both jaundice {1094} gradually appears; in both the liver is enlarged, but in hypertrophic cirrhosis much more than in occlusion; and in the latter the gall-bladder is full--may indeed be distended--whilst in the former it is empty or contains but little bile. The history of the case may indicate the nature of the symptoms. Previous attacks of hepatic colic, and the symptoms of occlusion supervening on the last, are highly significant of calculous occlusion.

TREATMENT.--To ascertain the nature of the occlusion is a necessary preliminary to any exact treatment. In many cases this must remain a mere conjecture, when, of course, the treatment is only symptomatic. When it is probable or certain that the duct is obstructed by a calculus, two methods may be resorted to for its removal: one method is to break up the calculus by mechanical means; the other is to effect its solution by chemical agents.

Fracture of an impacted calculus is not a merely fanciful expedient. If the site of the obstruction is ascertained, an attempt may be made to penetrate the calculus by an aspirator-needle passed through the abdominal walls, according to the method of Whittaker and Ransohoff. The dangers attendant on this mere puncture are great, and a fatal result has occurred in one of the very few cases in which it has been done. Less severe and dangerous methods for attempting the disintegration of a calculus should be first tried, as follows: Make firm friction with the fingers along the inferior margin of the ribs and toward the epigastrium and umbilicus, whilst the opposite side posteriorly is supported by the hand spread out and applied firmly. A strong faradic current sent through the region of the gall-bladder and ducts has in several instances seemed to do good--indeed, to remove obstructions. A calculus impacted may be dislodged either by the fracture of its surfaces or by the strong muscular contractions of the abdominal walls and of the muscular layer of the duct. Most calculi are easily broken, and when the smallest breach is made in the external crust disintegration follows; and some calculi are so friable as to yield to slight pressure. Furthermore, the slightest solution in the continuity of the rind disposes the whole mass to dissolve in suitable menstrua. Mechanical rupture is so important a step in the process of disintegration of an impacted calculus that so serious an operation as section of the abdomen as a preliminary to it should be considered. The cavity exposed, the obstructed duct is found, and its retained calculus is mashed without section of the duct. I find one instance[207] in which this was done as a subordinate part of a cholecystotomy, and the breaking up of the stone proved to be easy of accomplishment. It is also the method of Tait, who proposes to mash the calculus by means of suitable forceps fitted with padded blades.

[Footnote 207: Harley's case, op. cit.]

I have suggested a means of effecting solution of an impacted calculus which seems, on further reflection, well worthy of consideration. The proposal is to inject, through a canula introduced into the gall-bladder, one of the solvents of the cholesterin calculus before mentioned. I have already used the canula as a duct for the passage of an exploring-sound, and have by means of it explored the interior of the gall-bladder. It is quite as feasible to inject through the canula a solvent, successive charges of which can be thrown in and withdrawn by the aspirator.

{1095} That the usual solvents introduced by the stomach can effect the solution of impacted calculi has been declared impossible by Trousseau;[208] and with this conclusion I unhesitatingly agree. I have already discussed this part of the subject, and need now only refer the reader to that section.

[Footnote 208: Clinique médicale, loc. cit.]

The various causes of obstruction besides calculi do not offer an inviting field for the exercise of therapeutical skill. Each case must be treated according to the nature of the obstructing cause; hence to make an accurate diagnosis is an essential preliminary to suitable treatment.

IV. DISEASES OF THE PORTAL VEIN.

Thrombosis and Embolism of the Portal Vein; Stenosis; Pylephlebitis.

DEFINITION.--By the terms at the head of this section are meant the various pathological processes which induce coagulation of the blood in some part of the portal system. As the portal vein is made up of many branches coming from the various organs of the abdominal cavity except the kidneys, and as it empties, so to speak, into the liver, it is obvious that various and complex derangements will ensue on the formation of thrombi.

CAUSES.--Thrombosis of the portal vein occurs under three general conditions: the blood is in a readily coagulable state; the action of the heart is weak and the blood-current sluggish; the circulation through the vein is impeded by external pressure. The coagulability of the blood is increased in diseases characterized by an excess of its fibrin-producing constituents, of which cirrhosis of the liver may be mentioned as one having this peculiarity. In chronic maladies of a depressing kind there may be simply a weak action of the heart, or the muscular tissue of the organ may be affected by a fatty and atrophic degeneration. The external pressure by which the blood-current through the vein is impeded may be caused by the newly-formed connective tissue of Glisson's capsule, by enlarged lymphatics in the hilus of the liver, or by tumors of various kinds. The first named of these causes of compression--atrophic cirrhosis--is most frequently acting. Very rarely, organized exudations of the peritoneum may be so situated as to compress the portal vein. This result can only happen when the hepatic portion of the peritoneum is involved.

Pylephlebitis exists in two forms: the adhesive and suppurative. The former results in changes not unlike those of simple thrombosis. The blood coagulates in the affected part of the vessel, the clot is organized, and the vessel ultimately forms a solid rounded cord which is permanently occluded. The suppurative variety is so different in its origin and in its results that it requires separate treatment, and I therefore postpone the consideration of it to the next section.

{1096} SYMPTOMS OF THROMBOSIS AND ADHESIVE PYLEPHLEBITIS.--It is a remarkable fact that the biliary function of the liver is not necessarily affected in cases of occlusion of the portal vein. It is true, in advanced cases of cirrhosis, when the interlobular veins are obliterated by the pressure of the contracting newly-formed connective tissue, the functions of the liver are arrested in so far as the damage thus caused extends. Notwithstanding the blocking of the portal, sufficient blood reaches the hepatic cells by the anastomosis between the hepatic artery and the interlobular veins--an anatomical connection demonstrated by Cohnheim and Litten.[209] So long as this anastomosis continues bile will be formed, although the portal vein is occluded.

[Footnote 209: Virchow's Archiv, Band lxvii. p. 153, "Ueber Circulationsstörungen in der Leber."]

The most significant symptoms of thrombosis of the portal vein are the sudden formation of ascites, which quickly assumes a very high grade, and equally sudden passive congestion of the gastro-intestinal mucous membrane, enlargement of the spleen, and distension of the superficial veins of the abdominal parietes. When these symptoms succeed to cirrhosis of the liver, or appear after the formation of a tumor in the hepatic region, or come on in the course of phthisis or chronic inflammation of the hepatic peritoneum, the existence of thrombus of the portal vein may be reasonably suspected.

Coincidently with the occlusion of the portal vein the gastro-intestinal mucous membrane becomes the seat of a catarrhal process, and to the fluid thus produced is added a much more abundant transudation from the distended capillaries. Nausea, vomiting, and diarrhoea result, the rejected matters being serous, watery, and in many cases tinged with blood. Now and then quite a severe hemorrhage takes place, and the blood is brought up by vomiting (hæmatemesis) or is discharged by stool. Hemorrhoids form, and, in large masses protruding, much pain is experienced, and free bleeding may result from rupture of a distended vein.

The veins of the abdominal parietes, which in the normal state are invisible or at least not prominent, and which form anastomoses with the portal, when the obstruction occurs dilate, sometimes to a remarkable extent. The most important anastomosis is that between the femoral and saphena and internal mammary and epigastric veins. When the hepatic branches of the portal are closed, but the trunk remains pervious, the parumbilical vein enlarges greatly, and, communicating with the superficial veins of the anterior part of the abdominal walls, forms a radiating network of tortuous veins to which is given the striking title of caput Medusæ.

The most significant symptom of portal thrombosis is a quickly-forming ascites. It is true, ascites is a common symptom in advanced cirrhosis, but the rapid accumulation of fluid and the prompt filling of the cavity after tapping distinguish that which arises from portal thrombosis from all others. Besides its excessive extent, the ascites presents the usual symptoms.

Due to the same cause as the enlargement of the superficial veins, the hemorrhages, the ascites, etc., there occurs considerable hypertrophy of the spleen in many of the cases. It sometimes happens that the new compensatory circulation and the hemorrhages from some part in the {1097} usual route of the portal so dispose of the blood that the spleen does not enlarge sufficiently to be readily made out.

COURSE AND TERMINATION.--It is obvious that a condition such as that induced by thrombosis of the portal must be comparatively quickly fatal; but the cases vary in duration as the compensatory circulation is more or less complete. Whilst the majority of cases terminate within two weeks, instances of several months' duration are not unknown, but a fatal termination, sooner or later, is inevitable in all cases.

Coming on in the course of some chronic affection of the liver or some obstructing cause exterior to the organ, there soon follow ascites, nausea and vomiting, hæmatemesis, bloody stools of a liquid character, enlargement of the spleen, distension of the abdominal veins, and the distressing symptoms produced by an excessive accumulation of fluid in the peritoneal cavity.

DIAGNOSIS.--As there is no symptom of thrombosis of the portal which may not be caused by advanced cirrhosis, the diagnosis rests on the rapid production of the attendant phenomena and their conjoint appearance.

TREATMENT.--A symptomatic treatment is alone possible. The highly irritable and congested intestinal mucous membrane precludes the employment of hydragogue cathartics. Salines which cause outward diffusion from the vessels are the only cathartics which can be used with propriety. Action of the kidneys and of the skin must be maintained. To this end the resin of copaiba in pilular form and pilocarpine subcutaneously may be used. If the strength of the patient will permit, leeches around the anus can be applied, and much relief may be expected from free bleeding. It is probable that opening a swollen hemorrhoid would give the same kind of relief as that caused by a free hemorrhage. In any case the benefit derived from treatment must be merely palliative and temporary.

Suppurative Pylephlebitis.

PATHOGENY.--Primary pylephlebitis rarely if ever occurs. On the other hand, the secondary form is by no means uncommon; it succeeds to ulcerative or purulent inflammation at some point in the circuit of origin of the portal radicles. The most frequently-occurring cause is ulceration and suppuration of some part of the intestinal tube, and hence the most common result is multiple abscess of the liver. Pylephlebitis has often resulted from typhlitis; from ulcers of the large intestine, as in dysentery; from such traumatic injuries as tying hemorrhoids; from proctitis; from ulcers of the stomach and similar morbid processes elsewhere within the range of origin of the portal system. The pathogeny is clear. The inflammatory or ulcerative action extends to and involves the walls of the veins, or some morbid material diffuses through the vein walls. In either case coagulation of the blood in the vessel ensues, and the clot undergoes a series of changes resulting in the formation of emboli, which, carried into the main current, are subsequently lodged in the hepatic capillaries.

There are three steps in the morbid process: the changes in the vein wall; the production and transformation of the thrombus; and the formation of secondary suppurating foci in the liver.

{1098} The appearance of the tunics of the inflamed vessels varies with the stage at which they are examined. At first the walls of the vessels are reddish from congestion, succulent, and swollen, infiltrated by leucocytes and inflammatory exudation and the cellular elements undergoing proliferation. The intima especially is much altered in its appearance and structure, becoming thick, opaque, grayish or yellowish in color, and having adherent to it a thrombus passing through its characteristic changes. Ulceration of the intima then occurs, and the purulent elements, with shreds of tissue, mingle with the degenerating blood-clot, and ultimately there remains a purulent dépôt lined with sloughing, even gangrenous, contents. Emboli detached from such decomposing thrombus are arrested in the vessels of the liver, and there set up a suppurating phlebitis, ending in an abscess formation, or a quantity of pus from the original point of ulcerative phlebitis passes into the portal vein, and is generally distributed through the hepatic branches, here and there foci of suppuration being established by the deposit of decomposing emboli. There may be numerous small abscesses irregularly distributed through the liver, or there may be one or two larger collections of pus. Very often the vessel whose occlusion by a suppurating embolus has caused the mischief is destroyed, and hence no communication with the abscess-cavity can then be traced. These abscesses are not limited by a line of inflammatory demarcation or by a limiting membrane, but the hepatic tissue adjacent is congested and infiltrated with pus.

Ulceration, abscesses, or purulent inflammation occurring at any point within the area of origin of the radicles of the portal vein may induce pylephlebitis and consequent hepatic abscess. There are two points at which, suppuration established, secondary pylephlebitis is most apt to occur: the cæcum; the rectum. As respects the former, the symptoms of typhlitis precede the hepatic disturbance; and as respects the latter, usually dysentery, or rather proctitis, is the initial disease. In both sources of the hepatic trouble the inferior hemorrhoidal veins are chiefly concerned--a fact explicable by reference to the sluggishness of the circulation and the distended condition of these veins, whence it is that thrombus is very readily induced. Numerous instances of pylephlebitis following suppurative lesions of the cæcum have been reported. One of the most recent, and at the same time typical, examples of such conditions is that published by Bradbury[210] of Cambridge, England. The initial lesion was "an ulcer the size of a split pea" situated near "the junction of the vermiform appendix and cæcum." "The hemorrhoidal veins and the inferior mesenteric above were filled with breaking-down clot and pus," and "the liver contained many abscesses of various sizes, the largest about the size of a lemon, which had burst through the diaphragm." As is so often the case, the ulcer of the cæcum produced no recognizable disturbance, and important symptoms were manifest only when the emboli lodged in the liver set up suppuration, when there occurred the usual signs of hepatic abscess. In the West and South hepatic abscess due to pylephlebitis, induced by proctitis, with ulceration of the rectum, is a common incident. Various examples of this kind have fallen under my own observation. The relatively greater frequency of this form of pylephlebitis is due to the fact above {1099} stated, that the inferior hemorrhoidal veins are voluminous, have a sluggish current, and are liable to over-distension by pressure of feces and by external abdominal bands and clothing. Cases of a corresponding character arise from suppuration and ulceration elsewhere within the portal circuit. Thus, Bristowe[211] reports a case in which pylephlebitis resulted from an ulcer of the stomach, the neighboring veins becoming implicated and the usual results following.

[Footnote 210: The Medical Times and Gazette, Sept. 27, 1884, p. 450, "Proceedings of the Cambridge Medical Society."]

[Footnote 211: Transactions of the Pathological Society of London, vol. ix. p. 278.]

When inflammation has begun in a radicle of the portal vein, it may proceed to the liver by contiguity of tissue, the whole intervening portion of the vessel being affected. Probably more frequently the intra-hepatic portion of the portal is inflamed by emboli, and the adjacent hepatic tissue then undergoes suppuration, as has been already set forth.

SYMPTOMS.--There being two points of disease--the primary lesion of the peripheral vessel and the secondary results in the hepatic portion of the portal--the symptomatology must have a corresponding expression. The stomach, the cæcum, or the rectum, or some other organ or tissue, being occupied by a morbid process, there will be a characteristic complex of symptoms. Taking up the most usual primary disturbance, a typhlitis or an ulcer of the cæcum, there will be pain, tenderness, and possibly fever, occupying in point of time the period proper to such a malady and an amount of disturbance of function determined by the extent of the lesion. The symptoms caused by a single small ulcer of the cæcum, as in the example narrated by Bradbury, may present no characteristic features and may have little apparent importance, and yet the lesion is productive of very grave consequences.

When from any of the causes mentioned above a thrombus forms in a vein of the portal system in consequence of the extension of the inflammation about it, the case, what importance soever it previously had, now takes on new characters. The onset of the inflammation of the vein walls and the puriform degeneration of the thrombus is announced by a chill--a severe rigor, or chilly sensations at least. At the time of the chill, and sometimes before it, pain is felt, significant of the lesion in the vein. When proctitis or typhlitis precedes the pylephlebitis, pain appropriate to the malady is a significant symptom; but the pain which comes on with the beginning of the inflammation in the liver is a new sign. The most frequent sites of the pain are the right hypochondrium and the epigastrium, but it may also be felt in the left hypochondrium or in either iliac fossa. Unless there be diffuse peritonitis the pain is accompanied by a strictly-localized tenderness to pressure. The situation of the pain may afford an indication of the vein attacked, and when there are two points at which pain is experienced, one may originate at the first situation of the morbid action; the other will be due to pylephlebitis.

The fever succeeding the chill is decided, and in some cases may attain to extraordinary height--a manifestation indicative of the pyæmic character of the affection. The fever intermits or remits, with a more or less profuse perspiration. The febrile phenomena are similar in their objective expression to malarial fever, but there is an important difference in respect to the periods of recurrence of the chills. The paroxysms are very irregular as to time: there may a daily seizure at different hours, or there may be several chills on the same day. In other words, the {1100} paroxysms have the pyæmic characteristics rather than the malarial. After a time the intermittent phenomenon ceases, and there occurs a remission merely, the exacerbation being preceded by chilliness and succeeded by sweating. The sweats are characteristically profuse and exhausting. During the sweating the temperature begins to decline, and reaches its lowest point just before the chilly sensations during the early morning announce the onset of the daily exacerbation of the afternoon and evening. The thermal line exhibits many irregularities until the febrile movement assumes the remittent type, when there occur the morning remission and nocturnal exacerbation. The maxima may be from 103° F. to 105°, even to 106°.

When the pain and chill come on, disturbances of the digestive organs ensue. When a large vein of the portal system is occluded, the remaining veins must be over-distended, and congestion of a part or of all of the digestive tract will be a result. An acute gastric catarrh is set up. The appetite is lost, the stomach becomes irritable, and vomiting is a usual incident. Sometimes the disgust for food is extreme, and the nausea and vomiting are almost incessant. The vomited matters consist of a watery mucus mixed with thin bile after a time, and now and then of a bloody mucus. Thrombosis of a stomach vein may occur, to be followed by an acute ulcer, and from this considerable hemorrhage may proceed, when the vomit will consist of blood. Such an accident, happening to the mucous membrane of the intestine, will be indicated by bloody stools if the ulceration is low down, or by brownish, blackish, or chocolate-colored stools if higher up in the small bowel.

The tongue has usually a characteristic coating in these cases. Large patches of a rather heavy and darkish fur form, and, cast off from time to time, leave a glazed and somewhat raw surface. Sometimes there is a profuse salivary flow, but more frequently the mouth is dry. The lips are fissured or contain patches of herpes, and the buccal cavity may be more or less completely lined by patches of aphthæ.

Diarrhoea is a usual symptom, the stools being dark when mixed with blood, or grayish and pasty or clay-colored when there is jaundice.

Three-fourths of the cases of pylephlebitis are free from jaundice. This symptom may occur at the onset when the common duct is obstructed by a calculus, but in other cases it appears when the formation of pus in the liver exerts sufficient compression of the hepatic ducts to prevent the passage of the bile.

When jaundice occurs, it is accompanied by the usual symptoms. The urine, previously unchanged, is now colored by bile-pigment, and the alterations in the renal structure and function belonging to jaundice also take place.

It sometimes happens that the obstruction of the portal vein is sufficient to cause enlargement of the superficial veins of the abdomen, but the duration of the disease is usually too brief to permit much deviation from the normal, except rarely. In the cases characterized by the occurrence of diffuse peritonitis the abdomen will present a swollen and tense appearance, and there will be acute tenderness to pressure. The area of hepatic and splenic dulness is not increased from the outset, but is evident, as respects the spleen, soon after the obstruction at the liver, and as respects the liver when the formation of abscesses occurs.

{1101} COURSE, DURATION, AND TERMINATION.--The course of pylephlebitis is compounded of the disturbance at the original point of disease, and of the secondary inflammation at the several points in the liver where emboli set up purulent inflammation. There are, therefore, two distinct symptom-groups, and a short intervening period in which the first is being merged into the second. The duration is variable, but the extreme limits are not remote from each other, the condition of pylephlebitis terminating in from two weeks to three months, the shorter being the more usual. The termination is death, doubtless invariably; for, as in true pyæmia arising from other causes, the septic changes in the blood are such as to preclude the possibility of a return to the normal condition.

DIAGNOSIS.--The main point in the diagnosis consists in the occurrence of an evident local inflammation, followed by the signs of suppuration in the hepatic region coming on subsequent to ulceration and suppuration at some point in the peripheral expansion of the portal system. Thus, when a proctitis with ulceration of the rectum has been in existence for some time, there occur pain and tenderness in the hepatic region, accompanied by an irregularly intermittent fever and by profuse sweating, it can be assumed with considerable certainty that emboli have been deposited in some one or more of the terminal branches of the portal. The evidences of hepatic trouble--swelling of the organ, jaundice, etc.--and of portal obstruction, which then supervene, indicate with some precision the nature of the case.

TREATMENT.--Although pylephlebitis wears a most unfavorable aspect, the possibility of a favorable result should always be entertained by the therapeutist.

As absorption of medicaments must be slow--indeed, uncertain--by the gastro-intestinal mucous membrane when there is portal occlusion, it is well to attempt treatment by the skin and subcutaneous connective tissue. Gastro-intestinal disturbance--nausea, vomiting, and diarrhoea--should be treated by a combination of bismuth, creasote, and glycerin--remedies acting locally chiefly. Ammonia--the carbonate and solution of the acetate--is indicated, and should be given for the purpose of dissolving thrombi and emboli. Corrosive sublimate, carbolic acid, and quinine can be administered by the subcutaneous areolar tissue. Quinine may also be introduced by friction with lard, and in considerable quantity.

V. PARASITES OF THE LIVER.

Echinococcus of the Liver; Hydatids of the Liver.

DEFINITION.--The echinococcus is the intermediate or larval stage in the development of the Tænia echinococcus--the completed parasite--whose chief habitat is the intestine of the dog. As the natural and clinical history of parasites is elsewhere treated of, the subject is here confined to the development of echinococci cysts in the liver, its ducts, and vessels.

CAUSES.--The presence of echinococcus vesicles in the liver is due to {1102} the migration of the embryo from the intestinal canal. As Davaine[212] has ascertained by analysis of all the recorded examples previous to the publication of his treatise, echinococci are found in as large a proportion in the liver as in all the other organs combined. This statement is repeated with approval by Cobbold[213] and by Heller.[214] The embryo, set free in the intestine from the food or drink containing the ova, starts on its migration. There are several reasons why the liver is selected for its habitat: it is the largest accessible organ; the common duct and the portal vein offer the most convenient roadway for reaching and penetrating its substance. The exact route or routes of which the parasite avails itself in migrating have not been definitely settled, although Friedreich has shown that the portal vein is the medium of transmission of the Echinococcus multilocularis. The comparative frequency with which the liver is entered indicates that the portal vein is the favorite route of migration.

[Footnote 212: Traité des Entozoaires et des Maladies vermineuses, etc., par C. Davaine, Paris, 1877, p. 383.]

[Footnote 213: Entozoa, by T. Spencer Cobbold, M.D., F.R.S., London, 1874, p. 275.]

[Footnote 214: In vol. iii of Ziemssen's Cyclopædia, p. 561.]

PATHOLOGY AND SYMPTOMS.--The number of echinococci reaching the liver varies from one to ten or twelve or more. They increase in size from the time of their deposit in the organ, and ultimately attain to large proportions. The rapidity of growth depends somewhat on the character of the tissue in which imbedded, and the amount of disturbance of function is determined by the position of the parasite in the organ. Echinococci may be deposited in any part of the liver--in the substance of the organ, in the ducts, or in the vessels--but the most usual site is near the capsule, and, developing outwardly in the direction of least resistance, impart to the outline of the organ an irregular contour. As the echinococci develop, the adjacent parts of the liver pressed upon undergo atrophy, but the connective tissue of the organ contributes to the formation of the dense capsule which envelops them. But as the increase in size is not rapid, although continuous, if the cysts are situated at the periphery and adjacent to the capsule, they may be present for many months without causing any distinct symptoms. In a case occurring under my own observation last year the only symptom which attracted attention was an enlargement of the hepatic region, and on examination a characteristic elastic, irregular, and painless tumor could be readily detected by sight and touch occupying the right hypochondrium and extending into the epigastric and umbilical regions. When the echinococci cysts impinge on the portal vein or on the hepatic duct, there will be caused the usual results of such pressure--ascites or jaundice, or both conditions may occur simultaneously, with obstruction of both vein and duct. When the cysts develop downwardly, the stomach and intestines will be displaced, and nausea and vomiting, diarrhoea or constipation, and, it may be, considerable pain of a colic-like character, will be caused. An upward development of the cysts gives rise to more pronounced disturbances. The diaphragm is pushed upward, the heart displaced, and the lungs, especially the right, compressed. Occasionally the diaphragm is softened and perforated by the pressure of the enlarging cysts, and the lungs are ultimately tunnelled, the parasites being discharged by the bronchi.

{1103} The growth of an echinococcus tumor may spontaneously cease, and then retrograde changes take place, leading to its final disappearance. This arrest of development may occur without any obvious cause, but now and then such a change from the ordinary course of tumors may be effected by an external injury, as a blow on the abdomen, but more frequently the death of the parasite is caused by ulceration into a bile-duct, and the entrance of bile, which is a poison to these hydatids. It sometimes happens that, opening into a duct of large size, the daughter and granddaughter vesicles are slowly discharged through it into the intestine, and thus a cure is effected. Inflammatory action occurring in the cysts, adhesions may form and rupture into a neighboring cavity take place. Direct communication may be established with the intestine, or the cavity of the pleura or peritoneum be entered, with results entirely disastrous.

A necessarily fatal termination must also ensue when the hydatids penetrate the ascending vena cava, but this accident is, fortunately, very rare.

The passage outward through the abdominal wall is an exceedingly uncommon but fortunate issue of echinococcus of the liver, for in this mode the hydatids may be discharged without much difficulty.

The echinococcus vesicle is enveloped in a dense, resisting, and elastic capsule, constructed out of the connective tissue of the part in which it is deposited. The innermost layer of the vesicle is the germinative (endocyst), and from its granular surface are developed the brood-capsules and their scolices--i.e. the head with its suckers and crown of hooklets.[215] Each vesicle may contain not only daughter, but also granddaughter, progeny, numbering from a dozen up to many thousands, and they will vary in size from the head of a pin to a pullet's egg. It follows that the mother vesicles must also greatly vary in size: they range from a large pin's head to a child's head. The vesicles or sacs contain a clear, faintly yellowish, or opalescent fluid, neutral or slightly alkaline in reaction, and holding in solution a large per cent. of sodium chloride, but free from albumen. The specific gravity of the fluid ranges from 1007 to 1015, according to the quantity of sodium chloride present. Succinic acid and also hæmatoidin are usual constituents, besides the ingredients already mentioned.

[Footnote 215: Entozoa, Cobbold, p. 273 et seq., chapter viii.]

Although the form of hydatid or echinococcus cyst above described is the usual one, there is occasionally produced an anomalous development of the parasite, which from its resemblance to colloid cancer was supposed to have this character until Virchow[216] unravelled the mystery by demonstrating its true structure. This form of the parasite is designated Echinococcus multilocularis. Its resemblance to colloid cancer is the more striking because of the tendency of the interior of the mass to undergo degeneration, to disintegrate, and to break up into pus-sacs with greenish, cheesy, and bilious contents. An Echinococcus multilocularis tumor is of almost stony hardness; it has a very dense fibrous structure, intersected by cavities with thick gelatinous contents. These minor cavities[217] are sacs of echinococci, but they depart widely from the typical form, well-defined scolices being seldom encountered.

[Footnote 216: Archiv für Anat., Virchow, vol. xi. p. 80.]

[Footnote 217: Carrière, quoted by Davaine, op. cit., p. 961.]

{1104} Echinococci of the liver develop very slowly, and it is characteristic of them to attain to very large proportions in most cases without causing any very pronounced symptoms. There are certain signs common to hydatids in any situation; there are others which are due to particular circumstances.

A hydatid tumor of the liver is smooth but somewhat irregular in outline, and elastic, when it develops downward, extending below the margin of the ribs. If, however, it grows upward, the area of hepatic dulness extends in that direction beyond the usual limits; the diaphragm is pushed up, the lungs forced upward to the left and compressed, and the heart also displaced upward toward the left. The extension of the tumor downward, in the direction of least resistance, is more usual. If the walls of the abdomen are sufficiently thin, the tumor large enough, and if made up of many daughter vesicles, there may be evoked by palpation the very characteristic sign known as hydatid purring. To produce this effect an oscillation must be caused by a sudden impulse communicated to the tumor on one side, the hand resting against the other side. This sensation is likened to the impression on the eye of the vibration of a bowl of jelly. Even when there is a well-defined tumor this symptom is comparatively infrequent, but if present it is pathognomonic, since no other kind of tumor possesses the property of oscillation and elastic collision of its several constituents.

When the tumor is so situated as to occlude the hepatic or common duct, jaundice will be a symptom, and when the stomach is pressed upon there will be epigastric oppression and nausea. If the vena cava is impinged on or the portal vein, the usual results--ascites and oedema of the lower extremities and of the scrotum--will be manifest. There is, of course, nothing distinctive in these results.

The Echinococcus multilocularis, situated in the substance of the liver, causes the usual disturbances of a new formation in such a position. Much of the hepatic tissue is destroyed by its growth, and many of the minor ducts closed. Jaundice is an early symptom--the first, indeed, in many cases--and is also one of the most persistent. It is present, according to Griesinger, in 10 out of 13 cases. The usual gastro-intestinal disorders belonging to jaundice occur under these circumstances; also the nervous disturbances of cholæmia.[218]

[Footnote 218: Davaine, op. cit., p. 962.]

Enlargement of the spleen is a very frequent symptom, being present, according to Davaine, in 11 out of 13 cases, and, according to Heller, in 25 out of 29 cases, in which this fact was made the subject of direct inquiry.

Pressure on the vena cava causes oedema of the inferior extremities in a small number of cases; and on the vena porta, ascites. There may occur thrombosis of the portal, in which event the ascites will form very quickly, and return as quickly after tapping.

The usually placid course pursued by echinococcus of the liver may be much modified by inflammation and suppuration. Some external injury may develop the inflammation. Having occurred, the clinical history corresponds to other cases of hepatic abscess, and the reader is therefore referred to the section on that topic for fuller information.

DIAGNOSIS.--At the outset of echinococcus of the liver the {1105} differentiation of the tumor from other tumors, and of the disturbances produced by it as contrasted with the effects of other morbid growths, becomes exceedingly difficult, if not impossible. The size, painlessness, elasticity, the purring tremor of the echinococcus tumor, afford a sure basis for constructing a diagnosis, and as ultimately developed they become the means of accurate differentiation from other morbid growths of that locality. All doubt as to the nature of a given hydatid tumor of the liver may be set at rest by the use of the aspirator. The discovery of the characteristic hooklets of the scolex in the fluid withdrawn from the tumor will be conclusive as to the presence of echinococci. The hooklets may be absent, as in the case of acephalocysts, but the fluid is characteristic in other respects: it contains a large quantity of chloride of sodium and is free from albumen.

Very great difficulty is experienced in diagnosticating an echinococcus tumor developing from the upper surface of the liver, pushing the diaphragm and lungs upward and displacing the heart to the left. Whilst the physical signs may be, and are, usually alike when the condition calling for diagnosis has existed for some time, there are means of differentiating in the history of the cases and in the initial symptoms.

The origin and growth of the echinococcus tumor are obscure and free from constitutional disturbance; the onset of a pleuritic exudation is marked by pain, fever, and hurried respiration and by physical signs of a characteristic kind. It is true there are cases of so-called latent pleurisy in which a hydrothorax forms without any well-marked indications, but it will usually be found that some local pain, hurried breathing, or other symptoms existed from the beginning. Those cases of hydrothorax accompanying renal and cardiac diseases are readily enough associated with their original cause.

Echinococcus of the liver may be confounded with abscess of the liver, but a differentiation can be readily made by attention to a few considerations, except in the rare condition of the Echinococcus multilocularis which has proceeded to suppuration. In this latter condition there are no means of differentiation, since an abscess-formation has already occurred, nor is there any need to attempt a distinction without the occasion of a difference. Echinococcus differs from abscess in history, in the character of the swelling, and in progress. Abscess of the liver is preceded by paroxysms of hepatic colic, by inflammatory ulceration of some part of the intestinal tract, or by local injury--traumatism. The onset of a hydatid tumor is silent and painless. The swelling of the liver when an abscess forms is not considerable at any time, and appears to be a uniform enlargement of the organ, except when the pus tends to make its way through the walls of the abdomen externally. An enlarging echinococcus tumor is an obvious projection from the surface of the liver at some point, and it does not have the characteristic tenderness, the fluctuation of an abscess matured and ready to discharge, and the constitutional disturbance; but it does have a peculiar elasticity, and now and then may present that eminently characteristic sign, the purring tremor. The use of the exploring-trocar will usually suffice to clear up all doubts by the withdrawal of the characteristic fluid of the hydatid cyst or of pus.

DURATION AND TERMINATION.--The progress of an echinococcus {1106} tumor is exceedingly slow, and the development of symptoms produced by its extension is early or late according to its position and to the nature of the parts impinged on. A spontaneous cure may take place under the rather rare circumstances of an opening into the hepatic duct or one of its principal divisions, and the gradual discharge of the cysts by this outlet into the intestine. Next to this mode of termination, the most fortunate direction taken by the enlarging cysts is through the walls of the abdomen externally. When the growth is upward through the lungs, the symptoms belonging to empyema or hydrothorax, with pulmonary abscess, ensue, and the termination is fatal after a protracted course. Rupture into the peritoneal cavity is a fatal event. Ulceration into the intestine, and the discharge of the cysts through the route thus made, may effect a cure, but more frequently the fistulous communication becomes a means of forming a fecal abscess.

The result in any case of hydatids of the liver is much influenced by the mode of treatment adopted and the period at which it is undertaken. As these parasites can be readily reached and destroyed by safe means, obviously the more early the diagnosis is made and the treatment carried out, the less the injury done to the hepatic structures and neighboring parts.

TREATMENT.--Prophylactic.--As the intestine of the dog is the natural habitat of the Tænia echinococcus, and as the hydatid is the first stage in the development of the ovum and the second in the life-history of the parasite, the means of prophylaxis consist in preventing contamination of human food and water with the dog's excrement, which contains the ova of the parasite. In Iceland, where hydatid disease is very prevalent, dogs and human beings living in the same huts and obtaining their water-supply by melting the snow just about them, contamination of food and drink must readily occur. In this country such conditions cannot exist; nevertheless, cases of hydatids are not infrequent. The chief, if not the only, source of contamination is through the consumption of such uncooked vegetables as lettuce, celery, cabbage, etc., in the folds of which the ova may be retained, and from which an ordinary washing does not suffice to detach them. It follows that such articles of food should be minutely inspected and cleansed before being placed on the table.

Boiling and filtration are the means of removing impurities of this kind from potable waters.

Therapeutical.--The remedial management of cases of Tænia echinococcus is necessarily restricted to that stage in their development when by increasing size the functions of organs begin to be affected. Internal medicines given with the view to arrest the growth of the parasite are useless. Formerly, such attempts were made and successes were claimed, but it is now known that no medicine can act on organisms enclosed as these are in a dense capsule. It is needless to occupy space with therapeutical details of this kind, but mention may be made of the agents that were supposed to be effective. Laennec held that baths of a solution of common salt had a distinct curative effect. The internal use of iodide of potassium and the local application of iodine paint were believed to cure a case in St. George's Hospital, London, in the practice of Mr. Cæsar Hawkins. Kameela was, in Iceland, supposed to have a curative effect, but notwithstanding this the physicians of that island resort to very heroical surgical methods in the treatment of this affection.

{1107} The one means of relief consists in the removal of the vesicles, either by suitable incisions or by compassing the death of the parasite, after which the power of nature may be adequate to the cure. In Iceland large incisions are made into the tumor at its most prominent part, and, although accidents are not uncommon, the results in many cases are eminently satisfactory. The accidents are shock, hemorrhage, and especially peritonitis. Under favorable circumstances now no procedure is more satisfactory in its results than free incision and drainage. The tumor should be prominent, adherent all round to the peritoneum, and the walls of the abdomen thin to ensure complete success without accident. At the present time, so great have been the advances in abdominal surgery, this operative procedure may be preferable in some few cases presenting the favoring conditions above mentioned.

Very simple expedients, however, suffice in most cases. The most simple is puncture. This is now much practised in Iceland, and, as the statistics show, with considerable success. Thus, Hjaltelin[219] reports 100 cases cured in this way, and in his own hands this expedient proved successful in 41 out of 50 cases operated on. In Australia, where hydatid disease is also quite common, simple puncture has effected a large proportion of cures,[220] and is the method of treatment usually pursued. In England puncture has the approval of some of the best authorities.[221]

[Footnote 219: Davaine, op. cit., p. 605.]

[Footnote 220: The Medical Times and Gazette, August, 1873, p. 164.]

[Footnote 221: Transactions of the Clinical Society for 1872: discussion participated in by Gull, Bryant, Greenhow, etc.]

The mode of performing this operation consists in the introduction of an exploring-trocar into the most prominent part of the tumor. It may be withdrawn at once or be permitted to remain for a few minutes to several hours. The dangers are suppuration in the sac and peritonitis; but the former, although sometimes accompanied by severe constitutional symptoms, is not likely to endanger life, and even formidable disturbances due to the latter are usually recovered from. The facts show that puncture very rarely indeed causes dangerous, especially fatal, symptoms. An eruption of urticaria has been observed to follow puncture with the trocar, and also aspiration, in a considerable proportion of the cases, but it has no special significance.

Since the introduction of the aspirateur, puncture and withdrawal of the fluid by means of this instrument has been practised more frequently, and this appears to be a more effective procedure, than simple puncture with an exploring-trocar, although in most cases the escape of the contained fluids suffices to destroy the parasite. The aspirateur is less likely to permit the escape of fluid into the peritoneal cavity or the entrance of air into a vein punctured by accident. If puncture with the trocar or aspiration be practised, shall all the fluid be withdrawn at once? The answer to this question may be decided by the character of the sac. Does it contain daughter and granddaughter vesicles? If so, one puncture may not permit the escape of much fluid; but in any event it is the practice of the most judicious and experienced authorities[222] to withdraw as much as possible of the contents of the cysts at the first operation. Formerly, a method practised by some French surgeons consisted in successive tappings, a small quantity of fluid being drawn off each time.[223] {1108} There is no good reason for this method of treatment now, and it seems to have been discontinued.

[Footnote 222: Transactions of the Clinical Society, loc. cit.]

[Footnote 223: Davaine, supra.]

Yet another method of treatment, but less effective than puncture or aspiration, consists in injecting into the sac, after the removal of its contained fluid, certain agents toxic to hydatids. A solution of the extract of fern, alcohol, solution or tincture of iodine, and bile, are the chief remedies thus employed. It has long been known that bile is destructive of these parasites, and cases have occurred of spontaneous cure in which the opening of the growing cysts into a bile-duct has secured the entrance of bile and consequent arrest of growth and atrophy of the hydatids. Several successful cases have been reported in which the injection of aspidium (male fern) was the effective agent, but the threatening symptoms produced by it, and the comparative freedom of other methods of treatment from such disturbances, do not recommend the injections of fern. In the case reported by Pavy[224] the extract of fern was mixed with a solution of potassa.

[Footnote 224: Lancet (London), July, 1865.]

Injections of iodine in solution or in the form of tincture have been more frequently practised than of any other material. Davaine,[225] who finds it less successful than simple puncture and aspiration, recommends, as affording the best results, a dilute aqueous solution of iodine. Alcohol, a solution of permanganate of potassium, and various antiseptic agents have been used to some extent, but none of them possess any advantages over more simple measures.

[Footnote 225: Op. cit., p. 650.]

The latest proposal for the treatment of hydatid cysts, and probably the most effective consistent with entire safety, is electrolysis. Originally suggested by Althaus[226] to those who first employed the measure on any considerable scale, it had been mentioned thirty years before by Budd, and appears to have been first practised in Iceland on a single case. The first elaborate attempt to establish electrolysis on a sound basis as a regular procedure was made by C. Hilton Fagge and Mr. Arthur E. Durham.[227] They operated on eight cases, and all were successful. The method consists in the introduction of two needles connected with the negative pole, and the application of the positive--a moistened sponge--on the exterior in the neighborhood of the hepatic region. The strength of current employed by Fagge and Durham was that furnished by a battery of ten cells, and which by previous trial was found to decompose a saline solution. The two electrolytic needles, connected with wires attached to the negative pole, were introduced into the most prominent part of the tumor about two inches apart. The current was allowed to pass about ten minutes usually, sometimes a little longer, the sponge on the exterior--the positive pole--being shifted occasionally. The immediate effects are not considerable. The tumor may be rendered somewhat more tense and appear to be enlarged, but more frequently it becomes softer and is lessened in size, the increase of size being due to the disengagement of hydrogen gas, and the diminution caused by the escape of more or less fluid. The immediate effects of the operation varied. In one case no symptom followed, and in this the result was regarded as doubtful, although a cure was considered probable. In the others more or less {1109} constitutional disturbance followed, the symptoms being pain and fever, the temperature ranging between 100° and 103° F. The duration of the fever was from two to nineteen days, the latter in one case only. As has been observed in some of the cases treated by puncture or by aspiration, a rash appeared on the skin--in some instances scarlatinous, in others of urticaria. It is a curious circumstance that an eruption of urticaria is reported to have appeared in one subject in whom a rupture of the sac into the peritoneal cavity is supposed to have occurred.

[Footnote 226: On the Electrolytic Treatment of Tumors, etc., London, 1867.]

[Footnote 227: Medico-Chirurgical Transactions, 1871, p. 1 et seq.]

Although so little change in the tumor occurs immediately after the operation, yet it undergoes slow absorption, and ultimately disappears. The time occupied in the disappearance of the tumor varies from a few weeks to many months, the difference being due probably to the situation of the growth, those occupying the substance of the liver requiring a longer time to fill up.

Fagge and Durham report a case in which simple acupuncture was followed by a result apparently as good as obtained by electrolysis, and other similar experiences have been published. If the simple introduction of a needle suffices to arrest the growth of a hydatid cyst and induce its atrophy, of course the more complex procedures will be abandoned.

The tendency of the treatment of hydatid cysts has constantly been toward simplicity, and the success occurs in a direct ratio thereto. In forming an estimate of the relative value of the methods of treatment, the average of mortality of each plan becomes the most important factor. Simple tapping and paracentesis, the most frequently adopted mode of treatment, is not without immediate and remote danger. Of 46 cases carefully tabulated by Murchison,[228] there were 3 deaths properly attributable to the operation; but the after results--suppuration of the cyst and its consequences, peritonitis, etc.--cannot be measured so accurately. About two-thirds of the cases thus treated result in cure, and in a majority of these a single operation suffices. The injection of the various substances which have been employed for that purpose does not seem to increase the proportion of cures, and their use distinctly enhances the dangers of the treatment. At present, the decision as to the method of treatment to be employed in any case should be made between simple tapping, electrolysis, and acupuncture. Of these, the last mentioned, it can hardly be doubted, is the method which is most desirable, for although it has not been employed so largely as the others, thus far the results have been better: the percentage of recoveries without accident has been higher relatively than by other methods of treatment. As acupuncture presents no special difficulties or dangers, and is but little painful, it may be tried first, reserving more formidable measures for the failures by this simple expedient.

[Footnote 228: Clinical Lectures on Diseases of the Liver, loc. cit.]

Distoma hepaticum and Distoma lanceolatum (Liver-Flukes).

The Distoma hepaticum, entitled by Linnæus Fasciola hepatica, occurs very frequently in herbivorous animals and occasionally in the biliary {1110} passages of man.[229] It is, however, less important than the Distoma lanceolatum, which, although much smaller than the former, occurs in much larger numbers.

[Footnote 229: Davaine, Traité des Entozoaires, Paris, 1877, p. 240 et seq.; also, Cobbold, Entozoa, p. 148.]

Distoma hepaticum is a leech-like parasite from 25 to 30 mm. in length, of a brownish color, smooth to the naked eye, but thickly covered with minute spikes or spines to be seen with a low power, and provided with a cephalic (entrance to oral cavity) and an abdominal sucking disk, which are also organs of locomotion. The Distoma lanceolatum owes its name to its lancet shape; it is smaller than D. hepaticum, measuring about 8 mm. in length and half this or less in width; it is unprovided with spines, but contains two suckers at the side. Both parasites are hermaphrodite; the ova, according to Cobbold (p. 166), have "an average longitudinal diameter of 1/180, whilst their greatest transversal measurement is about 1/270." These ova are capable of some movement, provided as they are with a ciliated envelope.

The disease known as the rot in sheep, and a peculiar cachexia entitled by Davaine la cachexie aqueuse, are caused by the presence of distoma. The ova gain access to man through the use of unwashed cress, lettuce, and similar vegetables eaten in the raw state, and in drinking-water. Fortunately, this accident is rare. The number of reported examples collected from all sources by the indefatigable Davaine is twelve.[230]

[Footnote 230: Ibid., p. 253 et seq.]

The larger distoma passes into the common and hepatic duct and gall-bladder, whilst the smaller (lanceolatum) enters the finer ramifications, and, there multiplying, several consequences may ensue. The irritation caused by their presence and development will excite a more or less severe cholangitis, or, accumulating in sufficient numbers, an actual obstruction will be induced, and jaundice and structural alterations of the liver will in turn be brought on.

The DIAGNOSIS of such a malady is, in the very nature of the case, uncertain at best, and in most cases impossible. Nevertheless, it may be made in rare instances. The existence of the rot may cast suspicion on the mutton and kitchen vegetables so situated as to suggest the possibility of contamination with the ova of distoma. Definite and conclusive information will be afforded by the presence of the ova, still more of the more or less fully-developed parasite, in the feces of a patient effected by the symptoms of catarrhal jaundice or occlusion of the biliary passages. By tapping the gall-bladder parasites may be withdrawn.

The SYMPTOMS are those common to cases of catarrh of the bile-ducts (cholangitis), catarrhal jaundice, or occlusion of the passages, as may be. As these have been detailed under their respective heads, it is not necessary to repeat the observations already made.

As regards the TREATMENT, in addition to the methods of management recommended in such cases it may be stated that the use of certain parasiticides offers a reasonable prospect of good results. Creasote, bichloride of mercury, thymol, eucalyptol, oil of wintergreen (gaultheria), and similar agents are rational remedies and should be fairly tried.

{1111} Parasites in the Portal Vein.

The entozoön which by its presence in the blood causes the disease chyluria also inhabits the portal vein. In some parts of the world--Brazil more especially--this disease is exceedingly common. It has occurred also in two or three instances in England, and the writer has had a case within the past year (1884) in Philadelphia. The parasites in this case were found in immense numbers in the urine.

The blood of the portal vein sometimes is actually filled, and the liver substance itself is penetrated, by them, but nothing is known of the alterations they induce in these organs. When cases of hæmaturia or chylous urine due to the Filaria sanguinis hominis occur, the changes are not confined to the urinary organs, but often, doubtless, involve the liver. There are no signs in the present state of our knowledge by which the existence of these parasites in the portal vein and liver can be determined.

{1112}

DISEASES OF THE PANCREAS.

BY LOUIS STARR, M.D.

Until the middle of the seventeenth century the prevalent views upon the functions and diseases of the pancreas were vague in the extreme. By some the organ was regarded simply as a cushion provided for the protection of the neighboring blood-vessels and nerves; by others it was looked upon as the seat of lesion in many very diverse diseases, as ague, hypochondriasis, melancholia, and so on.

In 1642, Wirsung's discovery of an excretory duct demonstrated the fact that the pancreas was a special organ, and initiated the successful investigation of the physiology and pathology of the gland. For many years after this, however, little progress was made, and it is only comparatively recent investigations that have furnished definite and reliable information upon the subject. Even now our knowledge of the clinical and pathological features of diseases of the pancreas is far behind that of many of the other viscera of the body, the chief reasons for this being the uncertainty in regard to the physiology of the gland and the rarity with which its lesions are primary and uncomplicated.

ANATOMY AND PHYSIOLOGY.--The pancreas is a long, somewhat flattened, narrow, acinous gland, pinkish-white in color, and of looser texture than the salivary glands, which it otherwise closely resembles in structure. It is hammer-shaped, measures from six to eight inches in length, one and a half inches in breadth, and about three-fourths of an inch in thickness, and varies in weight from three to five ounces. The gland is situated in the upper part of the abdominal cavity; the expanded portion, or head, lies in the concavity of the duodenum; thence it extends transversely across the epigastric and both hypochondriac regions on a level with the first lumbar vertebra and in contact with the posterior abdominal wall. As it passes toward the left it gradually decreases in size, and the narrowest part, or tail, rests against the spleen. Behind the organ are the crura of the diaphragm, the aorta, the inferior cava, the superior mesenteric vessels, and the solar plexus; in front of it, the stomach and the left lobe of the liver. Its anterior surface alone is invested with peritoneum, being covered by the posterior layer of the lesser omentum. The ascending portion of the head is intimately connected with the duodenum by dense connective tissue, and at times the descending portion, by extending backward and outward, forms an almost complete ring around the gut; the body is loosely attached by connective tissue to the posterior abdominal wall, and the {1113} left extremity and tail are joined to the left kidney and suprarenal capsule and to the spleen by loose areolar tissue. The gland is supplied with arterial blood by branches springing from the pancreatico-duodenal and splenic vessels; its veins join the splenic and superior mesenteric veins; its lymphatics communicate with the lumbar glands; and its nerves are branches from the solar plexus. The principal excretory duct, the canal of Wirsung, has at its widest part the calibre of a goose-quill. It begins by the union of five small branches at the tail, and extends transversely through the substance of the gland from left to right, nearer the lower than the upper border, and the anterior than the posterior surface; it is joined throughout its course by numerous small branches from the acini, which enter it at acute angles. In the head the duct curves slightly downward, and as a rule opens with the ductus choledochus into the ampulla of Vater in the second portion of the duodenum; sometimes, however, it has a separate opening into the intestine. A second, smaller, duct runs from the ascending portion of the head, and usually joins the main duct, but may also open independently.

The acini of the gland are from .045 mm. to .090 mm. in diameter, and are composed of a very thin membrane lined with pavement cells. The thin walls of the excretory ducts are formed of connective tissue and elastic fibres, and are lined by a single layer of small cylindrical epithelial cells. The terminal extremities of the ducts form a complete network around the glandular cells, resembling the intralobular biliary canaliculi. The acini are imbedded in a mass of adipose tissue which contains the vessels and nerves.

The topographical relation of the head of the pancreas to the ductus choledochus is of clinical importance. As a rule (fifteen times in twenty-two, Wyss), the bile-duct descends near the head, toward the duodenum; frequently it runs through this part of the organ, being either partially or entirely surrounded by the gland substance. Now, when the bile-duct merely passes over the pancreas, any enlargement, unless excessive, would simply push it aside, but when it passes through the head, a comparatively slight amount of disease is sufficient to close it entirely and cause jaundice.

It is only since the observations of Bernard in 1848 that the prominence of the pancreatic juice as a digestive fluid has been recognized. It fulfils several important purposes: in the first place, it emulsifies the fatty articles of food; secondly, it converts starch and cane-sugar into glucose; and, finally, it supplements the action of the gastric juice upon nitrogenous materials and completes their digestion. Each of these changes is probably brought about through the agency of a special ferment (Danilewsky). The pancreatic juice is not secreted continuously. According to the observations of Bernstein, there are two separate secretory flows following each ingestion of food--one occurring shortly after the food enters the stomach; the other a few hours later, corresponding in time to the passage of the food from the stomach into the intestine, the latter being followed by a period of rest until the next meal. Both the condition of nausea and the act of vomiting arrest the secretion. When the vagus is divided and the central extremity of the cut nerve is irritated, the secretion is also arrested, and remains checked {1114} for a long time. The arrest in each instance is attributed to reflex action of the spinal cord and sympathetic nerve. At the same time, irritation of the mucous membrane of the stomach caused by the presence of food increases the flow of pancreatic juice, and so too does simple section of the nerves which accompany the arteries. It would seem, therefore, that the gland is under the influence of two sets of nerves from the vagus--one inhibiting, the other exciting, its secretion.

GENERAL ETIOLOGY.--Pancreatic disease occurs more frequently in men than in women. No period of life is exempt from it, but it is most commonly met with in the aged. The predisposing causes are constitutional syphilis, pregnancy, and hereditary tendency. Among the apparent exciting causes may be mentioned the habitual over-use of alcoholic drinks, gluttony, the excessive use of tobacco, suppression of the menstrual flux, the abuse of purgatives, excessive and prolonged mercurial medication, and mechanical injuries, either prolonged pressure or blows upon the epigastrium. As a secondary affection, disease of the pancreas is associated with chronic diseases of the heart, lungs, liver, alimentary canal, and abdominal glands, and the organ may be the seat of metastatic abscesses and tumors.

GENERAL SYMPTOMATOLOGY.--The objective symptoms are--rapid and extreme emaciation of the entire body; sialorrhoea; obstinate diarrhoea with viscid stools; fatty stools; lipuria; and the presence of masses of undigested striped muscular fibres in the stools.

The well-established fat-absorbing and peptonizing properties of the pancreatic juice furnish a ready explanation of the wasting of the body which occurs when this secretion is arrested, diminished in quantity, or altered in quality by disease. Emaciation is not a constant symptom of pancreatic disease. A number of cases are mentioned by Abercrombie, Claessen, and Schiff in which, notwithstanding disease of the gland and complete closure of the duct, revealed by post-mortem examination, the patients during life were not only well nourished, but even moderately corpulent. In such instances it is probable that the digestive functions of the absent pancreatic juice are more or less adequately performed by the bile and succus entericus. When present, emaciation is an early symptom; it is at the same time progressive, and is usually very intense in degree, being most marked in those cases where there is associated hepatic disease or obstruction to the passage of bile into the intestine, where the disease of the pancreas interferes mechanically with the processes of nutrition by pressing upon the pyloric extremity of the stomach or upon the duodenum, and when the organ is the seat of carcinomatous growths. In the last-named condition, in addition to the perversion or arrest of the secretion, the loss of flesh is attributable to the general causes of malnutrition attendant upon carcinoma wherever situated.

Sialorrhoea, or an excessive secretion from the salivary glands, is noticeable as a symptom of disease of the pancreas only when there is an associated lesion of the stomach, either of a catarrhal or cancerous nature. Under these circumstances a quantity--six or eight fluidounces--of a colorless, slightly opalescent, and adhesive and alkaline fluid may be expelled from the mouth at once as an early morning pyrosis; or by frequent and repeated acts of expectoration, following a sudden filling of the mouth with fluid, a large bulk of thin saliva may be expelled {1115} during the day. This hypersecretion must not be looked upon as any indication of an especial sympathy existing between the salivary glands and the pancreas, neither can it be regarded as a pancreatic flux with a regurgitation of the fluid from the duodenum into the stomach and thence through the oesophagus into the mouth, since during the nausea that must always attend the passage of the intestinal contents into the stomach the pancreatic secretion is arrested, and since the liquid contains salivary, and not pancreatic, elements.

The diarrhoea pancreatica is the least constant of all the objective symptoms; in fact, constipation is present in many pancreatic affections, notably carcinoma. The fecal evacuations in this condition are frequent, thin, viscid, and contain an abundance of leucin. Under the microscope the leucin appears either in the form of concentrically sheathed globules, or as small crystalline rods and scales collected together in the form of wheels or aggregated in clusters. This form of diarrhoea may be attributed to a hypersecretion from the pancreas.

That the presence of fat in the stools is an important diagnostic symptom of pancreatic disease is proved both by clinical and experimental observations. The characters of these stools vary considerably. The fat may appear mixed with the feces in small lumps, ranging in size from a pea to a hazelnut, yellowish-white in color, soluble in æther, and easily melted and burned. Again, after the evacuation has become cool fat may be seen covering the fecal masses, collected into a thick cake around the edges of the containing vessel, or, when the feces are liquid, floating as free oil on the surface. Finally, the fat may be in a crystalline form, the crystals being needle-shaped and aggregated into sheaves and tufts. The quantity of fat also varies. It may be present only in small quantities, or may even be entirely absent from the evacuations in those cases in which the secretion from the pancreas is simply diminished, and the amount is greatest in those instances where there is a simultaneous arrest of the pancreatic and hepatic secretions. It must be remembered, too, that even in health the stools may contain fat; this occurs when an excess of oleaginous food is consumed and after the administration of castor oil or cod-liver oil. These conditions must be eliminated, therefore, in estimating the value of fatty stools as a diagnostic symptom; if, then, at the same time, coincident disease of the liver can be excluded, the symptom becomes almost pathognomonic. The appearance of fat in the stools may be due not only to an arrest of the pancreatic secretion, but also to pressure upon the large lymphatic trunks, interfering with the circulation of the chyle and checking the absorption of fat from the intestine.

Usually, the amount of fat expelled is in direct proportion to the quantity consumed, but occasionally the former greatly exceeds the latter. In such cases there must be some other source for the evacuated fat than the food; and it is probable that fat from the adipose tissue passes into the blood, and thence through the mesenteric vessels into the intestine. This theory would likewise account in part for the rapid and extreme wasting, and for another less frequently observed symptom--namely, lipuria. A case is recorded by Clark of medullary cancer of the pancreas with nutmeg liver, and another by Bowditch of cancer of the pancreas and liver in which lipuria was noted. The fat was observed, after the urine had cooled, floating about on the surface in masses or globules; differing, {1116} therefore, from chyluria, for in this condition the fat is present in the form of an emulsion, and gives the urine either a uniform milk-like appearance, or, after it has been allowed to stand, rests upon the surface in a creamy layer.

When the pancreatic secretion is arrested, most of the animal food which has escaped gastric digestion will pass unchanged through the intestine and give rise to another characteristic condition of the evacuations--namely, the presence in the feces of undigested striped muscular fibres. The amount of these fibres, and indeed their appearance at all in any given case, will depend directly upon the nature of the food consumed.

SUBJECTIVE SYMPTOMS.--The subjective symptoms of disease of the pancreas are abnormal sensations in the epigastrium, and pain.

The abnormal sensations in the epigastrium are weight and pressure, attended at times by præcordial oppression and discomfort. The feeling of weight is usually deep-seated, may be intermittent or constant, and is generally increased or developed by pressure. It is often influenced by position, the assumption of the erect posture or turning from side to side giving rise to a stretching or dragging sensation, as if a heavy body were falling downward or moving about in the upper abdomen.

The pain may be due either to an inflammation of the peritoneum covering the gland or to pressure upon the solar plexus, and consequently varies in character. When it depends upon localized peritonitis, it is constant, circumscribed, and deeply seated in the epigastrium at a point midway between the tip of the ensiform cartilage and the umbilicus; it is rather acute, and is greatly augmented by pressure. The second variety occurs in paroxysms, and is neuralgic in character, the sharp, excessively severe lancinating pains extending from the epigastrium through to the back, upward into the thorax, and downward into the abdomen. These paroxysms--in reality attacks of coeliac neuralgia--are attended by great anxiety, restlessness, and oppression and a tendency to syncope. That calculi in the duct of Wirsung, tightly grasped at the position of arrest, may give rise to paroxysms of pain analogous to biliary colic, cannot be doubted, though there are no positive facts in support of this view.

PRESSURE SYMPTOMS.--When the pancreas becomes enlarged it encroaches upon the neighboring blood-vessels and viscera, interferes with their functions, and thus produces prominent symptoms.

The ductus choledochus from its close relation to the head of the gland is especially liable to become obstructed, with the consequent production of chronic jaundice and the general effects of the absence of bile from the intestinal canal. Pressure upon the portal vein gives rise to enlargement of the spleen; on the inferior cava, to oedema of the feet and legs; and on the aorta, occasionally, to aneurismal dilatation of the vessel above the point of obstruction and to subsequent alteration in the size of the heart. By encroaching on the stomach an enlarged pancreas may cause either displacement of the viscus or stenosis at its pyloric extremity, attended with occasional vomiting of large quantities of grumous, fermenting liquid, pain, constipation, general failure of health, and the distinctive physical signs of dilatation of the stomach. The duodenum may also be pressed upon and more or less occluded, and pain and vomiting occur several hours after food is taken. Occasionally hydronephrosis is {1117} produced, the accumulation being usually in the right kidney and due to obstruction of the corresponding ureter.

A sufficient number of cases have been collected to show that there is an intimate connection between disease of the pancreas and diabetes mellitus. One or other condition may take the precedence, melituria occurring during the progress of pancreatic disease, demonstrating the onset of diabetes, and the appearance of fatty stools in diabetes a secondary involvement of the pancreas. Various theories have been advanced to account for this association, but the true explanation seems to be based upon the experiments of Munk and Klebs. By experimenting upon dogs these observers found that extirpation of the solar plexus produced either permanent or temporary diabetes, whereas section of the hepatic and splanchnic nerves, removal of the pancreas, or ligature of the duct of Wirsung was without effect. From the intimate anatomical relation of the pancreas to the solar plexus it is easy to understand how disease of the gland may give rise to alterations in the nerve-structure, either by direct pressure or by the extension of inflammation along the nerve-fibres connecting the gland with the ganglia; and these alterations in time produce diabetes. In the instances in which diabetes is the primary affection the condition of the pancreas, as proved by post-mortem section, is usually one of simple or fatty atrophy; and it may be assumed that a lesion of the solar plexus is the cause of both diseases, the changes in the pancreas being produced in a similar way to the atrophy of the submaxillary gland after section of the vaso-motor nerves in Bernard's experiments.

The same nerve-lesion may give rise to bronzing of the skin, and two cases are recorded in which disease of the pancreas (cheesy infiltration, cancer) was attended by this symptom.

PHYSICAL SIGNS.--To make a successful exploration of the pancreas the stomach and colon should be as far as possible empty, and the patient placed in a position, with the head and shoulders slightly elevated and the thighs drawn up toward the belly, to relax the abdominal muscles; or if necessary this relaxation must be brought about by the administration of æther. The knee-elbow position is often preferable to the dorsal position in practising palpation.

The condition of the gland giving rise to physical signs is one of enlargement, affecting chiefly and primarily its head, and due generally to the presence of some morbid growth.

Inspection reveals either a diffuse bulging of the upper third of the abdomen to the right of the median line, or a well-defined tumor situated beneath the right costal border, about the line of junction of the right hypochondriac and epigastric regions. Often the pancreatic tumor does not come in direct contact with the abdominal wall, but presses against and thrusts forward the left lobe of the liver, producing simply a prominence in the epigastrium. In the first condition palpation elicits an ill-defined sense of resistance; in the second, the fingers readily outline a tumor, which is slightly movable, rounded in shape, firm or fluctuating, with a smooth or nodulated surface, usually tender to the touch, and often giving a false impulse transmitted from the aorta lying beneath; and in the third, the smooth surface and the sharp edge of the left lobe of the liver are easily distinguishable.

{1118} Percussion over a pancreatic tumor is commonly dully-tympanitic, absolute flatness occurring only when it is very large and comes directly in contact with the abdominal wall, pushing aside the stomach and intestines.

On auscultation a blowing murmur may, in some instances, be heard over the tumor. These murmurs are due to pressure upon the aorta, and must be distinguished from the sound produced in aneurism of this vessel.

The various complications of pancreatic disease, such as dilatation of the stomach, ascites, and secondary lesions of the liver, greatly modify the physical signs, and sometimes entirely prevent an exploration of the gland.

INFLAMMATORY AFFECTIONS OF THE PANCREAS.

Acute Idiopathic Pancreatitis.

This is a rare disease. It occurs most frequently in males during and after adult life, and the strumous diathesis appears to predispose to it. Intemperance, the suppression of normal or morbid discharges, and traumatism act as exciting causes.

ANATOMICAL APPEARANCES.--The pathological changes may be divided into two stages. In the first the gland is deep red in color, intensely injected with blood, greatly increased in consistence, enlarged to the extent of two or three times its normal size, and when an incision is made the divided lobules feel firm and crisp. The interlobular tissue is sometimes dotted with bloody points, and the same hemorrhagic changes may occur in the connective tissue surrounding the gland. In this stage resolution may occur or the inflammation may pass into suppuration. At the beginning of the second, or suppurative, stage numerous minute collections of pus are seen scattered throughout the gland in the interacinous tissue; these gradually collect into a single large abscess, and at times the whole gland is converted into a mere pus-sac, the capsule being much thickened. In other instances the formation of pus is entirely peripancreatic. The pus is usually inodorous and creamy, but is sometimes grayish-white or greenish in color; it then has a faint disagreeable odor, and occasionally is very fetid. When mixed with pancreatic juice it becomes clear and yellowish in color, and contains numerous minute curd-like masses.

In the first stage secondary peritonitis may arise from a simple extension of the inflammatory process, and bands of lymph are formed, gluing the pancreas to the neighboring organs. In the second, fatal acute peritonitis may result from the bursting of an abscess into the peritoneal cavity. These abscesses also occasionally open into the duodenum or stomach. Gangrene and peripancreatic sloughing occur very exceptionally, and are probably due to extensive hemorrhagic changes.

SYMPTOMS AND COURSE.--The disease may be preceded for an indefinite period by symptoms of impaired gastric or intestinal digestion, but its onset is usually sudden. The attack begins with colic or continuous {1119} deep-seated pain, starting in the epigastrium and extending toward the right shoulder or the back, and quickly becoming very intense. The pain is attended by pallor of the face, great restlessness, præcordial anxiety, dyspnoea, and faintness. The tongue is furred or dry and red; thirst is increased; the appetite is lost; there are frequent eructations, nausea, and constant vomiting of a clear, greenish, viscid fluid; the vomiting produces no sense of relief, and even increases the epigastric pain. The bowels are obstinately constipated. The epigastric region is tense, tumid, and excessively tender, so that it is usually impossible to elicit the physical signs of enlargement of the gland. There is moderate pyrexia, with evening exacerbations, and the pulse is increased in frequency. Jaundice does not occur.

These symptoms progressively increase in severity, and reach their maximum intensity in from three to five days. The pulse then becomes small, compressible, and irregular, the extremities cold, the face hippocratic, and death takes place in a state of collapse. The fatal termination is preceded by the symptoms of acute peritonitis in the cases which are complicated by an extension of inflammation or the rupture of an abscess into the peritoneal cavity.

Recovery is quite possible in the early stage of the disease. On the other hand, the course may be greatly protracted by a change in the type of the inflammation, resulting in induration and enlargement of the gland or in the formation of chronic abscesses. Again, when peritonitis from extension has been confined solely to the portion of the peritoneum that covers the gland, and has resulted in the formation of fibrinous bands binding the pancreas to the adjacent viscera, the symptoms of pancreatitis will on subsiding give place to those of obstruction of the stomach, duodenum, or bile-duct.

DIAGNOSIS.--The diseases most likely to be confounded with acute pancreatitis are biliary colic and the catarrhal form of acute gastritis.

From biliary colic it is distinguished by the absence of rigors, jaundice, enlargement of the liver, and a tender pyriform tumor corresponding in situation to the gall-bladder and due to its distension with accumulated bile. The pain in both affections is sudden in its onset, and very similar in character and distribution; but when caused by the passage of a gall-stone it usually begins either after a heavy meal or after some severe muscular exertion or shaking of the body--circumstances inoperative in the production of the pain of pancreatitis. The pain, too, in the former condition is less severe at first, increases gradually in severity, is more paroxysmal, is at the outset lessened by pressure, and is often temporarily relieved by the act of vomiting. The attacks at the same time are rarely isolated, and all doubt is removed when the pain ceases suddenly and a calculus is discovered in the feces.

Acute gastric catarrh is almost always traceable to the ingestion of some irritant substance, usually alcohol or food of bad quality. This history, together with the liability of the attack to occur during the course of chronic dyspepsia, the comparatively trifling severity of the pain, the headache, the irregularity of the bowels, the condition of the urine, which is either high-colored or deposits lithates abundantly, and the tendency of the affection to become chronic, are the points of distinction between this and the pancreatic disease.

{1120} Acute inflammation of the stomach, or gastritis proper, resulting from corrosive poisons, presents a train of symptoms entirely different from those of acute pancreatitis.

TREATMENT.--Absolute rest is essential. The diet should consist of milk guarded by lime-water and of meat-broths, this food being administered in small quantities--one to two or three fluidounces of the milk and lime-water or half as much broth--at proper intervals. In the early stage an effort must be made to reduce the inflammation by the application of ice to the epigastrium or of leeches to the same region, or preferably to the anus. The excessive pain demands the free use of opium. The nausea and vomiting may be relieved to some extent by directing the patient to swallow small lumps of ice, and by the employment of iced carbonic-acid water and the effervescing draught; and the tendency to constipation may be overcome by enemata. Later in the course of the disease, if the epigastric tenderness permits of it, light linseed poultices should be placed over the upper abdomen. During the stage of collapse alcoholic stimulants and the application of heat to the extremities are necessary. The occurrence of acute peritonitis or other complications and sequelæ demand appropriate treatment.

Acute Secondary Pancreatitis.

In this condition the pancreas may be the seat of either acute parenchymatous inflammation or of metastatic abscesses.

Acute parenchymatous degeneration of the muscles, kidneys, liver, and so on is recognized as a frequent lesion in the acute infectious diseases, particularly typhoid fever; and it is under these circumstances, and in association always with similar changes in some of the organs mentioned, that parenchymatous degeneration of the pancreas takes place.

Metastatic suppurative inflammation is very rare: it has been observed in cases of disease of the testicles after the operation of extirpation of these organs, and occasionally in puerperal peritonitis.

ANATOMICAL APPEARANCES.--In parenchymatous inflammation the gland at first is hardened, swollen, and reddened, and on section presents a reddish-gray surface, with indistinctness of the glandular structure, due to the amount of swelling of the acini. Under the microscope the gland-cells are found to be enlarged; they contain several nuclei, their protoplasm is infiltrated with fatty granules, obscuring the nuclei to a certain extent, and their outline is well defined. These alterations are most marked in the head of the gland. After a time the hypertrophy of the cells, by pressing upon the blood-vessels, produces an anæmic condition and the organ becomes pale; in the advanced stages softening occurs.

Metastatic suppurative inflammation leads to the formation of a single large abscess or to multiple minute purulent collections.

SYMPTOMS AND COURSE.--Parenchymatous degeneration gives rise to no distinctive symptoms. Its occurrence in typhoid fever or other infectious disease may be suspected when after prolonged hyperpyrexia there are enlargement of the liver and spleen and albuminuria. The appearance of jaundice (from pressure) increases the probability of involvement of the pancreas in the general gland-change.

{1121} The development of rigors, alternating with flushing, during the course of one of the lesions liable to be attended with metastatic abscesses in the pancreas might suggest the formation of pus in the gland, but an absolute diagnosis is impossible.

Several cases are on record pointing to the possibility of a metastasis of mumps from the parotid gland to the pancreas. In these the disappearance of the parotiditis was followed by symptoms resembling those of idiopathic pancreatitis--namely, thirst, fever, loss of appetite, anxiety, and burning in the epigastrium, with deep-seated pain extending toward the right side; in addition there was diarrhoea, with numerous, yellowish, watery stools. In one case that resulted fatally the secondary diarrhoea suddenly ceased and the parotid swelling reappeared. At the autopsy the pancreas was found to be swollen, reddened, engorged with blood, and indurated. Such a metastasis, however, must be very infrequent, and more extended observations are necessary to establish its course and clinical features.

The first form of acute secondary pancreatitis may be a comparatively unimportant complication of the acute infectious diseases, or, together with the parenchymatous degeneration of other organs, may form a distinct element in the fatal issue of these diseases.

Metastatic abscesses are prone to be followed by ulceration and the formation of fistulous communications with the neighboring viscera.

TREATMENT.--The management of secondary inflammation of the pancreas is regulated solely by the indications derived from the originating disease.

Chronic Interstitial Pancreatitis.

Inflammation of the connective tissue of the gland usually occurs after adult life, and depends upon a variety of causes.

The secondary form, due to long-continued venous engorgement resulting from lesions of the cardiac valves and from chronic disease of the lungs or liver, is the most frequently observed.

Other causes are closure of the duct of Wirsung, the retained secretion producing pressure upon the glandular tissue; the extension of inflammation from adjacent organs, as the bile-duct when there is an impacted gall-stone, or the stomach and duodenum, especially in cancer and perforating ulcer, where the floor of the ulcer is formed by the pancreas; the pressure of tumors, as aneurisms of the abdominal aorta and coeliac axis; chronic alcoholism; and syphilis.

ANATOMICAL APPEARANCES.--The lesion may be limited to the head or to isolated portions of the gland, or be uniformly distributed. The general changes are a hyperplasia of the interacinous connective tissue, with subsequent contraction and atrophy, or, in extreme instances, entire destruction of the glandular elements proper, the organ becoming granular and firmer and tougher than normal. A section shows a pale surface, studded at intervals with white spots, from which little cheese-like and fatty masses may be squeezed, and, when there has been intense hyperæmia, with minute collections of reddish pigment and small hemorrhagic cysts, indicating previous interstitial hemorrhages.

{1122} When the contraction causes closure of the small excretory ducts or of the duct of Wirsung itself, the section shows secondary cysts and beaded canals.

In exceptional instances of acquired syphilis the pancreas is the seat of gummata or sclerosis, but in congenital syphilis hyperplasia of the glandular connective tissue frequently occurs, being usually associated with specific lesions of the lungs, liver, kidneys, and general glandular system.

SYMPTOMS AND COURSE.--As chronic pancreatitis rarely attains a sufficient degree of development to interfere seriously with the function of the organ, the disease is usually latent, or masked by the symptoms of the originating lesion in secondary hyperplasia, or by the associated diseases of the abdominal viscera in alcoholism and acquired syphilis.

When due to hereditary syphilis, the foetus is stillborn or death takes place soon after birth, and there are no characteristic symptoms.

Occasionally, however, especially when it depends upon a complete obstruction of the duct of Wirsung, a diagnosis may be made from the presence of emaciation, fatty stools, and melituria, with epigastric pain of a neuralgic character, and the discovery of a deep-seated, dense tumor extending transversely across the epigastrium.

The duration is indefinite, and varies greatly with the cause. While a return to the healthy condition is possible during the early stage of the lesion, the usual course is similar to that of chronic interstitial inflammation in other organs.

TREATMENT.--The management, when a diagnosis can be made, must be guided mainly by the etiological indications. The restoration of the functions of the heart, lungs, or liver when these organs are at fault, the abstinence from alcohol in the drunkard, and an energetic use of mercurials or iodide of potassium in syphilis, are of the first importance in arresting the disease. A persistent course of mild purgatives and of cathartic mineral waters is serviceable. Pain should be relieved by belladonna or opium. The diet must be simple and digestible, and if an arrest of the pancreatic secretion be indicated by the appearance of fat in the stools, an effort should be made to supply the deficiency. For this purpose pancreatin, prepared by precipitation by alcohol from a watery extract of a calf's or pig's pancreas, may be used.[1] The pancreatin may be given in doses of from five to fifteen grains, in the form of a pill or in capsules, and at an interval of two hours after food is taken, or the same quantity of pancreatin may be added to the food a few moments before it is eaten. Probably the best substitute is a watery infusion of the gland containing all its soluble principles. To prepare an active infusion the pancreas must be taken from the animal during the act of digestion. It is then freed from its surrounding fat, and macerated for two hours in four times its weight of water at a temperature ranging between 25° and 30° C. (58.3° and 61.1° F.). Another plan is to beat a calf's pancreas in a mortar with six fluidounces of water until a milk-like fluid is obtained, and strain. One-third of the infusion obtained by either method is administered after each meal, an entire pancreas being thus used every twenty-four hours.

[Footnote 1: One gramme of pancreatin is sufficient to emulsify fifteen grammes of fatty substances, to convert eight grammes of starch into glucose, to digest fifty grammes of fibrin, twenty grammes of syntonine, and thirty-three grammes of boiled albumen (Raymond).]

{1123} The extractum pancreatis,[2] as it is now furnished to the profession, is a very useful preparation. It may be employed to peptonize milk, milk-gruel, and broth, or be given in combination with bicarbonate of sodium at a fixed interval after each meal, as in the following formula:

Rx. Ext. pancreatis, drachm j; Sodii bicarbonatis, drachm ij; M. et. ft. Chart No. XII.

S. One powder to be taken two hours after each meal.

[Footnote 2: That prepared by Fairchild Brothers & Foster of New York has proved the best in my hands.]

Peptonized milk is prepared by putting into a clean quart bottle 5 grains of extractum pancreatis, 15 grains of bicarbonate of sodium, and a gill of cool water; shake, and add a pint of fresh cool milk. Place the bottle in water not so hot but that the whole hand can be held in it without discomfort for a minute, and keep the bottle there for exactly thirty minutes. At the end of that time put the bottle on ice to check further digestion and keep the milk from spoiling.

Peptonized milk-gruel is made of equal parts of any farinaceous gruel and fresh cold milk. To a pint of this combination 5 grains of extractum pancreatis and 15 grains of bicarbonate of sodium are added, and the whole allowed to stand in a warm place for thirty minutes, when the process of digestion must be arrested by placing on ice.

Peptonized broth is made in the following way: Take one-fourth of a pound of finely-minced raw lean beef or mutton or chicken, and one-half pint of cold water; cook over a slow fire, stirring constantly, until it has boiled a few minutes. Then pour off the liquor, beat the meat to a paste, and put both into a bottle with a half pint of cold water. Add 30 grains of extractum pancreatis and 20 grains of bicarbonate of sodium; shake well, and set in a warm place (110-115°) for three hours, shaking occasionally; then boil quickly. Finally, strain or clarify in the usual way and season to taste.

MORBID GROWTHS OF THE PANCREAS.

Carcinoma.

Cancer is probably the most common of the chronic affections of the pancreas. It is usually secondary, being due to an extension of carcinoma of the stomach, duodenum, liver, or abdominal lymphatic glands, but there are enough cases on record to show that it may be primary. It has been discovered in the foetus at birth, but the vast majority of cases occur after the age of forty. Men are more frequently affected than women. Nothing is known as to the influence of inherited tendency in the production of the disease, and as little of the exciting causes, though some authors attach much importance to prolonged pressure upon the epigastrium and to blows and contusions on the upper part of the abdomen.

ANATOMICAL APPEARANCES.--Primary carcinoma may be either {1124} scirrhous, encephaloid, or colloid, the first being the variety most frequently observed.

The lesion begins in the head of the gland in the form of several small nodules which gradually coalesce. Sometimes the whole gland becomes involved in the new formation; again, isolated nodules may be scattered throughout its substance, and exceptionally the growth is limited to the tail or middle portion. When the head alone is involved, the remainder of the gland either remains healthy, undergoes fatty degeneration, or becomes indurated. The tumor is rounded in outline and nodular, and varies in size, density, and color according to the form of carcinoma present. The duct of Wirsung is ordinarily obstructed, large retention cysts, containing a yellowish-red liquid, are formed, and the changes already described under the head of Chronic Interstitial Pancreatitis take place in those portions of the gland which are free from carcinoma. The disease is very prone to extend to the surrounding organs, particularly the neighboring lymphatic glands, the duodenum, and the liver, rarely to the stomach. When the contiguous organs are not directly implicated in the carcinomatous changes, they are subjected to pressure by the tumor, and in the case of the stomach and duodenum adhesions often form, and are followed by perforation. There seems to be a tendency also to infiltration of the adjacent subperitoneal connective tissue and to hyperplasia of the fibrous tissue of the viscera, even when they are not secondarily involved in the morbid growth, leading to narrowing of the aorta, thickening of the walls of the stomach and duodenum, and a sclerosis of the liver. Obstruction of the common bile-duct, with dilatation of the gall-bladder from retention of bile, is a frequent result of the disease.

Secondary carcinoma of the pancreas usually first appears in, and is limited to, the head of the gland. It seldom occurs in isolated nodules, but the growth is generally continuous with the primary cancerous mass. The form is either scirrhous or encephaloid. Wagner records a case of cylindrical-celled epithelioma following a simple epithelioma of the mucous membrane of the duodenum; and a similar instance has come under the author's own observation;[3] but this variety of morbid growth is rare. The primary growth is almost uniformly situated in the stomach, duodenum, liver, or gall-bladder, though occasionally it may be seated in some distant organ; in such cases the pancreatic tumor appears as an isolated nodular mass.

[Footnote 3: Transactions of the Pathological Society of Philadelphia, vol. ix. 13.]

SYMPTOMS AND COURSE.--The symptoms may be divided into two classes--namely, first, those which arise from the lesion of the gland itself; and, secondly, those which depend upon the effect of this lesion on the neighboring viscera.

The features belonging to the first class are general marasmus, pain, the appearance of fat and perhaps undigested muscular fibres in the fecal evacuations and of fat in the urine, and the physical signs of an abdominal tumor.

Loss of flesh is one of the earliest symptoms: it is generally progressive, and is at times so great that the spine can be distinctly traced through the abdominal walls. Together with this emaciation there is debility, often extreme, but sometimes not so marked as might be expected from the degree of wasting. The skin is commonly pale and dry, and before jaundice is {1125} developed has the ordinary sallow hue of cancerous cachexia. The features are pinched, and the face wears an expression of anxiety and suffering. In cases uncomplicated by peritoneal inflammation the temperature remains about normal, or it may be lowered as the general exhaustion increases. The pulse is feeble and slightly increased in frequency.

Pain is the most uniformly present and the earliest symptom. It is always situated deep in the epigastrium, and from thence extends to the back, to the right or left side, downward to the umbilicus or lower part of the abdomen, and upward into the chest. It is generally continuous, but is subject to remissions and paroxysmal exacerbations. During the remissions sensations of distress, of burning, or of dull pain are experienced at the pit of the stomach; during the exacerbations, which may last several days, the pain becomes extremely acute and lancinating and extended in distribution. The ingestion of food and pressure upon the epigastrium have no constant effect upon the pain. Quick movements of the body from side to side often increase it and excite exacerbations. The suffering is greatest in the erect posture, and on this account the patient bends his body forward so as to relax the abdominal muscles. The paroxysmal and neuralgic character of the pain indicates implication of the coeliac plexus.

The appearance of fat in the stools is an important symptom, unless there be at the same time an obstruction to the passage of bile into the duodenum, indicated by jaundice. Lipuria has been noticed in a few cases only.

In many instances (nearly one-half of the number of recorded cases) physical exploration reveals the signs of enlargement of the organ. At times there is merely a sense of fulness and resistance to the touch, and a modified tympanitic percussion note in one of the three regions of the upper segment of the abdomen. But usually when a tumor is present it is readily mapped out by palpation. The tumor is seated in the epigastrium, and may extend into the right or left hypochondrium or downward into the umbilical region. It varies much in size, is rounded, nodulated, firm, slightly movable or fixed, and tender, though sometimes painless, to the touch. Percussion yields dulness or a dull-tympanitic sound. On auscultation a blowing murmur may be heard when the tumor presses upon the aorta; and when this murmur is present there is usually also transmitted pulsation.

The symptoms belonging to the second class arise when the adjacent viscera become involved in the cancerous disease, or when their functional activity is disturbed by the encroachment and pressure of the enlarged pancreas.

From the association of a catarrhal condition of the mucous membrane of the stomach, particularly when the pyloric orifice is obstructed, several prominent symptoms of gastric catarrh are frequently observed--namely, sialorrhoea, pyrosis, acid eructations, flatulence, abnormal sensations, such as burning, weight and oppression in the epigastrium after taking food, and increased thirst. The tongue varies in appearance: it may be dry and covered with a brown or yellow fur, but when the flow of saliva is increased it is peculiarly clean and moist; and this condition is rather characteristic. The appetite is also variable; sometimes it remains good {1126} until the end, and occasionally it is perverted. Hiccough in some cases is an obstinate and annoying symptom.

Nausea and vomiting are late but moderately constant features. Their relation to the ingestion of food is not fixed. The vomited matter may consist of food, of glairy mucus more or less tinged with bile, of colorless liquid, or of a fluid resembling a mixture of bran and water. If there is marked pyloric obstruction with dilatation of the stomach, large quantities of frothy and fermenting material containing sarcina ventriculi are rejected at intervals. In the rare cases in which secondary sarcoma of the viscus is developed the ejecta are bloody or have the coffee-ground appearance, and the vomiting occurs several hours after eating, as the new growth is generally situated at the pylorus. When there is adhesion of the pancreatic tumor to the stomach, with perforation, both blood and pus are vomited. Dilatation of the stomach is attended by prominence of the epigastrium and an extended area of gastric tympany, and in cancer of the pylorus a tumor is often appreciable on palpation. The bowels are usually constipated. The fecal evacuations are hard, and when the biliary secretion is absent from the intestine they are clay-colored, and often contain fat. When there is ulceration of the mucous membrane of the duodenum following secondary cancer or adhesion, the stools become black and tar-like from the presence of altered blood. Complete obstipation occurs in mechanical obstruction of the gut from direct pressure or from bands of lymph. Occasionally, just before death there is diarrhoea, and there may be an alternation of vomiting and diarrhoea.

The symptoms and signs of secondary carcinoma or sclerosis of the liver may be present, but the most commonly observed indications of impaired hepatic function depend upon pressure-obstruction of the common bile-duct. These are jaundice, fatty and clay-colored stools, and the appearance of a tumor in the region of the gall-bladder. Jaundice is a very common symptom. It occurs late in the disease as a rule, is progressive and persistent, resisting all treatment, and is extreme in degree, the skin becoming deep-yellow or greenish in color. The tumor of the distended gall-bladder is pyriform in shape, firm and elastic to the touch, yields a dull percussion sound, and occupies a position opposite the extremity of the tenth rib on the right side of the abdomen.

Dropsy occurs in a large proportion of cases (nearly one-half) during the advanced stages of the disease. It is due to vascular obstruction occasioned by the pressure of the enlarged pancreas itself or of the secondarily degenerated coeliac glands, and finally by secondary lesions of the liver. The dropsy appears either in the form of ascites or anasarca, is not often extreme in degree, and is subject to variations, disappearing and reappearing at intervals. Ascites is the more common form, but both conditions may exist in the same patient.

It is impossible in the majority of instances to definitely fix the date of onset of a pancreatic cancer, but the average duration of the disease may be stated to be about one year. The uniformly fatal termination usually takes place slowly from gradual exhaustion or with the symptoms of an adynamic fever, but death may occur suddenly from hemorrhage.

DIAGNOSIS.--The principal features of carcinoma of the pancreas are extreme emaciation, loss of strength, dyspepsia, pain of a neuralgic {1127} character in the epigastrium, constipation, obstinate jaundice, moderate ascites or anasarca, the appearance of fat in the stools, lipuria, occasional vomiting, and the physical signs of an epigastric tumor.

These symptoms are not pathognomonic, however, and the diagnosis can be certainly established only when it is possible to exclude primary disease of the surrounding organs, especially of the stomach and liver.

Cancer of the stomach may be excluded by the less-marked character of the functional disturbances of the viscus; by the absence of frequent vomiting, hæmatemesis, and the rejection of coffee-ground material; by the somewhat different situation and greater immobility of the tumor, by the seat, distribution, and constancy of the pain; and by the presence of jaundice and of fat in the stools and urine.

Diseases of the liver attended with alterations in the size of the organ, as cancer, abscess, albuminoid and fatty degeneration, sclerosis and hydatid tumor, have sufficiently characteristic physical signs and symptoms to be readily distinguished from cancer of the pancreas. On the other hand, the tumor of an enlarged gall-bladder is often confusing. The situation of this tumor opposite the tenth rib and its pyriform shape are important; other distinguishing points depend upon the cause of the enlargement. In enlargement from accumulated bile the tumor is elastic and fluctuating; from accumulation of gall-stones, hard and nodulated, movable, painless on palpation, and often the seat of crackling fremitus, produced by manipulation and due to the rubbing together of several calculi; from cancer, hard, nodular, the size of an orange, tender on pressure, rapid in growth, preceded by attacks of biliary colic, and attended by fistulous communications with the intestines and the passage of gall-stones per anum.

In aneurism of the aorta or coeliac axis the tumor may present in the epigastrium and produce analogous pressure symptoms. But the pain is more of the character described as wearing, and is usually augmented at night: on grasping the tumor a uniform expanding pulsation is felt in place of the to-and-fro movement appreciable in a tumor resting upon a healthy blood-vessel and receiving a transmitted impulse, while the constitutional symptoms and course are quite different.

The tumor of malignant disease of the omentum, although it appears in the epigastrium or upper part of the umbilical region, is much more movable, and is accompanied by ill-defined symptoms very dissimilar to those of pancreatic cancer.

In cancer of the transverse colon the mass may occupy nearly the same position as a pancreatic growth, but the pain occurs several hours after food is taken; vomiting is absent, and there is frequently hemorrhage from the bowels.

Chronic pancreatitis is accompanied by symptoms simulating those of cancer; the enlargement of the gland, however, is not so great, nor are the indications of pressure upon adjacent organs so prominent. The pain is less severe, the general failure in health more gradual, the progress slower, and constipation less common.

TREATMENT.--The indications are to maintain the strength of the patient, to provide a diet that is nutritious and at the same time easily digested, to allay pain by the employment of narcotics, and to relieve as far as possible the various symptoms as they arise. The plan of {1128} administering a calf's pancreas or extractum pancreatis will prove serviceable when the fecal evacuations contain fat. Nutritious and peptonized enemata may be of service in some cases.

Sarcoma and Tubercle of the Pancreas.

Sarcoma of the pancreas occurs with extreme rarity. It is impossible during life to distinguish it from carcinoma.

Tubercle of the gland is infrequently met with. Some pathologists deny its occurrence, and believe that the cases recorded as such are merely instances of caseous degeneration of the neighboring glands. When it does occur, it is always secondary, the primary disease being situated in the lungs or intestines. The alterations in the gland consist in the development of cheesy masses or of miliary granulations in the connective tissue between the acini. The condition gives rise to no definite symptoms, and its diagnosis during life is impossible.

DEGENERATIONS OF THE PANCREAS.

Fatty Disease of the Pancreas.

Two forms of fatty degeneration occur, either separately or combined--namely, fatty infiltration and fatty metamorphosis.

Fatty infiltration consists of a true hypertrophy of the fat-tissue normally existing in the gland, or of an increase and extension into the gland of the peripancreatic adipose tissue. Yellow bands and masses of fat-tissue appear between the acini, and by constantly increasing in size lead gradually to a total atrophy of the cells of the acini. The canal of Wirsung contains a fatty liquid. These changes are found associated with fatty liver, heart, and omentum, in drunkards especially.

Fatty metamorphosis of the gland consists of a change analogous to fatty metamorphosis of other organs. When hyperplasia of the interstitial connective tissue is absent, the organ is flaccid, soft, and diminished in size; the acinous structure remains distinct, though the acini and ducts are filled with a fatty emulsion: after this is discharged or absorbed the gland appears as a flaccid band, and finally becomes entirely atrophied. Fatty metamorphosis occurs in drunkards, in diabetes, in advanced age, in cancer, phthisis, and other wasting diseases.

Neither form of fatty disease gives rise to symptoms by which it can be recognized during life.

Albuminoid Degeneration of the Pancreas.

This is only found in combination with amyloid change in other organs of the body, and a diagnosis cannot be made.

{1129} Hemorrhages into the Pancreas.

Hemorrhages into the pancreas may be divided into three classes.

The most common form depends upon passive hyperæmia, the result of chronic diseases of the heart, lungs, or liver. In this condition the effusion of blood coexists with chronic inflammatory changes in the interstitial connective tissue. The appearance at first is of minute bloody points scattered throughout the areolar tissue; later, these change into round or oval pigment masses, or spaces containing reddish serum and surrounded by thickened, rust-colored, irregular walls.

The second class includes the rare cases of hemorrhage resulting from the rupture of one of the large blood-vessels of the gland, and due to some pre-existing change in the vessel walls. In these the pancreas is enlarged, may be converted into a sac containing blood, either fluid or coagulated or partially crystallized according to the duration of life after the hemorrhage has taken place, and a ruptured blood-vessel may be readily discovered on dissection.

The condition in which, without any evidence of passive hyperæmia or gross vascular lesion, the entire pancreas become hemorrhagic, constitutes the third class. The gland is then dark-red or violet in color, the meshes of the interstitial tissue are filled with recent or altered blood, and the acini are stained of a dull-gray hue. The hemorrhage may extend to the connective tissue surrounding the gland. Finally, the organ becomes soft, the peritoneal covering sloughs, and fragments of broken-down gland-tissue escape into the peritoneal cavity. These lesions are so analogous to those which attend thrombosis occurring in other organs that their dependence upon the same cause seems probable.

The first form of hemorrhage is unattended by special symptoms. In the second a pulsating tumor may suddenly appear in the epigastrium, and the ordinary indications of hemorrhage--vomiting, fainting fits, cold extremities, feeble pulse, and general exhaustion--are present. Death may occur suddenly or the patient may linger on for months. In the third condition death usually occurs very suddenly, probably from pressure upon the sympathetic ganglia. There are no symptoms, and the rapid termination prevents the development of general peritonitis, which would otherwise occur from the sloughing of the peritoneum.

There are no indications for treatment.

OBSTRUCTION OF THE PANCREATIC DUCT.

Obstruction of the excretory duct is a frequent occurrence in pancreatic disease, and is due to two classes of causes--namely, 1st, pressure from without; and, 2d, closure of the canal by catarrhal swelling of its mucous membrane or by calculi.

In the first class may be placed obstruction depending upon contraction occurring in sclerosis of the gland, upon carcinoma of the head of the gland, upon peripancreatic adhesions and indurations, upon the {1130} presence of large gall-stones in the ductus choledochus, and upon carcinoma of the pylorus and duodenum and enlargement of the neighboring lymphatic glands.

In catarrh of the canal of Wirsung the obstruction results either from simple swelling of the mucous membrane or from the presence of a plug of tough mucus.

The formation of pancreatic concretions is by no means a rare event, though these calculi are met with far less frequently than either gall-stones or salivary concretions. They result from precipitation of the inorganic ingredients of the pancreatic juice, and are usually seated in the main duct, although they may be situated in the smaller branches. They may be single or multiple, as many as twenty having been counted in one gland. In shape they are spherical, oval, or branched, with sometimes a smooth, at others a spiculated, surface; their size varies from that of a minute granule to a small walnut; they are usually white or grayish-white in color, but may be black; and are composed of the carbonate of lime or of a combination of the carbonate and phosphate with oxalate of lime. Coincidently with these calculi it is common to find concretions in the kidneys and gall-bladder.

Concretions composed of insoluble protein substances have also been found in the pancreatic ducts (Virchow).

The most probable causes of the formation of pancreatic calculi seem to be catarrhal conditions of the mucous membrane of the ducts and an alteration in the chemical composition of the secretion.

Whatever the cause, the obstruction, when complete, leads to retention of the secretion and the formation of retention cysts.

When the obstruction is situated at the duodenal extremity of the duct, the canal and its secondary branches are either uniformly dilated or sacculi are formed. These sacculi are round or oval, vary greatly in size, sometimes reaching the dimensions of the fist or of a child's head; they may be single, or several of them may be present, differing in size and causing irregular projections of the outer surface of the gland. When the obstruction occurs at some point in the course of the duct, the dilatations and sacculi are found only behind the point of occlusion. The small cysts contain a fluid resembling the pancreatic juice; the larger, a whitish, chalky fluid, which in old cases may contain white friable concretions composed of carbonate and phosphate of lime, and become purulent, or be stained bright red or chocolate-colored from the occurrence of hemorrhage. In such instances hæmatoidin crystals can be discovered by the microscope. The interior of the dilated ducts and of the retention cysts is lined by a single layer of thin flat cells, with irregular edges and with oval flat nuclei. The walls are thickened, and composed of superimposed layers of laminated connective tissue separated from one another by flat nucleated cells. The secreting structure of the gland undergoes atrophy from pressure, or fatty metamorphosis takes place, and, although the gland is increased in size from the presence of the cysts, its functional power is lost.

In addition to causing obstruction of the duct of Wirsung and the changes mentioned, pancreatic calculi may produce induration, atrophy, acute inflammation, or even suppuration of the surrounding glandular tissue.

{1131} SYMPTOMS AND COURSE.--The main feature is the presence in the epigastrium of a rounded, smooth, fluctuating, painless tumor. There are also indications of the absence of the pancreatic secretion from the digestive tract--notably, emaciation, general debility, and the appearance of fat in the stools. Jaundice resulting from a coincident obstruction of the bile-duct is a frequent symptom, and melituria has been noted in some cases. It is probable, too, that the passage of a calculus along the duct may give rise to pain resembling in character and distribution the pain of hepatic colic.

The duration is indefinite. Sometimes the termination is sudden from the rupture of a cyst into the peritoneal cavity or into the stomach or duodenum, with hemorrhage.

DIAGNOSIS.--The absence of pain, of tenderness, and of cachexia, together with the physical characters of the tumor, distinguishes it from carcinoma of the gland.

Though not likely to be confounded with this disease, both hydatid tumor of the liver and distension of the gall-bladder must be borne in mind in making the diagnosis of a fluctuating tumor situated in the upper third of the abdomen.

TREATMENT must be entirely symptomatic. Attention to the general health, proper regulation of the diet, and the employment of pancreatin or an infusion of calf's pancreas to supply the place of the deficient pancreatic juice, are the important steps. Attacks of pancreatic colic indicate the use of anodynes.

In two reported cases in which the cysts were very large paracentesis for the removal of the fluid contents was resorted to, and there are two cases on record in which the cysts were extirpated after abdominal section. Kulenhampff of Bremen records a case of a man, thirty-nine years of age, in whom, after a succession of severe blows upon the abdomen, a tumor appeared in the epigastrium. An exploratory incision was made, and a few ounces of pancreatic fluid evacuated by aspiration. Six days afterward the abdomen was opened, the peritoneum united to the incision, and antiseptic gauze inserted to produce adhesive inflammation between the sac and the abdominal wall. Adhesion taking place after four days, the cyst was opened, a liter of fluid evacuated, a tent inserted, and an antiseptic dressing applied. For sixteen days fluid constantly escaped in slowly diminishing quantities, and the tumor disappeared, a fistulous tract remaining. This completely closed under the use of tincture of iodine and nitrate of silver at the end of the seventh week. Thiersch opened a pancreatic cyst and evacuated three liters of chocolate-colored fluid; recovery with a fistula followed.

From a patient supposed to be suffering from ovarian dropsy Rokitansky partially extirpated a cyst connected with the tail of the pancreas; death from suppurative peritonitis occurred on the tenth day.

N. Bozeman[4] on December 2, 1880, successfully removed from a woman forty-one years old a pancreatic cyst weighing, with its contents, twenty and a half pounds. In this instance also the operation was undertaken for the removal of a supposed ovarian tumor, the diagnosis not being established until after the abdomen was opened.

[Footnote 4: New York Medical Record, Jan. 14, 1882.]

{1132}

PERITONITIS.

BY ALONZO CLARK, M.D., LL.D.

Italian physicians in the later years of the seventeenth century and in the early ones of the eighteenth had acquired some knowledge of the symptoms of the disease we now call peritonitis, but known to them as inflammation of the intestines. Indeed, it is claimed by some of the admirers of Hippocrates that there are passages in his writings that indicate some knowledge of the disease. But this claim will probably be always received with many doubts as to its validity.

In confirmation of the first statement I will transcribe certain passages from Morgagni's thirty-fifth letter: In inflammation of the intestines "Albertini had observed the pulse to be low and rather weak, such as you will find it to have been in general in the foregoing letter under Nos. 9, 11, 18, and 25." He also observed the abdomen to be tense and hard, the face and eyes to have something unusual in their appearance. "Medical writers, indeed, agree in the tension of the abdomen, but they add many other symptoms, which prove beyond a doubt the intestines to be inflamed; yet they mean that evident inflammation which all may easily ascertain, and not that obscure disorder which we now speak of, and which few suspect" (gangrene of the intestines). "By the same writers it is also supposed that there is an obstinate costiveness and continual vomiting."

Morgagni refers to the assistance rendered by Albertini, Valsala, Van Swieten, Rosa, and others in elucidating this subject. It is singular, considering the clearness of his perception of the symptoms of inflammation of the intestines, that he should be so greatly confused regarding gangrene and sphacelus of the same parts. He looks on these as the result of inflammation, and when the two classes of cases are considered and compared, the result is a contrast and not a resemblance. Yet he supposes that the differences are to be accounted for by the different modes in which the same disease may be developed in different persons.

Another thing obtrudes itself on the attention in these letters: that while a number of post-mortem examinations are reported of those who had died of inflammation of the intestines, of gangrene and sphacelus of the intestines, of hepatic abscess opening into the peritoneal cavity, there is no record of finding in the abdomen anything corresponding to what is now known as the inflammatory effusions from serous membranes.

Sydenham died in 1689. I have searched his works, not for {1133} peritonitis, for the word was not in use in his day, but for some account of inflammation of the intestines or of some disease in the description of which symptoms are named that distinguish or belong to peritonitis, and with the single exception of pain the search has been fruitless.

Cullen in 1775 mentions the disease, but says that so little is known about it that he will not attempt a description of it.

Bichat died in 1802 in the thirty-eighth year of his age. I am not able at present to lay my hand on his Pathological Anatomy; I therefore quote from Chomel's article on peritonitis in the Dictionnaire de Médecine to show his claim to important studies regarding that disease: "For a long time peritonitis was confounded under the name of inflammation du bas ventre with inflammations of the abdominal viscera; and it is to Bichat belongs the merit of having proved that inflammation of the peritoneum is a disease distinct, and that it ought to be separated from enteritis, gastritis, etc., as pleurisy is separate from pneumonia. The studies of Gasc and of Laennec soon confirmed the opinion of Bichat, and assured to peritonitis the important place which it ought to occupy in all nosological tables. It has become since then a subject of numerous observations and of interesting researches regarding the causes de sa marche and the lesions it causes."

The references are not given by Chomel, but they are probably these: Laennec, Histoire des Inflammations du Peritoine, 1804; and Gasc, Dictionnaire des Sciences Méd., p. 490, 1809.

Gasc says that the twenty years next preceding his publication witnessed the first stage of the true history of peritonitis. Walther in 1786 had contributed some facts, and S. G. Vogel in 1795, but the rounding off and completing their work was left for Bichat.

Acute Diffuse Peritonitis.

MORBID ANATOMY.--The first thing that strikes the observer in the post-mortem examination of a person who has died of this disease is the tendency of the intestines to protrude through the cut made in the abdominal wall. This is produced by their dilatation generally, both small and large, by gas. No gas, under these circumstances, ever escapes from the peritoneal cavity unless there has been perforation of the alimentary canal somewhere. While the intestines are in this manner dilated, the stomach is small and usually empty.

On the surface of the intestines there will be found a layer of coagulated fibrin, often very thin and delicate, requiring a scraping of the surface of the peritoneum to demonstrate it, but commonly obvious enough, and sometimes quite abundant. This same false membrane can be found on the viscera covered by the peritoneal membrane, on its anterior extension, and most at the point of contact of one coil of the intestine with another. Incorporated with this new membrane or lying under it will often be seen blood-spots, thin, translucent, diffused, and having ill-defined boundaries.

The blood-vessels themselves are not remarkably congested. Here and there may be spots where some redness remains, and the vessels are larger than natural. But the congestion and redness, which analogy leads us to {1134} believe belong to the active stages of the disease, have in great degree disappeared after death.

The peritoneal membrane itself has hardly become thickened, certainly not in marked degree, but it has lost its lustrous surface, is, at least in parts, of an opaline color, as if it had absorbed diluted milk, and there is an effusion of serum or slight oedema on its attached surface. Whatever may be the popular opinion regarding the termination of inflammation of the bowels in mortification, whatever the opinion of the older physicians, it is safe to say that gangrene of the peritoneum has never been the result of uncomplicated, diffuse, acute peritonitis. Peritonitis from strangulation of the intestine or analogous causes is of course excepted. But in puerperal peritonitis I have noticed a fact to which I have nowhere seen an allusion. The parietal peritoneum is at two points in the abdomen but loosely attached to the wall. One of these is on the anterior wall, anterior to and a little above the iliac fossa; the other is above and below the kidney on each side of the body. In these parts I have seen the membrane forced off from its attachment to the walls, which with it made a sac containing pus. Such an abscess, if the patient live long enough, would doubtless cause the death of the membrane.

There is in almost every case of peritonitis more or less of serous effusion, commonly not seen at first on opening the abdomen, for it has sunk into the pelvis. It is transparent, of a yellowish hue, and sometimes flocculi of lymph are found in it.

Whether the inflammation of the peritoneum extends to organs covered by it is a question that has been much discussed; but it is admitted that these organs, to a shallow depth on their surface, have an unnatural color; and when it is remembered that the peritoneum is nourished by vessels not exclusively its own, but running along its attached surface, and distributed as well to the surface of the organs it covers, it is easy to admit that to a very limited depth the organs partake of the inflammatory disease. This supposition gives an easy explanation of the constipation which is so prominent a feature among the symptoms of the disease.

The manner in which the false membrane is disposed of in those who recover is an interesting question. Forty or more years ago Vogel described the process by which the new effusion became a living tissue, and the manner in which blood-corpuscles and blood-vessels were formed in it; and another author had found that the time needed to complete this vascularization was twenty days. But now Bauer and most of the German writers inform us that the coagulated fibrin is converted into fatty matter and is absorbed, and that when adhesions occur they result from the coalescence of a new formation of the connective-tissue elements built up into granules. The question, then, arises, Will the chemical constitution of fibrin permit its conversion into oil? If it will, then the further question presents itself, By what chemical action is the change effected within the body? I do not intend to discuss these questions, but propose them by way of expressing some doubt regarding the accuracy of this statement.

I have always supposed that the epithelial layer of the peritoneum was pushed off by the first of the effusions in peritonitis, and that this was one of the causes of the lustreless appearance of the membrane. This {1135} opinion I have never attempted to confirm or correct by the microscope. Bauer confounds this idea. He says: "The deposition of fibrin occurs before the endothelium presents any changes. This fibrinous effusion encloses, primarily, hardly any cellular elements, and only a few cast-off endothelial cells are to be found in it. The endothelium itself is swollen and turbid; the cell-body is increased in size; the contents are granular; multiplication of the nuclei is apparent; the cells are, in fact, in active division. In the tissue of the serous membrane itself, soon after the deposition on its surface, an accumulation of indifferent (?) cells takes place, especially around the vessels, so that the spaces between the vessels are thus completely filled up. The fixed connective-tissue corpuscles take part in the inflammatory process."

Delafield says: "If the autopsy is made within a few hours after death, we find the entire peritoneum of a bright-red color from congestion of the blood-vessels; but that is all: there is no fibrin, no serum, no pus; epithelial cells are increased in size and number." For this kind of peritonitis he proposes the term cellular. He finds it in cases of local abscess of the abdominal cavity in which inflammatory action has extended over the whole membrane, and particularly on the omentum also, in the first two days of puerperal peritonitis. "The ordinary form of acute peritonitis is attended with changes in the endothelium and fixed connective tissue, and with the production of serum, fibrin, and pus." He describes the migration of white corpuscles of the blood through the walls of capillaries to become pus-cells, and then says: "Minute examination shows that two distinct sets of changes are going on at the same time: first, a production of fibrin, serum, and pus; second, swelling and multiplication of the endothelial cells. If the inflammation is very intense, the pus and fibrin are most abundant; if milder, the changes in the endothelium are more marked."

I have said above that the epithelium is early washed off by the inflammatory effusions. In opposition--or, perhaps better, in correction--of this idea, Delafield says: "There may be a considerable amount of pus produced, and yet the layer of endothelium remains in place." "If, however, the pus and fibrin are produced in large amounts, the endothelium falls off and leaves the surface of the peritoneum bare." The connective-tissue cells of peritoneum, he says, undergo but little change in the first three days of the inflammation, "but by the seventh day these cells are marked by increase in size and number in all parts of the peritoneum."

Two or three times in my life I have met with a peculiar arrangement of the false membrane and serum of peritoneal inflammation, of which I do not remember to have seen a description. It is this: the serum is enclosed or encysted in bladders, the walls of which are the false membrane. There may be two or three layers of these bladders, one upon another, all more or less flattened, and each holding from two to six ounces of fluid. It would seem that in these cases the inflammatory activity rose and fell in its progress, early reaching the point at which coagulable lymph was effused, then falling to the stage in which serum alone escaped. This serum lifted the false membrane irregularly, so that several pools were formed. After this the inflammation returns to the fibrous exudation stage, and gives to these bladders a floor which blends with the {1136} roof at the edges, and thus makes a complete sac. Once more the inflammatory action is changed in its intensity, so that the only effusion is serum; and this serum again raises the new layer of false membrane into bladders--not always or generally in the exact position of the first series. Still again, the inflammation may be so changed as to make a fibrinous flow to this second series of bladders. I am not certain that I have seen a third series of these rare productions. They have doubtless been seen by other persons, and may have been described. I have not been an exhaustive reader on the subject, but I can well understand how they may have been called hydatids on examination of the sacs without looking at the contents. The fluid in the cysts is simply serum, with no echinococcus sacs, and then the number of these inflammatory sacs greatly exceeds the probable number of the fibrous sacs of hydatids.

Pus in large quantity is not often a product of simple acute diffusive peritonitis, although it is frequently found in that form of the disease that attends puerperal fever, septicæmia, or erysipelas. Yet I have seen it a few times. The pus is not generally pure, but is mixed with serum in different proportions, and there will be seen at the same time deposits of lymph attached to the peritoneum or scales of it floating in the fluid effusion, or both. There is reason to believe that in the cases of this class a very large proportion are fatal in the acute stages, but in the cases that live for a few weeks the pus is disposed to collect in pools and become abscesses by adhesions around them at their borders. These abscesses are disposed to find an exit from the body. In one case four abscesses that were found in this way in different parts of the abdominal cavity had each burrowed toward the umbilicus, and were actually discharging their contents at this point when I saw the case. In another case one abscess only was formed, and in four weeks it had perforated the colon. The opening was nearly an inch in diameter.

Kalantarians says, in eight examinations of the solar and hypogastric plexus in persons who had died of acute peritonitis changes which he regards as inflammatory had occurred, with subsequent opaque swelling of the nerve-cells, ultimate fatty degeneration, brown pigmentation, and atrophy. In chronic peritonitis the cells are often converted into amorphous pigment matter, with increase and sclerosis of the ganglionic connective tissue. Still, it is worthy of notice that these changes do not express themselves in symptoms in those that recover.

ETIOLOGY.--Numerous writers have expressed a doubt whether a spontaneous acute peritonitis ever occurs, or if it is ever primary its occurrence in this way is very rare. Habershon[1] has presented the case with more apparent force than any other writer. He studied the record of five hundred autopsies of peritonitis made at Guy's Hospital during twenty-five years, but he "cannot find a single case thoroughly detailed where the disease could be correctly regarded as existing solely in the peritoneal serous membrane."

[Footnote 1: Medico-Chirurgical Trans., vol. xliii. p. 5.]

This statement must be received with some caution. In twenty-five years the records were probably made by a number of different persons, and persons of varying views and varying capacity and judgment. It is possible that the quotation may embrace some of the changes already referred to as the consequences of peritonitis. It does embrace the cases {1137} "when inflammation of the serous membrane occurs in the course of albuminuria, pyæmia, puerperal fever, erysipelas, etc." It also includes "peritonitis caused by general nutritive changes in the system," as seen "in struma, cancer, etc.," "comprising also those cases in which the circulation of the peritoneum has been so altered by continued hyperæmia (modifying its state of growth) that very slight existing causes suffice to excite mischief, as in peritonitis with cirrhosis, disease of the heart, etc."

With these explanations the statement differs widely from what it would seem to mean without them. It is far from saying that peritonitis always follows some abdominal lesion and is caused by that lesion.

Habershon's paper was published twenty-three years ago, and during all these years the curative treatment of peritonitis, to which the paper itself gave currency, has enabled us to study our cases after recovery as well as before the sickness, and it can hardly be doubted that a much larger proportion of the cases are primary and idiopathic than either Louis or Habershon found reason to admit. That a large number are produced by preceding lesions and constitutional conditions no one will be likely to doubt.

Among the 500 post-mortem examinations of peritonitis reported by Habershon, he found preceding disease or injury recognizable in the abdominal cavity in 261. The following is his table, viz.:

From hernia, of which 19 were internal obstruction . . . . . . . 102 From injuries or operations . . . . . . . . . . . . . . . . . . 35 From perforation of the stomach, ileum, cæcum and appendix, colon, etc. (other 13 mentioned with hernia, or with cæcal disease) . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 And leading to fecal abscess (2 otherwise mentioned) . . . . . . 17 From typhoid ulceration without perforation . . . . . . . . . . 5 From disease or operation on bladder and pelvis, viscera, etc. . 42 From disease of the liver and gall-bladder . . . . . . . . . . . 11 From acute disease of the colon (3 others enumerated with perforation) . . . . . . . . . . . . . . . . . . . . . . . . . 3 From disease of the cæcum or appendix (9 others previously mentioned) . . . . . . . . . . . . . . . . . . . . . . . . . . 3 --- 261

Habershon says that in the (his) second and third divisions of the cases the causes were as follows:

From Bright's disease . . . . . . . . . . . . . . . . . . . . . 63 From pyæmia, 13; erysipelas, 5; puerperal fever, 10; with pneumonia, 3 . . . . . . . . . . . . . . . . . . . . . . . . . 31 From strumous disease . . . . . . . . . . . . . . . . . . . . . 70 From cancerous disease . . . . . . . . . . . . . . . . . . . . . 40 From hepatic disease . . . . . . . . . . . . . . . . . . . . . . 27 From heart disease . . . . . . . . . . . . . . . . . . . . . . . 9 --- 240

I have drawn thus liberally from Habershon's paper because it is the only paper that I know, in any language, founded on the analysis of a large number of cases (for five hundred post-mortem examinations is a large number for a disease no more frequent than peritonitis), in the belief that he dealt with facts and that his conclusions must be of great value. He may differ with other physicians regarding what constitutes strumous disease and in the agency of heart disease. He may have mistaken coincidence for consequence, but the paper bears the marks of honesty and good faith from the beginning to the end.

In Habershon's second division, under which he ranks the cases of {1138} peritonitis caused by "a changed condition of the blood," he ascribes 63 to albuminuria. Every physician knows how often meningitis or pericarditis or pleurisy may occur under these circumstances, especially in young persons; but, for myself, I cannot but express surprise at these figures. In one capacity or another I have been connected with large hospitals for forty-eight years, and have seen many cases of albuminuria in private practice, and can recall but few instances in which kidney disease, excepting cancer and other tumors, has terminated in peritonitis. In modification of this statement, however, it is proper to add that the hospital physician cannot know how half the diseases he treats terminate, on account of the American plan of interrupted service, and even less can he know of the mode of death in cases which he sees in consultation. Even with this admission, from my standpoint it is not easy to believe that one-eighth of the cases of peritonitis are caused by albuminuria.

The word pyæmia used by Habershon, it seems to me, ought to be replaced by septicæmia, and it has been by many of the profession. Sédillot many years ago proved that laudable pus injected into the blood-vessels of the dog produced no signs of disease, but that septic pus, so used, was followed by grave symptoms, even death. Among the author's cases thirteen were associated with the septic poison. He also found five which he thinks were independent of erysipelas. One in one hundred is a proportion hardly large enough to establish the relation of cause and effect against the chances of concurrence.

I can make a remark with reference to the inquiry by C. Dubacy in the October number (1881) of the American Journal of Medical Sciences, whether diphtheria produces peritonitis. When diphtheria became epidemic among us in 1860 or 1861 for several years, I saw a great deal of it, but did not recognize any relation between it and peritonitis.

The relations of hernia, injuries, and operations to peritonitis need no commentary.

Perforations of the alimentary canal may require some illustrative statements. These occur most frequently in the vermiform appendix of the cæcum, and are almost invariably caused by some irritating substance imprisoned in its tube. In some cases it is a seed of some fruit, as the orange or lemon; in others, a cherry-pit; in one that I remember it was a small stone, such as is sometimes found in rice; in others, a hard fecal concretion; in one, a child, a singular formation: a strawberry-seed was the centre; around this a layer of fecal matter, around the fecal matter a calcareous layer, on this, again, a fecal layer, and so on to the number of six layers, the external one being calcareous. This body was about one-fourth of an inch in diameter, and may have been years in forming. In this connection I may state, per contra, that I am informed that in a pathological museum in Boston is preserved an appendix that contains, and did contain, a large number of bird-shot, which did no mischief except to enlarge the appendix. This was from the body of a man who had shot and eaten many birds. My observation has led me to the belief that a large proportion of the cases of peritonitis occurring in children are due to perforation of the appendix.

Of the diseases of the liver producing acute diffuse peritonitis, the foremost, I think, is abscess, single or multiple. The different modes in which gall-stones may produce it may be illustrated by the following {1139} cases: (1) A lady died of acute peritonitis. At post-mortem examination a large abscess was found, bounded above by the liver, in other directions by adherent intestines; it contained nearly a quart of pus: at the bottom of the sac was a single gall-stone, very large and very black; the gall-bladder was perforated and very much shrunken. The gall-stone had caused an ulceration of the gall-bladder, but none of the intestines, in this respect differing from the process known as painless transit of a gall-stone. So the calculus caused the abscess, and the abscess caused the general peritonitis. (2) A lady between fifty and sixty years of age had an attack of gall-stone pains; she had had them before. In a few hours symptoms of peritonitis were manifest, and she died. The post-mortem examination showed the ductus cysticus was ulcerated and perforated. Two gall-stones of large size had been formed in the gall-bladder, and had been pushed forward into the duct about halfway to the common duct, leaving it enlarged as they advanced. The foremost one had caused an ulcer on the anterior or lower side of the duct, and bile had escaped, staining all the right half of the abdominal cavity, and throughout this half only the parts were covered with false membrane and stained with bile.

These cases are not so very uncommon. John Freeland of Antigua had a patient, a colored woman sixty-five years of age, who had been suffering from intermittent fever, gastric disorder, and retching. In one of the vomiting spells she experienced great pain, which, being relieved by an opiate, soon returned and was attended by tympanitic and tender abdomen. Death occurred in collapse about eight hours later. The cavity of the abdomen was found filled with blood and bile, the intestines inflamed and gangrenous in spots, and there was general peritonitis. The gall-bladder was empty; the hepatic duct was lacerated, and contained pouches in which gall-stones were encysted. One of these bags was lacerated. This laceration was surrounded by evidences of recent inflammation, and caused the general peritonitis.[2]

[Footnote 2: The Medical Record, Dec. 9, 1882.]

The perforations of the stomach which I have seen have been attended by little inflammation of the peritoneum. Death has followed this accident in twenty to thirty-six hours. There has been little pain, little tumefaction of the bowels, little tenderness, but a sense of sinking and a peculiar feeling at the stomach which the patient finds it difficult to describe.

The ulcers of dysentery do at times perforate all the coats of the colon, and yet do not with any uniformity cause general peritonitis; but as the destructive process approaches the outer covering the latter becomes inflamed, and lymph enough is effused to close the opening and prevent the escape of the contents of the intestine; so that, while perforation is not uncommon, I have rarely seen diffuse peritonitis accompanying dysentery.

Habershon reports 5 cases in which incomplete typhoid ulcers of the intestines caused peritonitis, and 15 from the complete perforation. I believe that the physicians of this country and those of France have found the complete perforation much the most common.

I do not remember to have seen fecal accumulation in the intestines produce peritonitis at all general. I did see, years ago, a man of middle {1140} age in whom fecal impaction in the ascending colon had caused destruction of all the layers of the abdominal wall on the right side, so that the contents of the intestine were exposed to view in a space of three inches by two. This implies that there had been peritoneal inflammation enough to seal the intestine to the abdominal wall on all the borders of this extraordinary ulcer. The man recovered in about six months, and returned to his business.

The inconsiderable operation of tapping for abdominal and ovarian dropsy has sometimes been followed by acute peritonitis. In the early part of my professional life I met with several such cases, and have witnessed the same from time to time since. These were mostly cases of dropsy from cirrhosis of the liver. Habershon found 5 such cases, and 7 in the tapping of ovarian cysts.

The rupture of ovarian cysts has produced peritonitis, but in a larger number of cases such rupture, even when the result of violence, has not led to inflammation; but the kidney secretion has been greatly augmented and the fluid absorbed, so that the rupture has been beneficial rather than harmful.

Tumors, particularly those of a malignant character, are apt to grow to the surrounding structures by adhesions the result of chronic inflammation, but now and then they provoke an acute attack which becomes general. Benign tumors may, in rare instances, do this. In one case a man died of acute peritonitis, and the examination showed that a tumor noticed before death, a very large serous cyst standing out of the left kidney, downward-forward, was the only lesion that antedated the inflammation.

Infiltration of urine, in any of the several ways in which it can reach the peritoneum, is a cause of peritonitis. Pelvic cellulitis may also be a cause, though twenty or thirty cases in succession may run a favorable course with no secondary lesions; it is still recognized as one of the occasional causes of peritonitis.

Among the rare causes of diffusive peritonitis is perforation of the intestine by lumbricoid worms. In such cases the product of the inflammatory action is apt to be sero-purulent, with but a limited amount of fibrin. E. Marcus reports such a perforation, and it was called by Peris ascaridophagie. The worms were apparently not found in the peritoneal cavity, but in the intestines. The perforation had bloodless edges, which lay quite close upon one another, as if they had been separated by a piercing action of the attenuated extremity of the parasite not eaten through.[3]

[Footnote 3: N.Y. Med. Journal, Jan. 27, 1883.]

Lusk finds that certain vaginal injections excite a local peritonitis. Sentey gives the details of a case in which a midwife undertook to procure an abortion by the douche. She used a tube that was large with a spreading mouth or opening, which probably received the neck of the uterus in such a way as to prevent the return of the water. It was, in consequence, forced into the uterus and through one of the Fallopian tubes into the peritoneal cavity. By this a rapidly-fatal peritonitis was developed. He refers to two other similar cases. It would seem that this mode of procuring abortion can be frightfully misused, however safe it may be in skilful hands.

There is a word still to be said regarding the difference between peritonitis produced by wounds, operations, violence, and internal growths, or {1141} what, with a little liberty, may be called traumatic causes, and that which arises spontaneously or without recognizable cause. The first shows a tendency to limit itself to the immediate neighborhood of the injury, and more frequently does not become general; while the latter spreads pretty quickly over the whole extent of the peritoneum.

SYMPTOMS.--There is, perhaps, no grave disease whose symptomatology is more easily interpreted, in which the diagnosis is more easily made, than the average case of acute diffuse peritonitis. Yet there are obscure cases which it is difficult to recognize.

In a well-marked case the first symptom is pain. Chomel and even some later writers believe that chill precedes the pain, but to the best of my recollection it has not generally so occurred to me; and the question arises, Have they kept the symptoms of puerperal peritonitis separated from those of simple peritonitis?

The pain is first felt in a somewhat limited space in the abdomen, and pretty rapidly spreads, so that it is soon felt in every part of the bowels. It may remain greatest in the part where it first began, but there are many exceptions to this statement. As the disease advances the pain and tenderness become more marked, and the patient will try to diminish the tension of the abdominal walls by lying on his back and by bending the hip- and knee-joints, often also for the additional purpose of lifting the bedclothes from his abdomen. Often the patient will resist the physician's movement to examine his bowel with the hand. In the last few hours of life the pain ceases.

The pulse in its frequency follows the advances in the disease. At the onset it is not much accelerated, but in two or three hours it may reach 100 to 120 in the minute. Besides becoming more frequent, it becomes smaller in volume and more tense. Toward the end of a fatal case it may reach 140 to 160 in the minute and be very small.

In the early hours of peritonitis the bowels begin to swell, and percussion shows that the swelling is caused by gaseous accumulation. This increases as the disease goes on, so that in some the bowels become greatly distended--so much, indeed, as to diminish the thoracic space and interfere with the respiration. As the disease advances the tympanitic resonance may give place to dulness on percussion on the sides and lower part of the abdomen. This is due to fluid effusion.

Before the introduction of opium in the treatment of peritonitis the green vomit was a marked feature of the disease. It occurs in other conditions, but rarely, and its occurrence in this disease was so common that it was regarded as almost diagnostic. The fluid vomited is of a spinach-green color, and the color is probably derived from the bile; at least, I have examined it repeatedly for the blood-elements, and have not found them. In these days this symptom of peritonitis is not often observed.

Constipation is absolute in uncomplicated peritonitis of ordinary severity, and I believe is caused by a temporary paralysis of the muscular layer of the intestine. It has already been stated that the blood-supply of the peritoneum is through vessels whose capillaries are shared by that membrane and the tissues which it covers. Inflammatory action in the peritoneum of average severity would naturally extend to this muscular layer and render it inactive. When the inflammation abates it recovers its contractile power. Thus, the intestines become entirely insensitive to {1142} cathartic medicines. This fact is not observed in puerperal peritonitis, probably because the large share which the uterus takes of the disease may act, in some degree, as a derivative; and then, so far as I know, the muscular layer of the intestines does not undergo the change of color and appearance in the latter disease that has been observed in the former. This obstinate constipation has been noticed from the first discovery of the disease, and during forty years in the first part of this century many physicians believed that if they could overcome it their patients would recover. The present interpretation of this conviction is that if catharsis, which was very rarely effected, did precede recovery, the disease was not of a grave type--if, indeed, it was peritonitis at all.

Sometimes peritonitis occurs in the course of a diarrhoea; then the constipation is not at once established, but the symptoms of the two diseases concur for one or two days, when the diarrhoea ceases.

Abdominal respiration ceases when peritonitis is established, either because the movements of the diaphragm produce pain or because the diaphragm is partly paralyzed, as is the muscle of the intestines. Then the gaseous distension of the bowels obstructs the action of this muscle. As a clinical fact it is important, and has often helped me in a diagnosis. Another kindred fact is that all the indications of peristaltic action cease. I have a great many times placed my hand on the abdomen and patiently waited for a sensation that would be evidence of intestinal movements, but did not discover any--have placed my ear on the surface of the abdomen, and have long listened for the gurgling which is so constant in healthy bowels, and have listened in vain. In this respect my observations differ from those of Battey, who reports that he has heard the friction of the newly-made false membrane in respiration, while I concur with him in the statement that the sensation of friction can be felt by pressure of the ends of the fingers into the abdominal wall so as to produce indentation. It should be said regarding the friction sound in respiration that Battey has the support of Chomel, and he in his turn quotes Barth and Roger; so that there may be in this sign more than I have thus far found. (See case hereafter related.)

The temperature of the body is not, considering the extent of membrane involved, remarkably high. I have recently attended a most carefully-observed case in which the temperature never rose above 104° F. It falls below the temperature of health as the disease approaches a fatal termination.

From the time this disease was recognized as a separate and distinct affection the countenance has fixed the attention of writers. The face is pale and bloodless and the features pinched, and the general expression is one of anxiety and suffering. I do not remember to have seen a flushed face in peritonitis, although the degree of paleness differs in different patients.

The mind is almost always clear, unless disturbed by the medicines used in the treatment. Yet cases are recorded in which a mild, and still more rarely a violent, delirium has been noticed. Subsultus tendinum, and even convulsions, have been witnessed, but whether these symptoms belong to the peritonitis or to an accompanying uræmia has not received the attention of those who have witnessed them.

The urine is usually scanty and high-colored, but it does not often {1143} contain either albumen or casts. This statement is presumably untrue of the cases in which Bright's disease preceded the peritonitis and is supposed to be the cause of it--a variety of the disease with which I have already declared my scanty acquaintance. The urine is often voided with difficulty, and sometimes retained, so that resort to a catheter becomes necessary.

The symptoms of this disease are not invariable. In one case the inflation of the bowels is only enough to be perceptible; in another, as I have said, it becomes a distressing symptom, while in most the bowels are obstinately constipated. A case may now and then occur in which evacuations can be procured by cathartics. Pain is regarded by all physicians as the most constant symptom, and it has existed in every case that I have seen, or at least tenderness; but the late Griscom stated to me that a man once came to his office for advice in whom he suspected peritonitis; but the man asserted that he had no pain, and the doctor placed his fist on the abdominal wall and pushed backward till he was resisted by the spinal column, the man asserting that the pressure did not hurt him; yet he died the next day, the doctor declared, of peritonitis. This may be credible in view of the fact that absence of pain in puerperal peritonitis is not very uncommon. The green vomit, which was expected in all cases forty years ago, for the most part, as I have intimated, disappears under the opium treatment. There are persons in whom peritonitis does not accelerate the pulse beyond 100 beats in the minute. The pain, in rare cases, remits and recurs with some degree of regularity, in this respect resembling intestinal colic. Andral reports such a case; I have also witnessed it.

MORTALITY.--Up to the time when the opium treatment was adopted, peritonitis was a fearful word; a large proportion of those attacked by it died of it. In 1832, I began to visit hospitals as a medical student, and for eight years, at home or abroad, was almost a daily attendant. The number of recoveries of those that I saw in that time can be counted on the fingers of one hand. This may be regarded as its natural mortality, for the treatment of that day seemed to exercise little or no control over it. (Farther on this matter will be referred to again.)

DURATION.--Chomel believed that the disease might prove fatal in eighteen hours, while he regards its average duration as seven or eight days. I very much doubt whether peritonitis, not caused by perforation, violence, or surgical operation, was ever fatal in eighteen hours. I do not remember any case of shorter duration than two or three days. Then, on the other hand, the period of seven or eight days in the fatal cases appears to me too long. In the early part of my professional life I remember to have looked for death in three or four days. At present, in the fatal cases, life is prolonged to double or more than double that time. In the majority of those that recover at present the duration of the symptoms is from two days to a week; in a few they have continued fourteen days; and lately I have assisted in the treatment of a case in which there was little amelioration for forty days, and yet the peritonitis was cured.

DIAGNOSIS.--When the symptoms are fully developed there are few diseases that are more easily recognized. It is when these symptoms are slowly or irregularly manifested, or when some other disease which may account for many of the symptoms occurs with it or precedes it, that there {1144} should be any real difficulty. It is customary to regard the danger of confounding the transit of a renal or hepatic calculus with peritonitis as worthy of comment. But if the reader will turn to the articles in this work which relate to these topics, he will find the symptoms so widely different from those enumerated in this article as belonging to peritonitis that he will be surprised that this item in the diagnosis should have occupied so much room.

In a case already referred to, in which peritonitis followed gall-stone pains, the transition was so marked by the rapid acceleration of the pulse and swelling of the abdomen that each of the three physicians in attendance at once appreciated the significance of the change. A physician who resided in the country called on me to report his own case. He had a little before had a very painful affection of the abdomen which continued for three days. The pain was paroxysmal, confined to the region of the liver, back and front, for one day; after that there was some tenderness over most of the abdomen, but no tympanitis. His pulse became frequent and his temperature advanced to 103°. His physicians believed that these symptoms justified them in treating him for peritonitis. Yet his position in bed was constantly changed, and no one attitude long continued--a restlessness which never occurs in peritonitis, but is common in calculus transits. Add to this the absence of gaseous distension and of the green vomit, the paroxysmal character of the pain (though I remember one case in which peritoneal pain increased and diminished somewhat regularly, but only one), and, finally, the sudden cessation of the pain, such as often happens in calculus transit when the calculus passes into the intestine,--it is plain that his sufferings were caused by a gall-stone. The elevation of temperature was the result of a long-continued worry of the nervous system, and the abdominal tenderness came from the many times repeated contraction of the abdominal muscles which occurs in hepatic colic. And then, to make the diagnosis more complete, this gentleman, after twelve or fourteen hours of pain, became jaundiced--in the end very much so. There was no absolute constipation, and the stools were of the color of clay from the absence of bile.

The points of difference between renal colic and peritonitis are even better defined and easier recognized than those between it and hepatic colic.

In intestinal colic there may be some inflation of the bowels, and if it continues a day or two there may be some tenderness; but it is for the most part distinguished from peritonitis by the intermittent or remittent character of the pain, by its greater severity while it lasts, by its courting, rather than repulsing, pressure, by the moderate acceleration of the pulse, by no or only slight elevation of temperature (exception being made for long continuance), by the absence of the green vomit, by the absence of the fixed position of peritonitis, etc.

There does not seem to me any need of spending time to distinguish gastritis or enteritis or neuralgia from peritonitis, their symptoms are so wholly different; and if, as is said, the mucous inflammation can penetrate all the coats of the stomach or intestine, and so cause inflammation of the peritoneal layer, that is peritonitis, and will be distinguished by the proper symptoms of peritonitis.

TREATMENT.--Chomel[4] says: "If general peritonitis is intense, it {1145} should be attacked by the most powerful therapeutic agents. One should immediately prescribe a large bleeding from the arm--from 500 to 600 grammes, for example--and repeat according to the need once or even twice in the first twenty-four hours; apply to the abdomen, and particularly to the part of it where the pain was first felt, leeches in large number--fifty, even a hundred--as the violence of the disease may demand and the strength of the patient will permit." He recommends baths, presumably tepid, and describes an apparatus by which the patient can be put into the bath and lifted out of it without pain; prescribes a fixed posture, gentle laxatives, mercurial frictions, blisters; conditionally and doubtfully, paracentesis, emetics under certain circumstances--musk, etc. under others. In the treatment of general peritonitis there is no reference to opium. The word does not occur, but it does in the treatment of peritonitis following perforation. In this condition he would, among other things, give opium à haute dose, but he does not prescribe any repetition or give any details. It is probable that the idea was obtained from Graves, whose first use of opium in this accident was in 1821, although its first publication appears to have been by Stokes in 1832.

[Footnote 4: Dictionnaire de Médecine, 1841.]

Wardell,[5] who has written the latest treatise on the disease we are considering, relies greatly on bloodletting, but falls short of Chomel in the quantity of blood he would take--would bleed, not to withdraw a certain number of ounces, but to produce certain effects. The venesection is to be followed by the application of leeches--twenty, thirty, or forty--to the abdomen; after this turpentine applications to the bowels. After depletion, he says, opium should be given at once: "two or three grains may be given in urgent cases." Vesication he calls "another of our aids." He disapproves of cathartics, but when there is accumulation in the colon would use injections. "Opium in the asthenic form is the chief agent, and Graves and Stokes were among the first physicians who gave it very largely." "Two or three grains may at first be prescribed, and a grain every four or three, or even two, hours afterward." "In perforation there is sometimes great toleration of the drug. Murchison has known so large a quantity as sixty grains to be given in three days with impunity." Mercurials, he thinks, are of doubtful efficacy. In the paragraph devoted to the treatment of puerperal peritonitis the word opium does not occur, and it is only by a very doubtful inference that we can assume that he would ever use it. Chomel makes no allusion to the use of opium in the same disease.

[Footnote 5: Reynolds's System of Medicine.]

For two years (1834-36) I was connected with the New York Hospital as house-physician or in positions by which that office is reached. The treatment of acute diffuse peritonitis then and there was formulated as follows: First, a full bleeding from the arm, commonly sixteen ounces, then a dozen or more leeches to the abdomen; following this, another bleeding or not, in the discretion of the physician. Meantime, the patient would take half a grain to a grain of calomel every two hours, with a little opium "to prevent the calomel acting on the bowels," of which there was no danger, in truth. Mercurial inunction was used at the same time. The belief was that after depletion the most important thing was "to establish mercurial action in the system;" in other words, {1146} "to diminish the plasticity of the blood." Under this plan I saw one recovery in these two years.

In 1840, I went to Vermont to give a course of lectures in the Vermont Medical College, and while there was called by the physicians to see with them several cases of peritonitis. I found that they were treating the disease on the Armstrong plan; that is, bleeding freely, and then administering a full dose of opium, as they said, "to prolong the effects of the bleeding." In most cases there was a second bleeding and a second administration of opium. Leeches were also used, and irritating applications to the abdomen, and in some cases purges. I found they were getting better results than we were in New York, and I studied their cases as closely as I could, and reached the conclusion that opium was the curative agent, and that it would be safe to omit the abstraction of blood. This conviction grew in strength with every new case, and I saw, with different physicians, several cases, the disease being more prevalent among the mountains there than in the city--at least that year. The idea then formed was that to establish the narcotic effects of opium within safe limits, and continue them by repeated administration of the drug, would cure uncomplicated peritonitis--that a kind of saturation of the system with opium would be inconsistent with the progress of the inflammation, and would subdue it. There was no theory to build the treatment on, and no explanation of the action of the drug in my mind. What I saw of the action of two full doses of opium was the only foundation for the idea. I had in the course of two years after those observations in Vermont 9 cases of general acute peritonitis, 8 of which were cured. All these were reported in succession, as they occurred, to the medical societies and in my college lectures. The plan was adopted by many members of these societies and by others with whom I had opportunity of conversing on the subject, so that soon there were several--I may say many--workers in the field; and in all instances where the practitioner had the courage to carry out the treatment favorable reports were returned. Not that every case of peritonitis was cured, but the recoveries generally exceeded those that followed any other plan ever before used. No physician tried it with a proper understanding of its details, and with courage to execute them, who if living does not practise it to-day.

The treatment of puerperal peritonitis is not allotted to me, and I am very reluctent to encroach in any degree on the province of the very competent and highly-esteemed gentleman to whom that disease was assigned. But the history of the opium treatment is very incomplete without the statement I am about to make, and I trust to his generosity to forgive this encroachment; and all the more confidently because he was not at the time acquainted with the manner in which opium was first introduced into the treatment of puerperal fever.

After the curative action of the drug was demonstrated in general peritonitis, I was anxious to try it in puerperal fever, of which peritonitis forms a part. But I had no hospital and no obstetrical practice. In 1847, I was appointed one of the physicians to Bellevue Hospital, to which an obstetrical department was attached. After one or two years a single case occurred and was sent to my division. I gave her 100 grains of opium in four days, with more or less of calomel--I have {1147} forgotten how much. She recovered, but after the symptoms of puerperal fever passed away she had secondary abscesses of the lungs. These kept her ill for several weeks. At length her recovery was complete.

In 1840 there was a very fatal visitation of puerperal fever in this hospital, and on invitation of Vaché, who then had charge of the whole institution, I was a daily visitor and took notes of all the cases. It was from these notes that Vaché compiled his report of the epidemic published in the Medical and Surgical Journal. The disease was fearfully fatal, although every known mode of treatment was tried in different cases, including Brenan's plan by turpentine, but all, with one or two exceptions, with the same result. At this time the opium plan was on its trial, and I had not acquired a confidence in it that authorized me to try it in these cases. The time for it came in 1851. Then a sudden, vigorous attack occurred. One woman was sent to me in whom the disease was well advanced. I instructed my house-physician not how much opium to give, but what effects to produce by it. I found this woman dying the next day, and that she had taken only three grains of opium in three doses. In three or four days seven cases were sent me from the lying-in wards. One was returned for error in diagnosis, and six put under treatment. Having found that prudence in my house-physician was so much more conspicuous than courage, another house-officer, who combined them both, was selected to be in almost constant attendance. The instruction I gave him was in these words: "I want you to narcotize those women to within an inch of their lives." He did it, and saved every one of them. This gentleman is now known over the whole land as a learned and distinguished surgeon. I feel called upon to give his name in this connection, that he may be a witness to the facts I state, and for the admiration with which his nerve and prudence impressed me. One of these patients took first two grains, then three grains, then four, and so on till she took twelve grains of opium at a dose, the intervals being two hours. The state into which the patient was to be brought I have denominated a state of semi-narcotism. The quantity of the drug necessary to produce this state varied surprisingly in different persons. One of these women was pretty fully narcotized by four grains every two hours. She was watched with anxiety; restoratives were kept in readiness, but nothing was done but to suspend the administration of the medicine and to wait. In seven hours the consciousness was fully restored, and the improvement in her condition was wonderful. The disease seemed to be cured. But in a few hours more the symptoms recurred, and the same medicine was again given in three-grain doses, and again narcotism was produced. Taught by the experience of the day before, we waited, and when she recovered from this second narcotism her disease was completely cured. She took no more medicine of any sort. This case was very instructive, as it taught me that over certain cases of puerperal fever opium has absolute control.

From the time here referred to, so long as the obstetrical service was maintained at Bellevue Hospital, a large proportion of cases of this fever, as they occurred, were sent to my wards, and in all these years I have not lost faith in opium. This statement, however, requires an explanation. Puerperal fever is a compound disease. Its great inflammatory lesions are found in the uterus and its appendages and in the peritoneum. {1148} When the inflammation of the uterus is the dominant lesion, and is purulent, opium has little or perhaps no control over its fatality; but in the cases in which peritonitis is the ruling lesion, if begun early, it will show its power. In this connection I will only add that in private practice the drug has been perhaps more curative than in the hospital. I have seen many cases in consultation, and a decided majority have recovered. In some instances the patient has fallen into a pleasant sleep, only broken by some administration, and ending with her recovery. In one instance a very eminent physician had undertaken to treat a case by the opium plan, but he had administered the drug so timidly that for fourteen days he had done no more than hold the disease in check. After trial, I found that I could not induce him to give the drug in my way, and I asked him to give me sole charge of the patient for twenty-four hours. To this he assented, remarking, "If you cure her, doctor, I will have it announced to the profession that she was the sickest person I ever saw get well." In half the time allowed me I was able to establish the opium symptoms as given farther on, and the lady slowly recovered.

The treatment of any form of peritonitis by opium permits the use of the drug itself, or of any extract or preparation of it which contains its narcotic qualities, but it is wise to persevere with that one first chosen unless there is strong reason for a change. This caution is based on the fact that we cannot change from one to another and be certain to obtain the same drug activity. For example, we begin with laudanum, and find what it will do. We cannot take in its place the sulphate of morphia with the certainty that we can so graduate it as to get precisely the same effects. Then the quantity which will be effectual in one case may be quite inadequate for the next. The tolerance of opium in different persons varies remarkably, and probably the disease itself increases the tolerance in all. This will be illustrated by some of the details of this paper.

The drug symptoms to be produced are as follows: Subsidence or marked diminution of the pain; some or considerable tendency to sleep; contraction of the pupils; reduction of the breathing to twelve respirations in the minute; in the favorable cases a considerable reduction in the frequency of the pulse; a gentle perspiration; an itchy state of skin, or oftener of the nose; absolute inactivity of the bowels, and after a time a subsidence of the tumor and tenderness in them; some suffusion of the eyes.

Of these several signs of opiumism there is none more easily observed and none more valuable than the frequency of the respiration; and while the physician aims to reduce it to twelve in a minute, there are chances that he will see it fall to something below that. I have often counted it at seven, and in perhaps two cases it fell to seven in two minutes; and yet these cases of marked oppression from opium all recovered. In the cases in which the respiration has fallen so low there has been considerable obtuseness of the mind; but in no case except in the hospital patient already referred to have I seen unconsciousness. Then the sleepiness, so long as the patient is easily awakened, is wholly within the limits of safety.

As to the quantity of opium to be given, I have known two grains every two hours do the work, and in other cases many times this {1149} quantity was necessary to produce this condition of semi-narcotism. The plan is to begin with a dose that is safe--say two or three grains of opium or its equivalent of sulphate of morphia--and in two hours notice its effects. If any of the opium symptoms have appeared, repeat the dose; if none, increase by one grain, and so on at intervals of two hours till the degree of tolerance in the patient is ascertained. After that the case can be treated by a diminished occupation of the physician's time--two or three visits a day. The dose is to be increased if the opium symptoms diminish before the disease yields, but always to be diminished or discontinued if narcotism is approaching. The duration of the treatment will be sometimes no more than two or three days; it may be a week, or even a fortnight, and in one case already mentioned the symptoms persisted mildly for forty days, and then yielded. In this case the medicine used was the sulphate of morphia, and the enormous dose reached by steady and graduated increase was one grain and a quarter every forty minutes in a boy ten years old.

In some puerperal cases the doses have been so large as to require witnesses to make the statement of them credible, and the administration of them criminal had not the effect of each dose been carefully studied and the amount of each measured by the action or inadequate action of the next preceding one.

Here are the doses given a woman who fell sick October 13, 1857; the record was made by C. H. Rawson during the treatment, and was kindly given me two or three years ago: On the first appearance of her disease, while the diagnosis was uncertain, 10 grains of Dover's powder gave her a quiet night. The next day the disease was more manifest, and she took of Magendie's solution (2 grains of sulphate of morphine to a drachm of water) x minims every hour; growing worse, at night she took xxx minims every hour; the next day, xl minims every hour, and no change of symptoms. She took in twenty-four hours 32 grains of sulphate of morphia; slept, but was awakened by the slightest noise. On the fourth day 3-1/3 drachms of the solution, and opium as follows: at 4 P.M., 3 gr.; at 5 P.M., 4 gr.; at 6 P.M., 5 gr.; at 7 P.M., 6 gr., and 6 gr. hourly after 7 P.M. Sleep light. Fifth day, in twenty-six hours took in opium and morphine the equivalent of 208 gr. of opium. The sixth day, 212 gr. of opium; on the seventh day, 221 gr. of opium; on the eighth, 224 gr.; on the ninth, the same quantity; on the tenth, the same; on the eleventh, 247 gr., pulse subsiding; on the twelfth, 261 gr., other symptoms better; on the thirteenth, 144 gr.; fourteenth day, 4 gr. hourly; slept for the first time heavily, all other symptoms improving, bowels moved freely, ate well, tympanites subsiding; fifteenth day, 1 gr. of opium every two hours, and at night the last dose. Recovery was complete. The woman denied the opium habit, and the medicines were tested by the apothecary. Such doses can only find their justification in the demonstrated fact that smaller doses will not produce the degree of narcotism desired.

In Keating's edition of Ramsbotham's Midwifery a case is reported by myself in which a woman, by pretty rapidly increasing doses, reached forty-eight grain doses of opium, with the effect of curing her disease and substituting a temporary active delirium.

A word of caution is probably necessary regarding the use of opium in high doses when peritonitis and Bright's disease coexist. I have {1150} already said that I have but scanty personal knowledge of such a concurrence, but in Bright's disease alone I have known a large, non-heroic dose of an opiate fatal. For example: A young man had a felon on his finger, and did not sleep, so great was his pain. His physician prescribed 40 drops of laudanum at bedtime. Not sleeping on this, he took another portion of 40 drops, and in the morning he was found in a comatose condition, and in the course of the day he died. A post-mortem examination revealed Bright's disease, which was not before suspected. A woman took half a grain of the sulphate of morphine--for what reason I do not know. I was called to see her when she was in a semi-comatose state. The time between my seeing her and that of taking the morphine was fourteen or fifteen hours; its removal from the body was therefore hopeless. Her limbs were swollen with oedema, and the urine contained albumen and casts. Although the usual means of opposing the poisonous effects of opium were resorted to, they were of little use, and the patient died in the course of the day. These are selected from a considerable number of similar cases that show a similarity in their action on the brain of opium and urea. It seems that opium precipitates the uræmic coma, yet the coma produced by these agents combined is not so profound as that produced by opium alone. There is in it some movement of the limbs or body or some imperfect utterances, yet it seems to be more fatal than the coma of opium unaided. Notwithstanding all this, I have met with several cases of cardiac disease combined with Bright's--perhaps I should say many--in which half a grain of morphia sulphate has been taken every night to procure sleep with only beneficial results. This has been observed several times when physicians have been the patients.

These facts are stated to show the hesitation and prudence that should control the administration of opium when there is urea in the blood, whether there is peritonitis or not; but a case in which one form of Bright's disease preceded, and perhaps caused, peritonitis will be more instructive: A gentleman sixty-eight years of age was attacked by peritonitis on Thursday evening. There was a moderate chill at the onset (this being one of the few cases in which I have witnessed this occurrence). The diagnosis was then uncertain, and he took quieting doses of Dover's powder, which gave him sleep. The next day the diagnosis was easily made. The urine was examined for albumen, and none found. It was, however, scanty. He took only six-eighths of a grain of sulphate of morphine in the first twenty hours. It was then increased, so that in the next twenty-four hours he took two grains of the sulphate in divided doses--a quantity which has been greatly exceeded in hundreds of cases with the best results; but in this case coma was the result. At 10 A.M. on Sunday he was comatose, but not profoundly; he could be aroused. The breaths were five in the minute, the pulse increasing in frequency; secretion of urine next to none. The galvanic battery was used. After seven hours, while the respiration was growing more natural, the pulse grew more frequent and the stupor increased. At 8.30 P.M. the breathing was fifteen in the minute, and full and perfectly easy, but the pulse was running at 140, and the coma unbroken, and the pupils of good size. The effects of the opiate had passed off, but those of uræmia were profound. He died at 11 P.M. After the alarming symptoms occurred we tried to procure another specimen of the urine for fuller examination, but {1151} could not. It was only after his death that we procured the evidences that he had shown symptoms of contracted kidney for months. The urine contained no albumen at the time of our examination, as very often happens in that disease.

Regarding other points in the opium treatment there is little to be said. Purgatives are entirely inadmissible. The bowels should be left entirely at rest till they recover their muscular tone; then they will expel first the gas, and then the feces; or if, after the inflammation is subdued, they do not move of their own accord, injections are admissible. I have often left the bowels absolutely inactive for fourteen days without any recognizable consequences. If I meet a physician who believes that leeches are essential, I yield him his point, but never advise them. I do this because a moderate bloodletting will do no harm, and little if any good. The same rule I apply to irritating applications to the surface of the abdomen. Mercurials, I think, are harmful, and therefore I object to them. As to food, it should be milk, fresh eggs beaten up with water and pleasantly flavored, peptones, etc. selected from among those that leave no refuse.

The testimony of physicians who have adopted this plan within my own circle is unanimously in favor of it. B. R. Palmer of Woodstock, Vt., afterward of Louisville, Ky., who was the first to test it, told me after a few years' trial that he used to dread peritonitis as he would dread the plague, but with opium in his pocket he met it cheerfully and hopefully, as he did a pneumonia. Chalmers of New York, who is known by many readers of this article, has a very extensive practice, and he told me lately that he had not had a fatal case of peritonitis in twenty-two years. He embraced the plan early.

Now, how did this treatment originate? From whom did the profession adopt it? In 1836-37, I visited daily the hospitals of London, Edinburgh, and Paris, was in frequent intercourse with the physicians of those cities, and never saw a patient anywhere treated by opium, and never heard the least allusion to it. I can safely appeal to any physician who was familiar with the history of the profession before the year 1840, or for two or three years later perhaps, to inquire whether anything was generally known regarding this treatment of peritonitis, or whether he himself ever heard of it. Let the inquiry be made of Willard Parker of New York or Alfred Stillé of Philadelphia--men of a degree of intelligence and learning that has made them leaders in the profession--and of all the profession at that time. I venture to assume that they were as ignorant as I was of what Graves and Stokes had done.

The following fact is significant: In 1843, Graves published A System of Clinical Medicine, the preface of which is dated January, 1843. In this he says he had previously published essays, lectures, and articles in several medical journals. In this volume he intends, he says, "to revise what I have written, and to compress the whole within the limits of a single volume." There is nothing in the table of contents or explanatory headings of the several chapters of this volume which alludes to treating peritonitis by opium. It is fair to infer that the cases treated in 1823 had made little impression on his mind, and that he did not think his treatment could take rank as a discovery; and yet Stokes had made favorable mention of it eleven years before this publication. Graves, then, did not {1152} publish his cases, and the first knowledge which the profession could have of them was through Stokes's paper, published in the Dublin Journal of Medical and Chemical Science, No. 1, in 1832. Perhaps the reason why Stokes's paper produced so little impression on the profession may be found in the fact that first numbers of journals of every sort have few readers. Anyway, it was not till after the opium treatment had attracted much attention in this country that anybody here knew that Graves or Stokes had ever had anything to do with it. Besides, Graves and Stokes had only used opium in cases of perforation, and they had no plan or symptomatic guide in the use of the drug.

There is something new and strange in the following case copied from the Medical Record of May 12, 1883, under the heading, "Operative Measures in Acute Peritonitis:" "Dr. Reibel relates the case of a child, eight years old, suffering from acute idiopathic peritonitis. The disease had resisted all treatment, and the child being, apparently, about to die, it was determined to open the abdomen with a view to removing the fluid and washing out the peritoneal cavity with a solution of carbolic acid. The meteorism was intense. No fluid was found in the abdominal cavity. In prolonging the incision a loop of the intestine was punctured, as evidenced by the escape of gas and intestinal fluid. The wound was washed with carbolic acid and covered with a layer of antiseptic cotton. The following day the little patient was nearly free from pain, and was able to retain a little milk. The temperature had fallen from 104° to 101°, and the tympanitis was almost entirely gone. The (wounded) loop of intestine was adherent to the abdominal wall, and there had been no escape of fluid into the peritoneal cavity. The patient made an excellent recovery."

If the statements of this abstract are true, and the future supports the practice pursued in this case, acute peritonitis is likely to become a surgical rather than a medical disease. Reibel thinks that opening the intestine in the way he did is a better plan than the punctures with the exploring-needle to relieve the patient of the tympanitis. But it will require more facts than one to persuade the profession that this mishap of the scalpel can grow into a rule of practice. (The Record finds this report in the Journal de Médecine de Paris.)

I cannot say that I see the value of a distinction made in 1877 by Gubler between peritonitis and peritonism. By the latter term is meant the total of nervous and other symptoms that arise in the course of peritonitis. Trasour has lately revived this distinction, and thinks it important, and that a light peritonitis may be attended by a grave peritonism. He holds that the distinction is important, because "the treatment of peritonism consists in the administration of alcohol, chloral, and especially of opium in large doses. Of the latter fifteen grains may be given in twenty-four hours." "The symptoms [of peritonism] are produced through the agency of the great sympathetic."[6]

[Footnote 6: Med. Record, Aug. 28, 1883.]

I cannot say that I have seen great effects follow small causes, but think that, in general, the effects of peritonitis on the pulse, strength, nervous tone, etc. are, to some extent at least, a measure of its severity.

CONSEQUENCES OF PERITONITIS.--These are usually nothing. When recovery takes place it is commonly complete, but cases have been known {1153} in which the intestines have been left bound to the abdominal wall and to each other, and so made incapable of their natural action. The results of this are a swollen, tympanitic abdomen and impaction of the bowels, but the general health may be very good. A woman at Bellevue was left in this condition, yet she performed the duties of nurse in one of the wards for some years, and finally disappeared from the institution, and I do not know how it ended with her--probably by the breaking up of the adhesions and a return of the bowels to their natural condition.

In some few cases there remains new tissue, which in time is partly broken up and remains partly attached. In this manner strings and bands of considerable strength can be formed, and into these loops the intestine may pass, so as to form an internal hernia of a very dangerous character. In some bands are formed across the intestine, which by contraction flatten the tube and obstruct the fecal movement. There is reason to believe that such bands and bridles are formed by local inflammation of such imperfect manifestation by symptoms that the patient knows nothing about it. A very striking case illustrating the possible sequence of this inflammation came under my observation early in my professional life: A colored woman about twenty-five years of age gave a very clear history of a peritonitis from the consequences of which she had suffered two years before I saw her. About six months after recovery she began to have constipation and to suffer from small and frequent discharges of urine. The latter gradually grew milky and to have a bad odor; the constipation grew more and more, and at length came to be absolute for many days; then would come a diarrhoea of some hours' continuance, after which she would have a feeling of relief. This was her state when I saw her. She was emaciated, and so feeble as hardly able to leave her bed. She vomited occasionally, and her appetite for food was all gone. The urine was heavily loaded with pus, and was ammoniacal. She died after a few weeks. At post-mortem examination a firm membrane was found strained across the upper strait of the pelvis, wholly separating the abdominal cavity from the pelvic. It looked like a drum-head. The left posterior border was drawn very tensely over the colon where it passed into the pelvic cavity, flattening it down completely and making stricture. To the under or lower surface the fundus of the uterus and the base of the bladder were firmly adherent, and in this way both were suspended. The effect of this unnatural suspension of the inactive uterus did not seem to be noticeable, but with the bladder it was very different: it contained three to four ounces of water, ammoniacal and full of pus, and it could never have emptied itself. The explanation is very simple. During the peritonitis a false membrane was effused on the pelvic viscera in situ. When the period of contraction which is common to all such structures came, the new membrane was separated from the greater part of these two organs, but not from their bases. The firm attachment to the brim of the pelvis did the rest. So unusual a sequel of peritonitis I think deserves a record. I should add there were no adhesions above the pelvis. Such a structure as this, found long after the active symptoms of peritonitis have passed, as also the bands and cords before spoken of, does not give support to the doctrine that the false membranes are broken down into fatty matter, and in this condition absorbed.

{1154} The possible remote effects of peritonitis are shown in a case reported by E. A. Mearns to the Medical Record, published Sept. 15, 1883: A young man, aged nineteen, four years after he had had acute general peritonitis was attacked with constipation, which was absolute. He had had before occasional attacks of pain in the bowels and constipation, which were overcome. But this was invincible. He had the train of symptoms usual in intestinal obstruction. There was no fever or tympanitis, and this time but little pain. He lived eight days. There was a tangle and a constriction of the intestines at the middle of the ileum, caused by the contraction and hardening of the effusion of the old peritonitis, and the intestine was very much softened.

H. B. Sands reports in another number of the same journal: "The patient was a man about thirty who had suffered from acute obstruction for a week. No exact diagnosis was made. When the abdomen was opened the intestinal coils were found extremely adherent one to another in consequence of a former peritonitis. A careful search failed to discover the nature or seat of the obstruction. The abdominal wound was closed, and the patient died soon after."

Peritonitis from Perforation.

There is no part of the gastro-intestinal canal that may not, from one cause or another, become the seat of ulceration. The jejunum is the part of the tube long supposed to be an exception to this rule, but even in it one or two observers have found ulcers. These ulcers often exist without distinctive symptoms, and may go on to cicatrization without announcing themselves. In the stomach, however, there are commonly indications which will admit a conjecture of their existence, and perhaps a diagnosis. Sometimes these ulcers penetrate all the tissues of the tube and allow the contents of the intestine to escape into the peritoneal cavity, or they may have destroyed all but the external layer, and some succussion, as in coughing, sneezing, laughing, or perhaps straining at stool, may make the opening complete, with the same results. In these cases it seems to be inevitable that inflammation should follow, unless it has preceded, the complete opening and sealed it up by adhesions. The tendency of such an inflammation is to be local and limited, but when the contents of intestines escape into the peritoneal cavity it usually becomes general. These accidents are usually attended by the sudden development of local pain, by rapid increase in the frequency of the pulse, paleness, and prostration. The perforation of the vermiform appendix is often a partial exception to this statement, for, while the local symptoms are marked, the sympathy of the general system is not so quickly awakened. The same can be said of perityphlitis. The symptoms are often local for some time--a day or more; sometimes subside, as if the disease were cured, and then return in full form. This is produced by the tendency of the inflammation to limit itself to the immediate neighborhood of its cause. Lymph is effused at a short distance from the point of irritation, and seals the parts together, so as to shut in the offending substance; and though this substance may produce pus in contact with intestine or appendix, that {1155} fluid is held for a time, as in abscess. It may be permanently held in its new-made sac till it burrows into some near part, as the intestine or bladder, or remain an abscess till opened by Willard Parker's puncture. On the other hand, the contents of this sac may be increased till it breaks bounds and causes extension of the peritoneal inflammation or general peritonitis. In one particular case this process of setting limits and breaking through them occurred in a young lady four times at intervals of from one to two days. When the limiting adhesions were established symptoms would subside, so as to encourage in her physicians the hope, even the expectation, of recovery; but again and again the fire was rekindled, and she died eight days after the first attack. In the greater number of cases the first breaking of the adhesions is followed by full peritonitis, and this often by death.

The perforations of the stomach which I have seen have not been attended by the severe pain described by most authors, but by a sudden prostration of strength and a feeling of disquiet and sinking at the stomach; more of collapse than of inflammation in the symptoms; no tumefaction of the bowels; almost nothing to indicate the nature of the accident, but a sudden new sensation in the bowels, a rapid increase in the frequency of the pulse, it growing small as it increases in rapidity, and a pale and shrunken countenance, and death in from twelve to thirty hours. Then, on inspection, hardly any signs of peritonitis are found. The peritoneal vessels are fuller and the membrane redder than in health, and its surface covered with the thinnest possible film of lymphy exudation, and some serum in the deeper parts of the cavity.

These ulcerations of the stomach are not always fatal by peritonitis. A few instances are recorded in which adhesions of the outer surface of the organ to adjoining organs have taken place, so as to protect the peritoneum almost wholly from the fatal contact with the gastric fluids, and death has occurred in some other way. I have a remarkable specimen illustrating this fact. It was taken from the body of a woman of about middle age who had long had symptoms of dyspepsia, and had from time to time vomited a little blood. It was not difficult to recognize ulcer, but the extent and peculiarities of it could be learned only by inspection. She died suddenly of copious hæmatemesis. On examination an ulcer two and a half to three inches in its several diameters was found, beginning near the pylorus and extending toward the left, which in this large space had destroyed all the coats of the stomach and exposed an inch and more of the right extremity of the pancreas and about the same extent of the liver. The liver and pancreas were both perceptibly eroded when exposed, and in the latter an artery that would admit the head of a large pin was opened. The stomach, outside of this extraordinary ulcer, was strongly attached to the adjacent organs.

The ulcerations of typhoid fever penetrate the intestine about three times in a hundred cases of the fever. This result is reached by the study of a large number of cases, and appears to be pretty generally admitted. The point where this perforation occurs is in the ileum, near the ileo-cæcal valve--within a foot or eighteen inches of it in the great majority of cases, although it has been known to occur seventy-two inches above the valve, and it has been seen very rarely in the cæcum. The fever itself may be either severe or mild. Suddenly severe pain {1156} sets in, oftenest in the lower part of the abdomen, and spreads rapidly; the pulse is quickly accelerated and becomes small; and it has been lately stated that in this and other intestinal perforations the gases of the bowels, escaping into the peritoneal cavity, will give resonance to percussion over the lower part of the liver. Fetid gas found in this cavity after death is not without importance; for example, a distinguished Senator at Washington died not long ago of a very painful abdominal disease which his physicians declined to relieve with opium, though the patient pleaded for it. His family physician at home was summoned. Although the distance he had to travel was many hundred miles, he found the patient alive and still suffering. He at once gave morphine for the relief of the pain, but the patient died. Now, this gentleman had diabetes a year or more before his death, recognized by his physician at home and also by myself. While under my observation the urine ceased to contain sugar and its quantity became normal, but soon after this albumen was occasionally found in it. The quantity was generally small, and casts were only found now and then. This new disease was mild, and seemed to be, within certain limits, manageable. He went to Washington under injunction that he was not to let official and professional labors bear with any weight upon him. This last sickness and the death would naturally enough be supposed to be some new phase or consequence of the previous illness. But, while a post-mortem examination was not permitted, the family wished to have the body embalmed. The family physician accompanied the embalmer, and as the latter made a cut through the abdominal walls there was a gush of air laden with fecal odor, and he through this opening saw the intestines covered with false membrane. He satisfied himself that the intestine was not opened. This fetid gas came from the peritoneal cavity. An ulcer had perforated the intestine somewhere, and caused the death. The final disease could be only remotely dependent on the patient's previous illness, if at all. His impaired health may have made the ulcer possible.

All kinds of perforations in the bowels, except those of the stomach, cæcum, and appendix, even the cancerous, have one history and the same symptoms; and if treatment is ever successful in such occurrences it must all be based on one set of rules--absolute rest, no pressure on the bowels, and no movements of the muscles that will aggravate it; food that will be wholly digested and absorbed by the stomach; complete abstinence from cathartic and laxative medicines, and the free administration of opium or morphine. By these means, I fully believe, numbers have already been saved from the fatal consequences of peritonitis caused by perityphlitis and perforation of the vermiform appendix--some under my own observation and others under that of my friends. A boy fourteen years of age was brought to bed by a pain in the right iliac fossa. After a few hours his father, a physician, desired me to see him. There was already a perceptible fulness, with dulness on percussion, in the fossa, and some febrile excitement. I gave a portion of morphine, and promised to call the next morning. In the morning a message came from the father stating that the boy was better and there was no need of further attendance. In the evening I was recalled. The pain had returned, and had spread over most of the bowels. He had general peritonitis. He took tincture of opium, of which I believe the largest dose was 100 {1157} drops, reached after three or four days of gradual but steady increase of dose. From that point the patient got better, and the quantity of the medicine was correspondingly reduced. There were a relapse and a repetition of the treatment, and again the disease yielded. During convalescence, about fourteen days from the attack, the boy, after emptying his bladder, was suddenly pressed to continue the discharge. Now he voided what appeared to be blood, two or three tablespoonfuls. It was, however, pus with blood enough to color it. This purulent discharge from the bladder continued for about three weeks, the boy steadily recovering his health. This occurred twenty or more years ago, and that boy is now a well-known physician. Similar cases could be recited.

In 1850, or thereabout, I attended a physician through an attack of typhoid fever. In the third week there was a sudden outbreak of peritonitis. The opium treatment was resorted to, and he recovered, and had good health for twenty years after. Peritonitis occurs rarely in typhoid fever from any other cause than perforation, and its occurrence in this case at this time, when perforation is more likely to occur, renders it probable, at least, that this attack was produced by that cause.

March 3, 1883, autopsy of Wm. Fletcher, age 59, iron-worker. On Friday last, Feb. 23d, he was attacked with pain in the region of the right iliac fossa; it was severe. There was no chill, but little fever, and only slight acceleration of the pulse. His stomach was a good deal disturbed, and the bowels were soon distended with flatus. I saw him on the Tuesday following, with James D. Elliott. The bowels were a good deal swollen and very resonant on percussion; pulse 84. His stomach was still greatly disturbed, so that he retained no food, yet there was no green vomit, but much flatulency. The movements in respiration were particularly noticeable, being nearly or quite as much abdominal as in health. There was a short friction sound in inspiration, but an entire absence of the sound produced by peristaltic action. There was no dulness on percussing over the iliac fossa, and no pain on pressure over any part of the abdomen. I was careful in examining the right fossa, for the first pain was there, and it was severe; but there was no physical sign by which the perforation could be ascertained. Still, my mind dwelt on the probability of perforation, and I expressed my fears to Elliott regarding it. The respiration was of natural frequency. The bowels had not moved for two or three days.

The next day Flint was added to the consultation. The symptoms had changed but little; the pulse was 102; no pain, no tenderness, no peristaltic action; slight friction at one point only; the abdominal respiration was as marked as before. Frequency of respiration, 18; patient sleepy; pupils only slightly contracted. When we were in consultation I again expressed my fear of perforation, but Flint expressed the most decided opinion as to its absence, because there was dulness to percussion over the liver. I had read his paper on the intrusion of gas between the ribs and liver in cases of intestinal perforation, and felt as if I were almost reproved for entertaining the thought without this physical corroboration.

Thursday, March 1st, the stomach had become much more retentive; there were no pain and no tenderness on pressure; pulse 109; no friction sound, no sound of peristaltic action, no dulness on percussion over right iliac fossa, but resonance over the whole abdomen, excepting over the {1158} pubes; there the resonance was not clear; over a small space there was dulness; this was ascribed to moderate fulness of the bladder, and, as there had been no difficulty in emptying it, nothing was said of it. The abdominal respiratory movements were the same as before.

Friday morning, at 3 A.M., no marked change had occurred in the symptoms, but from this time onward there was a steady sinking of the vital powers. The pulse grew small and frequent, the hands became cool, the breathing more frequent, and without any sudden change or new symptom he died early in the morning. At the last visit there was no resonance on percussion over the liver.

Autopsy, Saturday, March 3d, 2 P.M. The bowels were distended, as they mostly are in peritonitis, but not extraordinarily. There was now pretty free resonance over the liver. The section to open the abdominal cavity was carefully made, with the aim of ascertaining whether there was air or gas in the peritoneal cavity. When a half-inch opening was made through the peritoneum, gas was forced out through it for some seconds with an unmistakable noise. The bowels were not opened by this cut. The bowels exposed, a very thin film of false membrane was found on all the middle and upper portions of the intestines, with a fringe of injection where the folds came in contact. But two or three inches above the symphysis pubis the section opened a collection of pus which extended downward into the pelvis. Somewhere hereabout--neither of us could say exactly where--was found a lump of fecal matter, not indurated, as large as a marrowfat pea, the intestine still unopened. Search was made for the vermiform appendix. At first it was not recognized on account of its remarkable shortness. It was found, however, pointing directly toward the median line of the body, and was short because a part had been separated from the rest by slough. The end of what remained was marked by a border, one-eighth of an inch deep, of a very dark-green gangrenous color. We did not attempt to measure the quantity of pus. It was six ounces or more. It was completely bounded and shut in by adhesions.

At no time during life was there resonance over the liver, but there was some at the time of post-mortem examination before the bowels were opened, due perhaps to the fact that at death the relaxation of the muscles allowed the gas to rise higher than it did during life. The unusual median position of the abscess is important in accounting for absence of dulness, when it is usually found in slough or ulcer of the vermiform appendix.

"A Fatal Case of Typhlitis without Recognizable Symptoms." Under this title José M. Fisser published a case of inflammation of the vermiform appendix causing general peritonitis in a young woman nineteen years of age. The peculiarities of the case were that the appendix was not perforated, and consequently there was no tumor in the right iliac fossa--that the symptoms were all referred to the epigastrium, without even tenderness in the fossa. She walked the floor and tossed about in bed; the highest temperature was 103°, and the most frequent pulse was 120, and these continued but a short time. Of tympanitis there was none till near death, and then but little. The obscurity in diagnosis led to the publication of the case. The cause of this disease was fecal matter, not very hard, in the appendix.[7]

[Footnote 7: Med. Record, Sept. 1, 1883.]

{1159} As much has been said in this article on the diagnosis of peritonitis, it may be well to introduce a case where that diagnosis was conjectural, and yet quite another state existed. I visited Mrs. H----, when her disease was advanced, twice. My impression was that she had peritonitis, but this opinion was held with grave doubt. After her death, Smith sent me the following record of the autopsy: "Mrs. H---- died Friday evening at ten o'clock; next day, at three in the afternoon, we made an autopsy. No gas or fluid in the peritoneal cavity; the small intestines inflated almost to bursting, with injection of the capillaries. In the left iliac region we at once discovered a portion of the intestine almost black, and on examination found a firm white band encircling and constricting that portion. Upon liberating the gas the intestines collapsed, and the constricted portion was released and easily removed. A further examination showed that two of the epiploic appendages, coming off from the colon above the sigmoid flexure, had united at their extreme points and formed a loop two and a half to three inches long, and through this loop or ring a portion of the ileum had passed, and was there constricted. The constricted intestine was about four feet in length. This examination has been gratifying to me. There was a small quantity of bloody serum in the peritoneal cavity low down in the pelvis. The dark grumous blood that passed the bowels on the second and third days can now be accounted for, and corroborates your remark that the hemorrhage looked like strangulation. This was at your first visit. This must be a new cause of strangulation, and one that we could not anticipate."

There was, before I saw her, a single vomit of a suspicious fluid, but the evidence was not strong enough to enable us to pronounce it stercoraceous. Some of the observers noticed bloody serum in the peritoneal cavity, and perhaps some shreds of lymph, but that was in consequence of the strangulation.

Local Peritonitis.

This may occur anywhere in the broad extent of the peritoneum, and will be more or less limited in different cases, or may be limited for a time, and then become general. It is either acute or chronic. The product of the diseased action may be serum or lymph or pus, or all of them. The cause of this local inflammation is sometimes very obvious, in other cases wholly unknown. The consequences vary all the way from harmlessness to death; the symptoms are as variable as the consequences, making the diagnosis easy in some cases, in others impossible. Some cases in which it was not difficult to recognize it have already been recorded--those caused by perityphlitis and perforation of the vermiform appendix, for example. In such cases the local pain, the swelling, the dulness or resonance on percussion, depending on whether the tumor is made by inflammatory exudation or gas, together with the general symptoms and the history, leave but little ground for doubt regarding the character of the disease. Perhaps one-half the local abscesses which form between the folds of the peritoneum are recognizable during life by the local, associated with the general, symptoms. When situated in the posterior and upper part of the abdominal cavity, the hand gives little, {1160} perhaps no, assistance, as in the most widely-known case of abscess that has been recorded in all time. While the physicians were giving to the country hopeful reports day by day, thousands of medical men shook their heads and spoke sadly of the prospects. The illustrious patient was losing rather than gaining strength and flesh, his appetite poor, his digestion poor--a strong man growing helpless--and, above all, a pulse that for months never fell below 100. With an adequate cause of abscess, whether there were chills or not, what else could it be? Thus, in peritoneal abscesses that cannot be felt the general symptoms are of great importance to the diagnosis. When abscesses tend to discharge their contents soon or late--sometimes into the intestine, sometimes into the bladder, sometimes externally: in such cases there is a fair chance. Sometimes they burst into the peritoneum: such cases are almost inevitably fatal; even opium will not cure them. The pus of these abscesses often has the fecal odor, which it acquires by the transmission of the intestinal gases through the intestinal walls. I was attending, with the late James R. Wood, a young lady in whom peritoneal abscess had been recognized. It was anterior to the intestines. In the consultation, while we were discussing the propriety of using the trocar, the mother became alarmed at the odor and appearance of the urine just passed, and summoned the doctors back to the chamber. The abscess had opened into the bladder. The urine contained pus which gave off the fecal odor strongly. This patient recovered. It should be added that these abscesses, as well as those of the convex surface of the liver and those that are post-peritoneal, sometimes pierce the diaphragm and produce empyema, or by previous adhesion of the lung to its upper surface find a way into a bronchial tube, and so the pus is expectorated.

The history of local fibrinous exudations is not as easily told as that of the purulent. We find from time to time, on the peritoneum, bands, patches, or cords of false membrane, which were produced in so quiet a way that we can get no information regarding the time when they were formed, and perhaps the subject of them was not aware that anything was wrong with the bowels till he began to have the symptoms of obstruction. These unnatural structures are formed in great variety. The omentum is found thickened and contracted. The mesentery and mesocolon are seen in a similar condition, causing wrinkling and shortening of the bowels. The spleen has on its surface patches or even plates, or one great plate, of firm fibrinous deposit, often cartilaginous in density, sometimes calcareous; and we can rarely fix the time of these occurrences by any symptoms. It is not always so with the liver. We are acquainted with a perihepatitis which is acute, attended by pain in the right side, a febrile movement, and, if the inflammation reaches the under surface of the organ, by jaundice, and have learned to combat this with cups and opiates, the latter in rather free but not heroic doses, and to expect recovery in a few days. This may leave the liver wholly or partly invested with a layer of false membrane which may have a sequel of importance. Then, again, we find the organ invested with a thick contractile membrane, but cannot learn that the symptoms of perihepatitis have ever occurred. The diseased action which produced this bad investment appears to be analogous to that which not only covers the organ with a thinner coat of similar new tissue, but inlays it everywhere with the same material in cirrhosis. This also is {1161} unattended by local pain. The effects that may result from this encasing of the liver in a strong contractile capsule may be illustrated by the following case (the late Buck was the physician): The patient was an unmarried lady of middle age who had consecrated her life to charitable works. In searching for the suffering poor she often had to ascend several flights of stairs. The time came when she found this fatiguing and a tax on her respiration. She observed at the same time that the bowels were enlarged. She called Buck, and he had no difficulty in discovering ascitic fluid. He was surprised, as he knew that her habits were perfectly good, and she had very little the appearance of an invalid. Notwithstanding the proper use of the usual remedies for dropsy, the fluid slowly increased, and at length he was obliged to draw it off. He found it to be a clear, yellowish serum. In the course of about two years she was tapped four times. I saw her, with Buck, after these tappings, when the fluid had again been effused in quantity that half filled the peritoneal cavity. The emaciation was not considerable; there was nothing of the semi-bronzed color of the skin so common in cirrhosis of similar duration; her appetite and digestion were not materially impaired; the temperature was natural; the pulse was increased in frequency only a few beats. The skin over the abdomen was in a soft, natural state, and there was nothing that suggested a hyperæmic or inflammatory dropsy. The liver on percussion appeared to be reduced in size. Taking all things into account, and especially the patient's habits and the absence cancerous cachexia, it seemed probable that the dropsy arose from atrophy of the liver, and that the atrophy was caused by an adventitious capsule of the organ, although the patient had never had symptoms of perihepatitis. From this point the fluid did not increase or diminish, but remained stationary till she died, perhaps two years after, of some other disease. Meanwhile, the lady resumed her favorite charity-work to a limited extent. At the post-mortem examination the capsule was found investing nearly the whole liver, but not materially obstructing the gall-duct. The new membrane was thick and strong, having a thickness of at least one-twentieth of an inch. The remaining liver structure was of natural appearance. The organ was reduced to one-half its natural size. No other cause of dropsy was found.

Chronic Peritonitis.

I have doubted whether any disease deserving this name really exists independent of such low inflammatory action as may arise from the irritations of tumors or heterologous deposits. This statement refers to general not local peritonitis. I have never seen anything that would lead me to believe that acute diffuse peritonitis can be deprived of its acute character and still continue an inflammation. With me it has always been death or cure. I have already referred to a case in which after recovery the bowels were greatly disturbed by tympanitis for years. But this came from adhesions: her general health was good. I have at long intervals met with cases of ascites in which the peritoneal membrane was redder than natural, and in which no obstruction to the portal {1162} circulation was discovered. This, however, I have regarded as hyperæmia rather than inflammation.

Bauer,[8] however, gives to these cases the title latent general peritonitis, especially when after death an abnormal adhesion is found here and there. In the cases that I have seen there was a peculiar state of the surface of the abdomen. The skin there was more or less scaly and dry, but I do not remember whether there were internal adhesions. Bauer regards the diagnosis of this form of disease as difficult, but refers to the constantly present meteorism as well as serous fluid. I have met with three or four instances in which at the time of puberty an abdominal dropsy has rather suddenly occurred, lasting one to three months, and disappearing on the use of diuretics. I have had no reason to attribute this effusion to inflammatory action, except in one case. A lady of extraordinary symmetry and beauty of form, in excellent health, whom I had treated for this disorder twelve years before, applied to know whether there was anything in that disease that would prevent her having children. She had been married seven or eight years, and had not been pregnant. The question then occurred to me, At the time of the dropsy could there have been lymphy exudation that has since confined the ovaries in an unnatural position? The question I could not answer. The treatment which Bauer prefers for his latent peritonitis consists in "painting with iodine, the use of diuretics, and the regulation of diaphoresis by means of Turkish baths."

[Footnote 8: Cyclopædia of the Practice, etc., vol. viii. pp. 297-302.]

Another form of general chronic peritonitis is, according to Bauer, that which follows acute peritonitis. He quotes several authorities in support of his views. I must draw on him for a description of it, for, as I have said, practically I know nothing about it.

The symptoms of acute peritonitis are all toned down, but do not all disappear. Vomiting occurs occasionally; tenderness is diminished, but is quite perceptible; meteorism diminishes, but fluctuates greatly; appetite is poor or variable; constipation alternates with diarrhoea or is followed by dysentery; now there is a febrile heat, and then the temperature is normal--this fever is most likely to come in the evening; the pulse is frequent and varying; ultimately extreme emaciation and anæmia. The most striking feature of this condition appears to be sacculation of the fluid in the abdomen, wholly or partially; this fluid then is not freely movable, but will give dulness on percussion, which may contrast well with intestinal resonance in its immediate neighborhood. When the tension of the abdominal wall is diminished these sacs can be felt by the hand as uneven tumors. Colicky pains occur, and in a case cited it was at one time very severe, at another only slight. The majority of the cases terminate, after a protracted course, fatally. Recovery may occur by absorption or external evacuation of the fluid. He gives no special treatment.

Bauer makes still another class of cases of chronic peritonitis--those arising in the course of old ascites; he, however, does not make much out of it. He thinks the cases of this kind occur with cardiac and hepatic disease, and particularly with the nutmeg liver. The symptoms, he admits, are neither well defined nor severe, and the anatomical changes consist "in thickening of the serous membrane by a slight deposit of fibrin, {1163} slight turbidity of the ascitic fluid, and a few flakes of fibrin suspended in it." He then, strangely, gives, as if they were illustrations of such a disease, two cases in which death by acute peritonitis followed the last of many tappings, in one of which a pool of pus was found encysted in front of the intestines. Both are borrowed.

Probably most practitioners who are in the habit of making post-mortem examinations have seen the flakes of lymph in the ascitic fluid, etc., but the German physicians have been the first, I believe, to regard such cases as belonging to separate forms of disease.

William Pepper has published[9] a case observed by himself and G. A. Rex which shows non-malignant chronic peritonitis better than any I can recall to mind. The report forms the sequel to the case of the young woman on whom he successfully performed paracentesis of the pericardium.

[Footnote 9: Am. Journ. of Med. Sci., April, 1874.]

This young woman began to have double pleuritic effusion, and this was soon followed by ascites three and a half months after the operation. From that time the ascites was better or worse, but did not wholly leave her, and became considerable before her death. This was sudden, she having some convulsive movements in extremis. Lesions were found in the thoracic cavity like those discovered in the abdominal, showing, it was believed, a special tendency in this person to plastic exudation on the serous membranes. "The lower part of the abdomen was found occupied by an extensive effusion. The intestines were floated upward. There were few if any signs of inflammation of the intestinal peritoneum, but marked changes were observed in the parietal peritoneum and in the capsules of the liver and spleen. The peritonitis was most marked in the upper segment of the abdomen, while the parietal membrane presented large patches of irregular thickening. No tubercles were found on any part of the peritoneum. The capsules of the liver and spleen were greatly thickened, whitish, opaque, and densely fibrous. The liver was enlarged and heavy, and so tightly bound by its thickened capsule that its shape was somewhat altered.

"The diaphragm, especially that part of it underlying the pericardial sacs, had undergone marked fibroid degeneration. The muscular tissue was much atrophied; many fasciculi had evidently disappeared, while many others were markedly narrowed, some of them shading off to a width of less than 1/3000 of an inch, and finally disappearing altogether. They retained, however, even in their narrowest dimensions, their transverse striæ."

(It may be remarked, in passing, that this substitution of fibrous for muscular tissue follows the same law that it does in the heart when that organ is the seat of fibrosis or fibrous degeneration. Here it was supposed to be the consequence of a low grade of inflammatory action. Is it when it occurs in the heart?)

In the abdomen these observers found nothing which suggested the possibility of tubercles or any obscure form of cancer. In the pericardium, on the heart side, were found numerous small nodular roughnesses. Irregularities of the pericardial false membrane are so common that nothing but the close and universal adhesions would raise any question of these relations. But tubercles would hardly be here and nowhere else.

{1164} Delafield says that one form of the chronic disease is the continuance of his cellular peritonitis. In this, he says, the surface of the omentum is covered with cells which look as if they were derived from the endothelium and connective-tissue cells, although they differ from the normal shape of these. The new cells are for the most part polygonal, of different size, with one or several nuclei, and giant-cells--large granular masses filled with nuclei. Although these new cells are produced over the entire surface of the peritoneum, yet, as a rule, they are more numerous in little patches here and there. These little patches may be heaped together in such numbers as to form nodules visible to the naked eye. There is never any stroma between these cells.

This form of peritonitis occurs most frequently with organic heart disease, with cirrhosis of the liver, with chronic pulmonary phthisis, and with acute general tuberculosis. In the two latter diseases he thinks they have been improperly called tubercles.

He describes a form of chronic adhesion of peritoneal surfaces that occurs without the intervention of fibrin, but, as he supposes, by coalescence of the branching cells and a production from them of a fibrillated basement substance, the fibrils crossing in all directions. In the midst of these fibrils he finds the nuclei of these cells. He finds also in the immediate neighborhood of these adhesions thousands of branching cells that are attached one to another and float free in the water, the fixed end being attached to the peritoneum. He regards such a peritonitis with adhesions as a more advanced stage of the forms of cellular peritonitis already described, and the new cells are changed into membrane.

Sayre has published an extraordinary case in the Transactions of the Pathological Society. He calls it chronic proliferative peritonitis; it might be called more aptly the consequence of peritonitis.

A large, strong man fell from a hammock, the rope breaking, upon his shoulders, and felt a severe pain in his stomach, and soon developed symptoms of peritonitis. This pain never entirely subsided. The peritonitis was recognized. About one month after he was tapped, and 240 ounces of serum were drawn. He was tapped one hundred and eighty-seven times, and 1203-5/16 pounds of fluid were taken from him during the remainder of his life. At post-mortem examination 3000 cc. of yellow serum were found. The liver and spleen were covered by a thick layer of false membrane, intestines were glued together in the upper part of the abdomen, and the stomach was adherent to the lower surface of the liver. The portal vein was contracted by this membranous coating. There were numerous other lesions in the heart and pleura, but these will account for the dropsy.

This man was unusually strong and hearty until 1876, when he had an attack of double pleuro-pneumonia, and in 1878 he slipped on the front steps and fell, but seemed to recover from the effects of this. The fall from the swing occurred in July, 1879. He died in February, 1884.[10]

[Footnote 10: Med. Record, April 19, 1884.]

{1165} Tubercular Peritonitis.

This form of disease is by no means uniform in its first symptoms or in its progress. The only things uniformly attending it are tubercles on the peritoneum and more or less of inflammatory effusion, chiefly lymph and serum; tumor and hardness of the bowels, general or local; deranged function of the stomach and intestines; emaciation; and extreme fatality.

In some cases the invasion is acute and marked--a chill followed by fever, vomiting, early development of meteorism, and in a few days a point or points of resistance to pressure, but not necessarily dulness on percussion. In a few days the febrile action and the meteorism may subside, leaving the symptoms of local peritonitis. But we have not long to wait for a renewal of them and an evident extension of the inflammatory action. Remission and relapse alternate at varying intervals, until the whole extent of the peritoneal surface seems to be involved in inflammation. With this mode of development meteorism may not be renewed in the most common way. The lymphy product of inflammation may so bind the intestines to the posterior walls of the abdomen that they cannot extend forward, but are pushed upward against the liver and diaphragm, and so encroach on the thoracic space. But then the anterior parietes are tense and hard, and do not move in respiration. The febrile heat may not continue more than two or three months, but the pulse will be frequent to the end. There will be a thinning of bowel walls, and here and there a knuckle of adherent intestines may cause some prominence and give some resonance on percussion. There will be also occasional vomiting, and the dejections will be irregular--maybe only deficient or thin; there may be an alternation of constipation and diarrhoea.

Tuberculous ulcerations of the mucous layer of the bowels is not uncommon in tubercular peritonitis, and these ulcers have in rare cases perforated and allowed the fecal matter to accumulate in considerable quantity in a sac limited by previous adhesions. In all forms of tubercular peritonitis death is caused as often by grave complications as by what appears to be the primary disease. The affection occurs in probably every instance in those who had at the beginning, or had acquired in its progress, what we call the tubercular diathesis. We are not surprised, therefore, to find on inspection a wide diffusion of tubercles in the body, particularly on other serous membranes, and in the lungs. Death may occur, then, from phthisis pulmonalis or from pleurisy or meningitis, as well as from the exhaustion and accidents of the peritoneal disease. The effusion serum or turbid serum is very common in tubercular peritonitis, and can be recognized by the dulness it produces in part of the cavity, and sometimes by fluctuation. It is often sacculated, but it is not constantly found after death, it having been absorbed before, and perhaps long before, that event.

In other cases the invasion of the disease is stealthy and deceiving. It comes so quietly that the patient is not conscious of any local disorder beyond a dyspepsia and irregular action of the bowels. He has a pulse of growing frequency, but if he knows it he ascribes it to his dyspepsia. He is slowly losing flesh and strength; this he accounts for in the same way. At length a perceptible swelling of the bowels attracts his attention. At this stage the physician finds that the swollen bowels are tympanitic everywhere or only in the upper, while there is evidence of fluid {1166} effusion in the more depending, parts. He discovers some, it may be little, tenderness on pressure, and a pulse of 85, or maybe 90, increasing in frequency toward evening. The appetite is poor, the digestion slow, and occasionally there is vomiting; the complexion is pale and a little dingy; the skin of the abdomen may be dry and rough or may be natural; some colicky pains have been or soon will be felt. From this point the disease gradually advances. The distension of the bowels slowly increases or they are firmly retracted; the emaciation increases; the strength diminishes; there is often cough, which is generally dry; the bowels are slow or diarrhoea alternates with constipation; with the distended bowels there is always more than natural resonance on percussion, except when there is fluid effusion, though not often the full tympanitic sound observed in acute diffuse peritonitis. This resonance is not equal, always, in different parts of the abdomen; the respiration is embarrassed and almost wholly thoracic. The abdomen is often as large as that of a female at full term of pregnancy, and indeed the condition has been mistaken for pregnancy. This is an inexcusable blunder in a case like that which I have in mind--a young unmarried woman. She had no dulness on percussion in the space that would be occupied by the gravid uterus, but rather resonance. The case might have been a little less clear if there had been fluid effusion in the abdominal cavity, but if this were not encysted it would flow from one side of the abdomen to the other when the patient turned correspondingly in bed; if it was encysted, there would be small chances that it would have the shape and position of the gravid uterus; if it had, there would be no chance of hearing in it the foetal heart or feeling the foetal movements; and after all this there remains the experimentum crucis--a vaginal examination.

At first the diagnosis is unavoidably uncertain. Some aid is found, possibly, in the medical history of the family, in tuberculous antecedents, yet I remember cases in which no phthisis could be found in any living or dead member of the family on the paternal or maternal side as far back as it could be traced. Some aid is found if the patient himself has any of the physical or rational indications of pulmonary phthisis, and yet there are recorded cases in which the abdominal symptoms were the first to appear. The prominent German physicians attach great importance to the pre-existence of a cheesy mass or degeneration somewhere in the body as the real parent of tubercles wherever they appear. The truth of this doctrine, I do not think, has received anything like universal recognition; and if it had, as this cheesy degeneration is often, perhaps commonly, only discoverable after death, it could rarely give any assistance in diagnosis, so that the early diagnosis is always difficult, and a very early one often impossible. But as time goes on, and the symptoms are better defined and show themselves one after another as they are above described, it seems as if a careful observer could not confound it with anything except perhaps one of the other forms of chronic peritonitis or cancerous peritonitis. As to the latter, the cough which exists in most cases of tubercular peritonitis will assist in the distinction, but a physical examination much more; for a cough does not always attend phthisis when this disease exists; for example, I visited a daughter of one of the distinguished gentlemen of Vermont. She had had the bowel symptoms that indicated tubercular peritonitis for eight or ten months, and the diagnosis was not {1167} difficult. Remembering Louis's opinion that if tubercles invade any other part of the body, they are likely to be found at the same time in the lungs and in a more advanced condition, I examined the lungs, and found in the upper part of the right a cavity so large that it could have received a fist. I was only surprised by the fact that she did not cough, and had not coughed. She herself assured me of that (she was twenty-one years old); her physician, who was present at the visit, had never heard her cough, and had no suspicion of any pulmonary complication; but, more than all, her mother, who had walked with her, slept with her, eaten with her, travelled with her, and from the beginning of the illness had not been out of her company more than twenty minutes in any twenty-four hours since the disease began, had never heard her cough. Here, then, the nervous deviation to the abdomen, or whatever else it may have been, had so benumbed the sensibility of the pulmonary nerves that the alarm-bell of phthisis had never been sounded; but the cavity, had there been any doubt whether the bowel disease was cancerous or tuberculous, would have almost fully settled the question. But more of the peculiarities of cancerous peritonitis a little farther on.

The lesions of this disease (or its pathological anatomy) differ considerably, but the differences are in the amount of tuberculous deposit and the secondary results, not in the real nature of the disease. Lebert has published among his plates of pathological anatomy one which shows the peritoneum thickly sprinkled over with small tuberculous grains, and represents each particular grain surrounded by a little zone of inflammatory injection. There is yet no exudation, but that would soon follow. A fibrinous exudation will soon come over this primary deposit, and undergo a kind of organization, or at least get blood-vessels, which in their turn can furnish the material for a new crop of tubercles. These again provoke a new layer of fibrous tissue, which also becomes studded with tubercles, and so on, till a thick covering is formed over the intestines. But the same material is interposed between their folds, separating one from another and compressing them and diminishing their calibre; at the same time this agglomerated mass is firmly adherent to the abdominal walls everywhere. The new material may have a thickness of half an inch or even more. I remember how surprised and confused I was when I made my first inspection of such a case. The abdominal walls were cut through, but they could not be lifted from the intestines, but were firmly adherent to something. They were carefully dissected off and the bowel cavity (?) exposed; there was apparently an immense tumor filling the whole space: no intestines, no viscera, could be seen. A section was made through this mass from above downward, and another parallel with it and an inch distant from it, and this part removed. It appeared like a large, hard tumor, through which the intestine made several perforations. The new material appeared to be fibrous, with grayish-white tubercles sprinkled in through it everywhere, and pretty abundantly. In another case this fibro-tubercular material may occupy one part of the abdomen, and a large serous cyst or serous cysts another. The tuberculo-fibrous material may be found in markedly less quantity than is so far described, till there will be no more than in a case from Ziemssen's clinique, quoted by Bauer: "In the peritoneal cavity about four liters of yellowish-brown, slightly turbid fluid. Omentum {1168} thickened, stretched, adherent to the anterior wall of the abdomen and beset with hemorrhages; the same was true of the parietal peritoneum; between the hemorrhages whitish-yellow and entirely white tubercles occur, varying in size from the head of a pin to a lentil. The intestinal serous membrane was similarly invaded. The intestines intensely inflated; a number of ulcers on the mucous membrane, one approaching perforation. Covering of the liver thickened by fibrinous deposition."

The lungs and serous membranes generally will, in all probability, show more or less of tubercular deposit, the pericardium less frequently than the others.

The result in this affection, after it is fully established, is believed to be uniformly fatal, and at its commencement the difficulty of diagnosis may lead one to doubt whether his apparent success is anything better than apparent. Still, a plan which I have relied on is, I believe, worth announcing. As soon as the disease is recognized the patient is put upon the use of the iodide of potassium and the iodide of iron, in full average doses, and a solution of iodine in olive oil is applied to the whole surface of the abdomen by such gentle friction as will produce no pain; and after a minute or two of such friction the oil is brushed thinly over the surface and the whole covered with oiled silk. This dressing is repeated twice a day. The quantity of iodine to an ounce of oil will vary considerably in different persons; for some, seven to ten grains will be enough; for others, thirty will be needed. The iron is to make the application moderately irritating, and if it produce pinhead blisters or blisters a little larger, all the better. When the application becomes painful the oil is washed off, and the application is not renewed for two or three days. In this manner it may be continued for two or three months. Meantime, the patient is put upon the diet and regimen of the consumptive, the appetite encouraged; he takes sustaining food, with plenty of milk and cream, or cod-liver oil, as much fresh air as possible, and friction is applied to other parts of the body with dry flannel.

Cancerous Peritonitis.

Benign tumors of the abdomen are not frequently the cause of general peritonitis, and when they are, the grade of the disease is acute rather than chronic. They very often provoke local inflammation and become adherent to the neighboring structures. The same is true of malignant growths in the abdominal cavity, except that the adhesions are earlier formed and more likely to occur. Localized cancer, of whatever variety, is not very prone to produce general peritonitis, even though there be multiple developments of it. But when the disease takes the disseminated form, and is sprinkled over the whole extent of the peritoneum, then inflammation is almost certain to occur--not of high grade, and yet deserving the name subacute rather than chronic. A case which illustrates this statement has come under my observation within the last year. I will recite it with sufficient detail to make it intelligible.

A lady about forty years of age had, up to the summer of 1881, enjoyed very good health, though she was never robust. At that time she felt her strength abating and her stomach disordered. She sought {1169} health in various places, and took professional advice in September. It availed her little; the bowels were gradually swelling and fluctuation could be felt. She was losing strength and flesh. There was not a cachectic countenance, but the features were growing sharp. She had suffered but little from pain till October. At that time she was at the family country home. Then she began to suffer from a severe pain in the left thigh; and this, it was noticed, increased as the accumulation in the bowels increased, and at length her physician felt compelled to tap her--not so much on account of great distension of the bowel as in the hope of relieving the pain. He drew off nine quarts of gluey, viscid fluid, and her pain was wholly relieved. Twelve or fifteen days after this she was brought to her city home, and her city physician, seeing that her case was a grave one, sought the aid of a distinguished gynæcologist. She was then again tapped to give him a more satisfactory examination. He found the ovaries considerably enlarged and hard. They could not, however, be felt by pressing the fingers into the pelvis from above--only by the vagina. I saw her on the 10th of November. The fluid had again made considerable tumefaction of the bowels, and she was again suffering great pain in the region of the right kidney and in the leg of the same side, together with cramps. The relief given by the first tapping induced us to propose its repetition. It was, however, delayed till the 14th, that the physician who had tapped her before might be present and assist. The quantity of water drawn was again nine quarts, and again the pains and spasms were quieted. The examination of the abdominal fluid was interesting. It was nearly clear, reddish, of syrupy flow and consistence, and so viscid that while a portion of it had remained on the slide of the microscope long enough for the examination of its constituents the thin cover became so firmly attached to the slide that it could not be removed without breaking or long maceration. The albumen was so abundant that the fluid was completely consolidated on boiling. Fibrinous threads were running through it in great numbers, and here and there was a cell of large size, round, granular, but not plumped up with granules, with a nucleus barely less in size than the cell itself; its outer border within, but only just within, the boundary or wall of the cell. It was the nucleus that was granular, for there was little room for granules between the nucleus and the cell wall. The vial containing the fluid had been standing three or four hours for a sediment. This in a vial four inches high occupied the lower half, and gave nothing to the dropping-tube till the sedimentary matter was drawn into it by suction. This matter consisted of fibrillated fibrin in large quantity; a great number of the cells just described, some grouped, but most separate or single. There were pus-cells in moderate quantity, each having the amoeboid movements, and a considerable number of red blood-corpuscles, some of natural form, some crenate.

Immediately after the tapping the flaccid condition of the abdominal walls admitted an examination. A solid, hard mass was found running across the upper part of the bowels, a nodule of which was lying on the stomach at the point of the ensiform cartilage. A harder mass of irregular shape was also found just above the pelvis on the right side, extending upward and to the right. This was in extent two by three inches. The ovary, however, could not be detected by pressure from above {1170} downward. The diagnosis up to this time was hardly doubtful, but these revelations made it complete, and crushed any lingering hope of the patient's recovery.

While the pain and spasm ceased after the tapping, the oedema of the left leg, which came on some time before the last tapping, did not diminish. The hard spot near the right iliac fossa was tender on pressure, but otherwise hardly painful. While the fluid did not exceed six quarts or so, she had little pain anywhere. There were no external glandular swellings. Her appetite was poor, and she took but little food. She vomited very little till the end was approaching. The urine contained a few globules of pus, some pigment matter, two or three hyaline casts, but no trace of albumen. For sixteen days following November 14th the patient was comfortable, but the fluid was slowly filling the bowels again. At that time the pains already referred to began to return. On December 5th they required another tapping, and preparations were made for it, but vomiting, rather severe, led to its postponement to the next day. The quantity of fluid drawn was nine and a half quarts. It was of the same syrupy consistence as that previously drawn, and under the microscope showed exactly the same constituents and gave the same quantity of albumen. The next day stercoraceous vomiting commenced, with no movement of the bowels, except what was produced by 10 grains of calomel given on the second day of this vomiting. That acted well and produced a temporary relief. She after this took no food by the mouth, but milk and beef-tea were injected into the rectum. Still, the fecal vomiting returned, and she died on the 15th.

The post-mortem examination was made on the 17th by William H. Welch. I could not attend it. His report is complete as to the main features of the case, though it does not furnish an explanation of the spasms and the oedema of the left leg, regarding which Welch was not informed. The pain and spasm were doubtless due to backward pressure of a diseased part on a nerve or nerves, and the oedema to a narrowing of the iliac vein by pressure or constriction by fibro-cancerous matter on its outer sides. "The peritoneal cavity," he says, "contained somewhat over a gallon of clear, yellow serum. Both the visceral and parietal layers of the peritoneum were thickened, in some places more than in others; this was especially marked on the anterior of the stomach and on the lower part of the ileum and in the left iliac region. The omentum was greatly thickened and retracted into a firm mass (or roll), which extended somewhat obliquely across the body, more to the left than to the right. The mesentery was much thickened and contracted, drawing the intestines backward. In a few places only was the peritoneal surface coated with fibrin, and the intestines were mostly free from adhesions. The coils of the lower part of the ileum, however, were firmly matted together by organized connective tissue in such a way that they were twisted, often at a sharp angle, so as greatly to constrict the calibre of the gut. The serous and muscular layers of the intestine at this point were greatly thickened. By these causes there appeared to be a complete obstruction at a point about six inches above the ileo-cæcal valve. By careful dissection these coils were straightened out, so as to remove the main cause of obstruction. The peritoneal covering of the liver was adherent to the parietal layer.

{1171} "The surface of both the visceral and parietal peritoneum was studded over with hundreds of small, firm, whitish nodules, generally not larger than a pea, and often not larger than a pin's head. In some places they had coalesced and made firm patches an inch in extent. This same material was found in the contracted omentum in considerable quantity. In a few places, particularly on the uterus, a blackish pigmented deposit appeared.

"The ovaries were not adherent, but both were enlarged to the size of a hen's egg. The outer surface of each was rough and corrugated. The new growth was deposited on the exterior and penetrated each a quarter to half an inch. It was of uniform white color and of firm consistence.

"The stomach wall was thickened nearly throughout its extent, but particularly in the anterior part, where it amounted to thrice the normal thickness. This consisted wholly of hypertrophy of the muscular coat and increase of fibrous tissue in the peritoneal layer. This new growth was traced, in the interlacing bands, from the surface into the muscular coat. In the outer layer of the stomach were found three small white nodules. The mucous membrane of the organ was healthy or a little pale.

"The retro-peritoneal glands along the aorta were enlarged, soft, and of a reddish-gray color. A nodule was found in the wall of the duodenum outside the mucous membrane, and one in the Fallopian tube."

Every organ in the abdomen and chest was examined, but nothing important found except what is here recorded. Welch concludes his record with the following diagnosis: "Primary scirrhous carcinoma of the ovaries. Secondary deposits in the peritoneum, in the outer layer of the right Fallopian tube, of the stomach and duodenum, and in the retro-peritoneal glands. Chronic peritonitis, intestinal obstruction."

This case presents to the reader so accurately the usual course of cancerous peritonitis, and the inspection its lesions, that a treatise on the subject is hardly called for. It often happens that cancerous antecedents in the patient or his relatives will lend an aid to the diagnosis, which this case did not present. To distinguish this disease from tubercular peritonitis no question can arise except in its dropsical form, and then the lungs in every case of the latter that I have met with have the physical signs of tubercles, though not always the rational indications. The pulse is much more accelerated in the tuberculous variety. I omitted to state that the temperature of this patient was often taken, and till the closing scene was never found more than one or two degrees above the healthy standard, and the morning and evening heat did not materially vary; the opposite of both, then, would be expected in a tuberculous case. The existence of meteorism is much more common in the tubercular disease; indeed, in the cancerous case recited there was none of it. The duration of the two is different--that of the cancerous kind is recorded in months, while the tuberculous variety may continue two years. The cancerous is more likely to be attended by alarming accidents, like the complete obstruction of the bowels, large hemorrhages, and a sudden lighting up of acute peritonitis. Finally, in the light of the case here recorded, it seems probable that the examination of the abdominal fluid will become of great importance. I have never carefully examined the fluid of tubercular dropsy, but it does not seem probable that it will have the syrupy {1172} appearance, the large amount of albumen, the abundance of fibrin-fibres, and the granular large cells with nuclei only perceptibly less in size than the cells themselves, that were repeatedly found in this case--found by two observers, and at every tapping after the first.

TREATMENT cannot be curative; it therefore consists of such administrations as will relieve pain, give sleep, improve the appetite, increase the flow of urine if it be scanty, and relieve the bowels if there is a tendency to constipation. It is as much the duty of the physician to put off the fatal day, when he can, in incurable affections as it is to cure those that will yield to his prescription and advice. In the case just narrated opium or an opiate alone produced such unpleasant after-effects that she was unwilling to take it, but when the extract of belladonna was given with it she slept pleasantly, and could take her food the next day.

Infantile Peritonitis, or Peritonitis of Childhood.

Bauer, in Ziemssen's Cyclopædia of Practice of Medicine, and Wardell, in Reynolds's System of Medicine, have each devoted a chapter to this form of disease. They refer to the fact that the foetus may have peritonitis before birth or be born with it, or may have it when a few days old. They say that this form of the disease occurs most frequently in lying-in asylums or foundling hospitals, and that it has been supposed to depend on a syphilitic taint. They say, too, that it follows erysipelas, scarlet fever, measles, etc. I do not perceive that the description of either of these authors makes any marked distinction between this and the same disease in adults, except what may arise from the inability of the infant to describe its sensations, and the more rapid course of the disease to a fatal result--in some cases twenty-four hours. Having myself had no obstetrical practice, or next to none, I have nothing to add to their statements, and can from my own knowledge abate nothing. I therefore refer the reader to these chapters, and to the references given by the first of these authors, for a fuller knowledge of the matter.

Regarding the comparative exemption of children, after the first few weeks of life, from spontaneous peritonitis, referred to by one of these authors, I can fully confirm his statement. Though I have assisted in the treatment of many children suffering from peritonitis, I have difficulty in recalling to mind a single case in which the disease was not caused by perforation of the intestine or vermiform appendix of the cæcum, and in much the greatest frequency perforation of the appendix.

B. F. Dawson,[11] after reciting a case in which the liver had undergone a peculiar degeneration and was attended by peritonitis before birth, states that Sir J. Y. Simpson observed nine cases in his own practice "and notes more than a dozen from different sources." These cases seemed to have been caused by the ill-health of the mother during gestation, or excessive labor, injuries, venereal disease, and were mostly attended by grave disease; the viscera often, the liver; but sometimes the mother was perfectly healthy, and the peritonitis was the primary disease. Death almost always occurred in utero or shortly after birth. In one instance the child recovered.

[Footnote 11: N.Y. Med. Journ., Dec., 1882.]

{1173} The Med. Record takes the following from Schmidt's Jahrbucher for Jan. 7, 1883: "Dr. Oscar Silbermann recognizes two varieties of peritonitis in the new-born. The non-septic or chronic is developed usually in the first third of foetal life, and is generally syphilitic in origin. If the peritoneum covering the intestines be involved, as well as that over the liver and spleen, various forms of intestinal obstruction may result. Most frequently there is occlusion of the anus, less often stenosis or complete stricture of the small intestine. Of a number of cases of congenital occlusion of the intestine collected by the author, all ended fatally, only one living beyond twelve days.

"The second, acute or septic, form of peritonitis in the new-born the author divides into two varieties, according as the peritonitis is only a part of general infection or is the sole manifestation of the septic poison. In either case the point of entrance of the poison is always the navel wound. The symptoms, which need not all be present in a given case, are vomiting, watery stools, meteorism, ascites, abdominal tenderness, icterus, etc. The pulse and temperature may vary in degree in different cases. A cure of the septic form is possible; therefore the treatment should be carefully considered. The navel wound should be cleansed, and the child is to be isolated from its mother. To control the fever quinine may be given. Priessnitz's sheet is of value; vomiting may be checked by chloral (one-half to one grain in water). The strength should of course be maintained by stimulants if necessary."

Ascites.

The accumulation of fluid indicated by this name has already been referred to in its relations to several causes. There are, however, conditions producing it which have not been considered or only considered partially.

The most prolific source of abdominal dropsy is obstruction of the portal circulation on its way to or through the liver. Condensation of the liver structure in cirrhosis, with destruction of many of the portal capillaries and compression of many more, is prominent in this connection. The compression of the liver caused by an adventitious external covering, referred to under the head of Local Peritonitis, acts similarly, whether it compresses the vein at its entrance into the liver or not, although it is not known to produce any destruction of the portal capillaries. Some enlargements of the organ are attended by the same result, but they are always associated with a hardening of its structure. The disease lately called waxy liver, now often denominated lardaceous, belongs to this class, as does that condition in which the organ is enlarged, hardened, and fissured, regarded as syphilitic liver. That both these diseases may have a syphilitic and mercurial origin is not a point now under consideration. They both harden the hepatic structure and obstruct the portal circulation, while they may not in equal degree hinder the progress of arterial blood. This is explained when we remember the diminished force that propels the portal blood. Neither of these diseases produces dropsy early in its progress, but, as I have seen it, always before it reaches its fatal termination. Fatty liver has not, in my observation, produced dropsy, {1174} although I have seen livers made very large by that disease, and the absence of dropsy when the liver has been large has aided me in distinguishing it from the waxy disease. Cancer of the liver in some instances does, and in others does not, produce dropsy of the bowels. It is only certain to have this result when a tumor is in position to press upon and obstruct the portal. Hypertrophy of the liver, caused by mitral regurgitation or other disease of the heart, does not generally produce dropsy, but, aided by anæmia or watery condition of the blood, such a result is possible. In children, however, it is not very rare to see the bowels distended by dropsy, and to discover that the liver is enlarged at the same time. It is common in such cases that the dropsy and the hypertrophy disappear after a few weeks of treatment. This may occur in a child that is anæmic, but without any disease of the heart. Such a case was brought to me two or three months ago, and after four weeks of treatment by tonics and diuretics the health was re-established. There is one point in these cases of some importance. When the child lies on his back, if the abdomen is much distended, the liver cannot be felt. It has sunk away into the fluid, and in this position ordinary percussion cannot ascertain its dimensions. In the July number (1840) of a quarterly journal edited by Swett and Watson, I published an article in which I reported the conjoined labors of the late Camman and myself on a new method of combining auscultation and percussion, with its results, under the heading "Auscultatory Percussion." By the method described in that article--viz. by placing a solid stethoscope, or for that Laennec's first stethoscope, a rolled-up pamphlet, on the chest at a point where the liver has not fallen away from its walls, and percussing on the abdomen from below upward--a point is reached whence the percussion sound is brought sharply to the ear, while half an inch below the sound is dull and distant. The lower edge of the liver is thus easily recognized, and its upper boundary is found in a similar manner or by ordinary percussion, so the difficulty of measurement disappears.

In such case, when the dropsy disappears and the liver recovers its natural dimensions at the same time, the inference is that the hypertrophy caused the dropsy, and that the hypertrophy was of the kind called simple. The nutmeg liver is thought to have an agency in producing dropsy, but as it is for the most part associated with diseases that have been called dropsy-producing, its bearing on this effusion may yet be regarded as uncertain.

It is common to speak of heart dropsy in such a way as to imply that disease of the heart alone can produce abdominal effusion. I doubt it. I even doubt whether the heart alone can cause the anasarca that is so often attributed to it. In following a great multitude of heart diseases from the time they were recognized to their termination, I have been struck with the ease with which the patients attend to their business, sometimes even laborious business, for years--in one instance fifty years--with almost no complaint, and how rapidly their condition changes as soon as albumen and casts appear in the urine. I have been compelled by these observations to ascribe the anasarca and oedema that makes this last stage of heart disease so distressing to the kidneys, and not to the heart. Double pleuritic effusion is not uncommon under these circumstances, but every physician must have noticed the rareness of troublesome abdominal {1175} dropsy, while there is sometimes--perhaps often--a little effusion; and when in the exceptional cases there has been much, it was almost always accounted for by a dropsy-producing change in the abdominal organs, not, perhaps, discovered during life; so that for me, while they produce overwhelming effusions in other parts of the system, they are minor agents in the production of ascites. Phthisis is occasionally attended, toward its close, by oedematous legs and albuminous urine, but I cannot report any important relation between these and peritoneal effusion. I can say the same of chronic bronchitis. I record this negative testimony regarding the two last-named diseases, because I find them enumerated among the causes of abdominal dropsy.

Cancer may invade the portal vein, tumors of adjacent parts other than those of the liver, or an aneurism may compress it and cause dropsy. Hydatid tumors may do this. Diseases of the pelvic organs, both acute and chronic, may produce it, but then the disease would fall into the class of those produced by chronic or subacute peritonitis.

DaCosta thinks he has lately had a case of chronic peritonitis attended by ascites. It was in a woman thirty years of age, who had been thrown with force upon the frame of an iron bedstead, striking the lower part of the bowels. Pain and tenderness followed. These were not confined to the injured part, but extended to the whole abdomen; and there was menorrhagia. After a time there was fluid effusion in the peritoneal cavity, which slowly increased till her state demanded relief from tapping. The fluid after this operation did not return. The pain and tenderness were constant symptoms all through. She slowly improved, and at the time the case was reported it was believed that she would soon be discharged from the hospital. The only doubt which DaCosta finds regarding the diagnosis is in the facts that the liver was diminished in size and that the spleen was moderately enlarged, and he admits the possibility that an adventitious capsule of the liver may have caused the ascites, but believes that it was dependent on chronic peritonitis.

Acute peritonitis subsiding into chronic, with increase of fluid effusion, as I have already said, I am not familiar with. That occurring in cancerous and tuberculous peritonitis has already been considered. But in relation to these some facts regarding frequency of occurrence, collected by Bristowe, are worth quoting. He says that in 48 cases of tubercular peritonitis, dropsy was found in 12, and that in 22 of peritoneal cancer, 12 had more or less ascites. He further adds, regarding cirrhosis, that of 46 cases observed post-mortem, there was dropsy in only 20. This is not surprising, as in all the diseased conditions of the liver that produce dropsy the anatomical changes must reach the point at which there is considerable portal obstruction before the effusion will occur.

The amount of fluid found in ascites varies greatly. In some it may remain for a long time stationary at four or five quarts; in others the suffering caused by an accumulation of nine or ten quarts will demand its removal; and in a few cases twenty quarts have been removed in one operation. It is in cirrhosis that the largest quantity is found, and it is in this disease and in cancerous peritonitis that the most frequent tappings are required. The quality of the fluid also varies markedly: from being almost as clear and thin as spring-water it may be almost ropy, or in color greenish or yellowish or slightly red; it is very likely to contain {1176} albumen; and it is probable that a further study of its microscopic elements may enable us to resolve doubts regarding the cause of the effusion. It very often contains blood-corpuscles.

Bristowe finds from hospital records that ascites occurs in about equal frequency in males and females, but, as everybody has noticed, that hepatic dropsy is much more frequent in men than in women. Ascites, he says, is most frequent between the ages of thirty and fifty, and next between twenty and thirty and between fifty and sixty, but is not uncommon above the latter age; and it occurs in children.

SYMPTOMS.--In general, ascites is easily recognized by the swollen state of the bowels: a well-rounded swelling when the patient stands or sits, but spread out in the flanks when he lies on his back; the fulness of the side on which the patient may be lying, and the flattened condition of the opposite side,--belong to this disease, and as a group to no other. The results of percussion are significant in the movement it causes in the fluid, and for the resonance or flatness it produces. When the patient lies on his back, tapping with the finger-ends on one side of the abdomen sends a wave of the fluid across to the other side, where it is perceived as a gentle blow by the applied fingers of the other hand. If the abdomen is not full, this wave will be produced at the upper level of the fluid, but not above that. If this wave cannot be sent across the body, it may be found on either side by percussing above and feeling for it below; percussion also teaches where the fluid is, and where it is not, by the dull sound it produces. It is rare in ascites that the intestines do not float on the surface of the fluid, at least from the umbilicus upward, and there give a loud percussion sound, while toward the back, and often toward the pelvis, it is dull, or even flat; changing the position of the body, the resonance will be uppermost and the dulness in the most dependent part. Then the softness or impressibility of the abdomen till the tension becomes great is noticeable. The changed position of the fluid as the body is turned from side to side is important. A very small quantity of fluid can be detected in this manner. The patient is placed on his right side and percussion is made in the right flank: there is dulness, while in the left flank there is resonance. The patient turns on to the left side: dulness now changes position, and is on the left, and on the right resonance. If it is feared that some undetected fluid remains in the pelvic cavity, the pelvis may be raised by pillows and the same examination repeated, or he may be placed in the knee-and-elbow position referred to by Bristowe, and the percussion will then be made upward in the umbilical region. In some cases the contraction of the mesentery will not allow the intestines to rise through a large amount of fluid and float on it; but such cases are almost confined to the cancerous and the tuberculous varieties of the disease; and as in these the symptoms are grave, the physician will probably have visited his patient many times before this contraction will embarrass him. Besides, when mesenteric contraction occurs there is a very strong probability that the omentum will also be contracted, be rolled up, and lumpy; as this can almost always be felt above the level of the umbilicus, he has in it an explanation of the absence of resonance on the fluid. It has happened that oedema of the abdominal walls or fatty accumulations there have given a delusive though feeble fluctuation on percussion. In such cases, if the patient make moderate pressure with the back of a small book in {1177} the course of the median line, that kind of wave will be broken, while a wave in the abdominal cavity will not be prevented. When there is considerable distension of the abdomen by fluid, weak spots in the abdominal wall often yield and make a tumor. This is very common at the umbilicus, where a little bladder is lifted half an inch or more above the general curve of the abdomen. The fluid frequently follows the track of hernias. In females it has been known to press the anterior wall of the vagina backward and downward, so as to make it protrude at the vulva. It has, in one of my own cases, by downward pressure caused complete prolapse of the uterus. It is very often attended by oedema of the lower limbs. This is accounted for by the pressure of the abdominal fluid on the veins that return the blood from these parts, or in cirrhosis by contraction of the ring or notch through which the vena cava passes in the liver. If there is general oedema, the cause will probably be found in disease of the kidneys; or if in one limb, in pressure or thrombosis of one iliac vein. As the disease advances the accumulating fluid forces the diaphragm upward, diminishes the breathing room, and threatens the life still more. Then the patient cannot lie down in bed, but spends his nights as well as days in an easy-chair, and sleeps leaning forward on a support for his forehead. The veins on the abdominal surface will fix attention. With almost any large tumor in the cavity they become more or less enlarged. But in cirrhotic dropsy this becomes more striking than in any other affection. The enlargement is attended by a reversion of the blood-current on the lower half of the abdomen. This is early shown by emptying an inch or two of a vein with the finger, drawing it either upward or downward, and noticing from which direction it is refilled when the pressure is removed. The pelvic veins do not readily discharge their blood by the natural channels, and by anastomosing branches it is forced over the surface of the abdomen and into the thoracic veins, these latter becoming in turn greatly enlarged. The appetite is commonly poor, the digestion flatulent, the pulse accelerated. Emaciation is gradual or rapid. The urine is commonly scanty, and in cirrhosis of a reddish hue. The skin is apt to be dry, particularly so in simple chronic peritonitis. The tongue has no characteristic fur, and is often, almost always toward the close, dry. The mind is not affected till near the end; then often the patient is delirious, commonly mildly. Diarrhoea is not uncommon, and even dysentery has been observed. The result is almost always unfavorable, or, as has been said, lethal.

The diagnosis is not often difficult. When, as in chronic peritonitis and in tuberculous peritonitis, the fluid is confined in a sac or sacs, each particular pool will be yielding to pressure, but elastic, and will give the percussion wave, though it may extend but a short distance. To distinguish ovarian dropsy--ovarian cysts, as it is now called--from ascites may require a few words. Ovarian tumors of all kinds are found to be more prominent on one side when they rise from the pelvis than on the other. This is not the case with ascites. The uterus and its appendages lie in front of the pelvic intestine, and when any of them ascend above the pelvis they must occupy the same relative position. In other words, a large ovarian cyst must lie in front of the intestines, while intestinal resonance should be found behind and in the sides. But if the ovarian cyst does not occupy the whole height of the bowels, intestinal resonance {1178} may exist above it, and the dulness may be found below, bounded by a portion of a circle, and sometimes the cyst walls are resisting enough to allow its boundaries to be ascertained by the fingers. This cyst can also be felt in the vagina; and the uterus, instead of being pressed down, is sometimes lifted upward, so that it cannot be reached in the vagina, but can be felt through the abdominal walls just above the pelvic bones. A condition more troublesome than this is when ovarian cyst and ascites occur together. Then the posterior or lateral resonance is lost when the patient lies on her back, but can be found on one side when she lies on the other. In that concurrence, in dorsal decubitus it is possible by pressure or a little blow to send a wave of the ascitic fluid over the front of the cyst. This can be seen as well as felt. Should the patient take the knee-and-elbow position, the intestinal resonance may be restored in both flanks.

TREATMENT.--In opening the chapter on the treatment of ascites it is usually said, Give principal consideration to the diseased conditions that have caused the dropsy; in other words, cure cirrhosis, cancerous peritonitis, tubercular peritonitis, heart disease, and the secondary affections of the abdominal organs, release the liver from the dangerous compression to which it is subjected, and all will go well. But they do not inform us how these impossibilities--at least in most cases impossibilities--are to be achieved. It is true that the physician would not shrink hopelessly from the treatment of simple chronic peritonitis. But this is one of the rarest causes of ascites. A physician in a long lifetime may not have seen a case. It is true, ascites is a symptom, always a secondary, or even a tertiary, affection; and theoretically there can be no better advice, but practically it cannot amount to much. Then, if the cause cannot be removed, it remains to do our best to relieve the patient of his load and strive to prolong his life to its utmost possible limit. In doing this the physician will often find himself able to give gratifying relief, and once in a great while to rejoice in a cure.

The three great emunctories, the skin, the bowels, and the kidneys, are chiefly appealed to for relief in this as in other serous accumulations. Most physicians prefer to use the diuretics--first, because if they will act at all, they act so quietly and produce so little debility that whatever can be gained by them is obtained at small cost to the system. The form of ascites that most resists diuretics is that which originates in cirrhosis. Often a full trial of them, with suitable changes from time to time, is of no avail, yet now and then the kidneys yield to persuasion and act freely. The saline diuretics and digitalis are most in favor with some. In the early part of the present century a pill composed of squill and digitalis in powder, and calomel, each one grain, given three times a day, was almost universally chosen. In place of the calomel the blue mass was often preferred. When this prescription had produced a little ptyalism the mercurial was omitted and the squill and digitalis continued. It has often been observed in dropsies of all kinds that diuretics act better after a little mercurial action is set up in the system. The diuretic that I most frequently prescribe is made of the carbonate of potass. ounce ss and water ounce vj; to a tablespoonful of this a tablespoonful of fresh lemon-juice is added. This is taken every two hours, and at the same time a dessertspoonful of the infusion of digitalis or more is taken three times a day. This is an {1179} old prescription. Sometimes the old sal diureticus is used. This is the acetate of potassium. It is not always kindly received by the stomach. At Bellevue Hospital the following is much used: viz. infusion of digitalis, ounce iv; bitartrate of potash, ounce j; simple syrup, ounce ss; and water added to make a pint. This is taken pretty freely. But it would require many pages to exhaust the diuretics. I will only add that I have more confidence in the salts of potash and soda, singly or combined, aided by digitalis and a mercurial, than in any others.

The diaphoretics that are most efficient are warm water and steam. A foot-bath long continued and frequently repeated, the patient covered with blankets, and the water kept at 90° or warmer, are very effectual in producing perspiration. Bricks heated or hot water in bottles, or potatoes heated, and enveloped in damp cloths and laid alongside of the body and limbs, form an extemporaneous vapor-bath of considerable efficiency. A vapor-bath can be easily extemporized in the following way: Have a kitchen vessel furnished by the tinman with a cover which has an inch tube fitted to this and bent so as reach the floor six feet from the fire. The pot should have a capacity of a gallon or more, and should be kept boiling briskly. Meantime, the patient, in his night-dress, has a double blanket brought over his shoulders from behind, and another from before, and fastened. Now he takes a chair (wooden), under which the steam is delivered. The blanket from behind is kept off his body by the back of the chair, and the front one by his knees. The steam, shut in in this way, soon brings on a sweat, and when it is sufficiently active the front blanket is thrown off, and the patient wrapped in the rear one and put to bed, when the sweating can be regulated by blankets. This is better than what is called the alcohol sweat, for in that the patient is bathed in carbonic acid gas as well as heat. A patient is sometimes enveloped in a hot, wet blanket with good effect. Pilocarpine has come into use lately as a sudorific. I have witnessed its effects many times and can testify to its certainty as a sudorific; but it is too debilitating for common use. Digitalis has sometimes acted with extraordinary power in this way, but there are grave risks in administering large doses.

Among the cathartics that may be used in ascites, it has seemed to me that the milder hydragogues are safest. One ounce of Epsom salts with a drachm of the fluid extract of senna can be taken every second or third day for months, if need be, with little reduction of strength, and sometimes with an increase of it. I had charge of a young man in the hospital in whom cirrhosis was unquestionable, and dropsy at one time extreme, in whom the abdominal veins had made furrows that would receive the little finger, who was wholly relieved by a drastic dose of elaterium every second day. I saw him three years after his discharge, and then his health was good. Notwithstanding this, I prefer the milder medicines.

Bristowe has seen no cures from either sudorifics, diuretics, or purgatives. I have seen one or more from each of those agents, all cirrhotic. He "has seen cures occasionally from mercury, iodide and bromide of potash, copaiba, and a combination of fresh squills and crude mercury." I agree with him in his statement that counter-irritants are useless, making exception for chronic peritonitis and the early stage of the tubercular variety. He thinks quinia, iron, and cod-liver oil are useful.

{1180} Paracentesis in almost every case will at length become necessary, and the question comes whether it should be practised early or late. If it be delayed till the oppression of the breathing makes it imperative, the walls of the abdomen will be so stretched as to present little resistance to the reaccumulation of the fluid, and a second tapping will be required in fifteen to twenty-five days. A bandage is a poor substitute for muscular contraction. If, on the other hand, the fluid is withdrawn before the muscularity is not stretched out of the muscles, then accumulation will be less rapid and the patient will be spared the suffering which large accumulations cause. But tapping is not always an innocent operation. It is sometimes followed by acute peritonitis. By the early tapping this risk is oftener taken. Reginald Smith suggests the use of a small canula by which only ten or twenty ounces of the fluid can escape each hour. This mode, he thinks, removes the danger of syncope and makes the bandage needless.

Hemorrhagic Effusion

in the peritoneum is a topic on which there is little to be said. A primary effusion of this kind probably does not occur. In hæmatophilia, where the mucous membrane of the nose and wounds bleed dangerously, there is no record of spontaneous bleeding into the peritoneal cavity. The same thing can be said of that very rare disease which has been called bloody sweat. An unmarried lady applied to me fifteen years ago with this disorder. The blood would ooze out at hundreds of points on the inner face of the arm; these would run together and drop off the arm, or the same thing would occur on the chest and in the bend of the knee. This would continue for two or three minutes, and then cease of itself, but to recur in one or more, rarely several, places. For years this habit continued. There was no irregularity of the menses. I could find no visceral disease; there was no nose-bleed. She lost strength, but only moderately. This kind of bleeding continued for several years. She is now approaching fifty years of age, and for the last two or three years has had no recurrence of the bleeding. There was never anything in this case to lead to the suspicion of peritoneal or other serous hemorrhage. In the few similar cases on record there is the same absence of all evidence of internal bleeding.

It has already been said that a certain amount of blood, as shown by its corpuscles, is to be expected in cancerous ascites, and with less uniformity in tubercular ascites, and not unfrequently in hepatic dropsy, as well as in acute peritonitis. This may not deserve to be called hemorrhage, on account of the moderate quantity of blood that is effused; but aside from that which results from rupture of blood-vessels it is about the only kind of it with which we are familiar.

Scurvy, and conditions of the blood analogous to those produced by that disease, make it almost certain that if pleurisy or pericarditis occurs while these conditions exist, it will be hemorrhagic. I am not, personally, acquainted with a single instance in which peritonitis in this condition has occurred. Copeland, however, says that hemorrhage in peritonitis has been noticed by Broussais and others. The blood is mixed {1181} with the serum and stains the surface of the false membrane, as in hemorrhagic pleurisy and pericarditis, and the disease is of an asthenic type, "occurring in the hemorrhagic diathesis." "The symptoms are inflammatory from the beginning, and rapidly pass into those indicating great depression; the pulse becomes rapid, small, and soft, death quickly supervening, with convulsions, cold and damp extremities and surface," etc.

Copeland has himself not seen a case, and regards its occurrence as very rare. Delafield states that "Friedreich describes two cases occurring in patients with ascites who had been frequently tapped. He says that both the parietal and visceral peritoneum was covered with a continuous membrane of a diffuse, yellowish-brown color, mottled with small and large extravasations of blood. The membrane was thickest over the anterior abdominal wall. It could be separated into a number of layers. These layers were composed of blood-vessels, masses of pigment, branching cells, and fibrillated basement substance. In many places the extravasated blood was coagulated in the shape of round, hard, black nodules. The new membrane could be readily stripped off from the peritoneum, and there were no adhesions between the visceral and parietal portions of the peritoneum."

The erosions of abdominal cancer sometimes open vessels of considerable size, causing large hemorrhage into this cavity and sudden death.

When aneurisms of the abdominal aorta rupture, they sometimes flood the abdominal cavity; oftener they open into the structures under the peritoneum on the left side, and make a large flat tumor extending from the point of rupture downward to the brim of the pelvis, and even beyond it.

A gentleman whose health was usually good, thirty-five years of age, felt an unwonted exhaustion and feebleness creeping over him. His countenance became pale, his pulse rapid, growing smaller and smaller. It seemed certain that there was hemorrhage somewhere, but until it was noticed that the bowels were growing tumid and hard there was nothing to guide us to its seat. Even then we were left to conjecture regarding the bleeding vessel. This sinking continued for thirty-six hours. After death it was found that a small aneurism had been formed on one of the vessels of the omentum, not larger than a small walnut, and had ruptured by a very small opening, and that it was by this small opening that life had oozed away.

Bleedings from stabs and other wounds of the bowels, from lacerations of the liver, spleen, uterus, and sometimes of the kidneys, should be mentioned in this connection; but as they, for the most part, fall into the hands of the surgeons, this is not the place to give the details regarding them.

{1182}

DISEASES OF THE ABDOMINAL GLANDS (TABES MESENTERICA).

BY SAMUEL C. BUSEY, M.D.

DEFINITION.--Tabes mesenterica may be briefly defined to be tuberculosis of the mesenteric glands. This definition may seem too limited, because it recognizes the identity of tuberculosis and scrofulosis of the lymph-glands, and excludes those hyperplastic conditions which do not certainly undergo the cheesy degeneration. It is supported, however, by the absence of any essential difference in the histological changes which take place in tuberculous and scrofulous (Wagner) lymph-glands; by the frequent simultaneous occurrence of each in the same subject; by the secondary development of tubercles during the course of scrofulous affections; and by the fact that the cheesy transformation is alike common to both these conditions of new formations. Schüppel maintains that the presence of tubercles is necessary to the production of the cheesy metamorphosis of lymph-glands, and that "scrofulous glands are always tuberculous glands." In this view Rindfleisch coincides, and expresses the belief that the inflammatory and hyperplastic changes are secondary to the formation of the tubercles. Birch-Hirschfeld asserts that cheesy degeneration of the mesenteric glands is always accompanied by tubercular formations.

This definition is therefore adopted as the expression of the result of the most recent investigations. It must, nevertheless, be admitted that a few equally competent observers deny the identity of the tuberculous and scrofulous new formations in lymph-glands. It must also be conceded that occasionally hyperplastic processes in the lymph-glands undergo the cheesy metamorphosis independent of tubercular development.

SYNONYMS.--The differences of opinion, especially among the older authors, in regard to the nature of this disease are very distinctly indicated in the varying significance of the numerous synonyms, of which the following list is only a part: Atrophia mesenterica; Atrophia infantum (Hoffmann); Febris hectica infantum (Sydenham); Scrofula mesenterica (Sauvages); Paralysma mesentericum (Good); Physconia mesenterica (Baumes); Mesenteritis chronica (Stewart); Mesenteric fever, Hectic fever, Marasmus (Underwood); Carreau, Entero-mésentérite of the French; Darrsucht der Kinder and Gekröschwindsucht of the Germans; Tubercles of the mesentery; Tuberculous disease of the abdomen; Phthisis mesenterica; Tabes glandularis; Tabes scrofulosa; Macies infantum; Pædatrophia; and Rachialgia mesenterica.

{1183} Some of these synonyms indicate the theoretical and unsupported opinions of their authors, and others refer merely to a symptom. The name carreau refers to a hardness of the abdomen; physconia, to the presence of a non-fluctuating and non-sonorous abdominal tumor; and that of entero-mésentérite presupposes a secondary origin from a primary enteritis. Good classes it among his numerous varieties of mesenteric turgescence, but characterizes this special form as a scrofulous turgescence always associated with the strumous diathesis. The terms tabes and atrophy originated when the nomenclature of disease was derived from symptoms, and not from pathology.

HISTORY AND PATHOLOGY.--The history of tabes mesenterica is coeval with that of scrofula and pulmonary consumption. The ancient authors recognized the existence of a chronic disease of the mesenteric glands, characterized by enlargement and induration, followed by destruction of the gland-parenchyma, which was associated with digestive disturbances, emaciation, hectic fever, and usually terminated in death. At first, the degenerative process was regarded as suppurative. But as the study of scrofula progressed, and frequent observations were made of the occurrence of disease of the external lymphatics and of the mesenteric glands in the same subject, disputes arose as to the identity of the two affections. These controversies led to the general acceptance of the belief that the scrofulous degeneration of lymph-glands and the process of destruction in tabes mesenterica were identical. Consentaneous with these investigations, and for a long time subsequent, even down to a very late period, which is, perhaps, not yet concluded, the relation of scrofulous disease of the lymph-glands to pulmonary consumption was discussed and studied with great assiduity. As the knowledge concerning these diseases advanced, and the results of investigations were accepted, the doctrine of the identity of the morbid processes in scrofulous disease of the external glands and mesenteric phthisis became firmly established. The history of scrofulosis and tuberculosis cannot be separated. The connection and identification of the two processes have been subjects of constant discussion from the discovery of tubercle to the present time. Occasionally, the dividing-line seemed definitely fixed. Then would follow the general acceptance of the doctrine of identity. With the discovery of miliary tubercle a determined reaction took place against this view, and for a while many regarded scrofulosis merely as a form or stage of tuberculosis. As the conclusions in regard to these questions changed, so did the opinions concerning the true nature of tabes mesenterica change, until, finally, the investigations of Rindfleisch, Schüppel, and others seem to have established the tuberculous nature of the disease. Many authors of a comparatively recent date have applied the term tuberculosis to this condition, not because they knew or believed the development of true tubercle was a constant or essential characteristic, but because they regarded the words scrofulosis and tuberculosis as synonymous.

Notwithstanding the obscurity in which, for so long a time, the pathology of this disease was involved, certain facts well known to the earliest writers have been confirmed by continuous observation down to the present. Its secondary character has been so uniformly recognized that some of the older authors based its origin upon the absorption and conveyance along the lymphatic vessels to the glands of some peccant material originating {1184} in a primary focus of disease. The constant coexistence with scrofulous affections and pulmonary consumption had long ago established the direct and primary relation of these diseases to tabes mesenterica, and authors of recent date, though not so generally holding the opinion that it is always an intercurrent complication of these maladies, yet maintain its secondary development. Even Schüppel, whose investigations and conclusions lead in the direction of an idiopathic origin, admits that the only primary element is the tuberculosis, which finds its cause in some peripheral irritation.

In the earlier times, as now, tuberculosis of the mesenteric glands has been observed during every period of life from birth to advanced old age, but then, as at the present time, the greater number of cases were known to occur during infancy and childhood. But few cases have been observed during the earlier months of life or before weaning. Between the ages of two and eight years is the period of greatest frequency. Though rarer during the later years of childhood, the older the child the more rapid its progress to a fatal termination. Nursing infants are not exempt, but those nursed by healthy mothers are much less liable than the wet-nursed. Among hand-fed infants it is not an uncommon disease, but it is much more common among the farmed-out children. While, as has been stated, the greatest number of cases occur in those between two and eight years of age, statistics show that the liability to it increases from the age of two and a half years up to the eighth, and, according to some authors, up to the tenth year. At the latter age there is a remarkable diminution in the number of cases. This fact is probably due to the greater prevalence of the acute diseases of the respiratory organs and of the exanthematous diseases among children during this period of life. Some have attributed it to the more rapid development and increased functional activity of the mesenteric glands. This circumstance might afford a plausible explanation for the apparent sudden increase in frequency after the completion of the second year because of the independent subsistence of children at that age, and the additional duties imposed upon the alimentary tract and its dependencies; still, if this were so, the period of greatest frequency ought to begin at an earlier age and more nearly correspond with the time of weaning. It is, however, a fact that tubercularization of the mesenteric glands is more frequently associated with chronic intestinal inflammation in those over one year than in those under that age. This fact, together with the greater liability of artificially-fed infants, would seem to connect, at least in such cases, its secondary origin with some primary irritation of the intestinal canal.

Authors are not yet agreed in regard to the relative frequency of this disease in boys and girls, though opinions predominate in favor of the greater number among the males. The statistics of Rilliet and Barthez and Schmalz show a decidedly greater prevalence among boys.

The comparative frequency of tuberculosis of the mesenteric glands cannot be determined. Louis found disease of the mesenteric glands in one-fourth of the autopsies of persons dying of phthisis; in 100 adults dying of the same disease Lombard found tuberculosis of these glands in 10; and in the bodies of 100 tuberculous children he found the glands tuberculous in 34 cases. In the Hôpital des Enfants Maladies tubercles were found in the mesentery of one-half of the children dying of {1185} tuberculous affections. In the bodies of children dying of tuberculous disease in the Children's Hospital of Washington tuberculous degeneration of the mesenteric glands has been found in two-thirds of the cases, and without a single exception in those dying of rickets. Authors differ also, and the statistics are equally unreliable, in regard to the relative frequency of tubercularization of the bronchial and mesenteric glands. The general opinion seems to be in favor of the greater frequency in the bronchial glands. In a majority of cases both sets of glands are found diseased.

The geographical distribution of tabes mesenterica is as universal as that of scrofula and pulmonary phthisis. No country or climate is exempt, yet there is no locality in which it is endemic. It has been observed among all civilized nations, in the cold regions as well as in the tropical countries. Wherever scrofulous and phthisical diseases are known, there also are found cases of tabes mesenterica. Livingstone has stated that scrofula is unknown in some regions in Central Africa, and other travellers have made similar statements in regard to some Indian tribes. The statistics of the Children's Hospital of Washington show a far greater frequency among the African race than among the whites. It belongs to no class or condition of life, but occurs more frequently among the children of the squalid than among the children of the affluent and well-to-do.

ETIOLOGY.--Predisposing Causes.--Modern as well as the older authors have very generally accepted the conclusion that a constitutional tendency or liability to this disease is its most frequent and potential etiological factor. This predisposition may be either inherited or acquired. The ancients called it the strumous, and the more recent writers the scrofulous or tuberculous, diathesis. Lugol maintained that this diathesis is begotten of old and syphilitic fathers, and others state that children of parents nearly related and of those broken down by disease and excesses may inherit it. That it is transmitted by scrofulous and phthisical parents no one can doubt, but as yet it cannot be defined to be anything more than a peculiarity of the constitution which may exhibit abnormal reactions against irritating influences. The scrofulous habit is believed to be indicated by physical appearances which represent two extremes. The erethic form is characterized by a feeble and delicate frame; deficient muscular development; transparent, smooth, and florid skin; light hair and blue eyes, large pupils; precocious intellect and sanguine temperament; the torpid form, by a large head; large and tumid upper lip; soft and flaccid flesh, bloated appearance; short and thick neck; muscular incapacity, tumid abdomen, and sluggish intellect. Some of these features are more frequently symptoms of the actual disease than of the existence of a predisposition to it, and, except so far as they may refer to a primary scrofulous or pulmonary disease, cannot be accepted as indicative of the presence of a constitutional tendency to tuberculosis of the mesenteric glands. A tumid abdomen, rapid emaciation, and anæmia are far more valuable signs of the disease of these glands.

Bad air and bad food are also important predisposing causes. They are conditions to which the children of the poor, especially in large cities, are constantly exposed. Insufficient protection from climatic influences, neglect of person, and unhygienic surroundings must be classed in the same category. It is claimed that vitiated air, unwholesome habitation, {1186} insufficient or improper food, squalor and filth may cause the constitutional tendency, as they will certainly precipitate the development of the disease in those predisposed to it.

Exciting Causes.--The border-line between the predisposing and exciting causes cannot be positively fixed. The presence of tuberculosis or of some form of scrofulous disease in some other part of the body so constantly precedes the development of tuberculosis of the mesenteric glands, even in those who have not exhibited the characteristic phenomena of the scrofulous diathesis, that such affections must be regarded as exciting as well as predisposing causes. No one can doubt the frequent infection of the mesenteric glands in cases of pulmonary tuberculosis. The probability of systemic infection from a single focus is universally admitted. These facts and circumstances do not exclude the possibility of localized tuberculosis of the mesenteric glands. Whether such exclusively local development of tubercles ever occurs independent of the scrofulous diathesis cannot be determined, but that the disease does find its exciting cause in inflammatory conditions of the intestinal mucous membrane cannot be doubted. Schüppel, who asserts the primary development of the tubercle-formation in lymphatic glands, does not claim an idiopathic origin, but admits the necessity of a primary peripheral irritation in direct connection with the affected gland. The intimate connection between diseases of the intestinal mucous membrane and of the mesenteric glands is established beyond a doubt. Vogel and Steiner assert that tabes mesenterica is a common result of enteritis folliculosa. A primary inflammatory process may not contain any element which could be classed as tubercle, yet it may excite secondary tuberculosis of the glands. Whether such a result only occurs in those who may have acquired or inherited the predisposition is yet undecided. In many of the cases of tabes mesenterica tuberculous ulcers are found in the intestines, but it cannot be claimed that such ulcers are always the primary foci of tuberculous development. If primary, it is not difficult to understand how the virus may be transmitted to the glands.

It has been claimed that certain articles of food will produce the disease. Potatoes and rye bread in large quantities and a coarse vegetable diet have been mentioned among the exciting causes. Deficiency in the quantity of food is a much more frequent cause than inferiority in quality, yet there can be no doubt that any and every article of diet that will set up catarrhal inflammation of the intestinal mucous membrane may become a cause. Irritation of the mucous membrane of the alimentary tract, induced by coarse, stimulating, or imperfectly-digested food, or by the improper and frequent use of purgative medicines, may give rise to disease of the glands; and, even though the irritation may in itself be trivial, its long continuance or frequent renewal may prove sufficient, especially in those in whom the predisposition is present. Malarial and exanthematous diseases have also been considered exciting causes, and among the latter class measles and scarlet fever, because of the inflamed condition of the intestinal mucous membrane which they leave, are the most frequent. Difficult dentition and whooping cough must also be classed in this category.

Recently attention has been called to the probable transmission of the disease through the milk of diseased cows, but further investigation and {1187} more reliable data are necessary to establish this connection. Klebs has deduced the conclusion from recent experiments that the use of the milk of cows in advanced phthisis will always produce tuberculosis, which begins as an intestinal catarrh and extends to the mesenteric glands.

Some of the older authors believed that the cure of some chronic diseases of the skin and mucous membranes and the suppression of chronic discharges might induce tuberculosis of the mesenteric glands; but these conditions are now known to be most frequently the initial manifestations of the scrofulous diathesis, and the mesenteric complications are far more likely to occur when these primary foci are neglected and the patient is left to suffer the unabated progress of the disease.

MORBID ANATOMY.--It is not usual to find all the glands of the mesentery affected at once, nor of those affected all in the same stage of disease. Newly-affected glands may be found alongside of others in an advanced condition. In the first stage the glands are enlarged, but rarely exceeding the size of a filbert; they are firm, but not inelastic. This change consists in hyperplasia of the gland-constituents. Microscopic examination shows abundant cell-proliferation, but the cells are badly constructed and prone to undergo retrogressive metamorphosis. The cells accumulate in clusters without any intercellular substance, and compress the lymph-sinuses and blood-vessels.

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