Volume 2 — DISEASES OF THE DIGESTIVE SYSTEM. (continued 27)

One of the most interesting complications which arises during the existence of obstruction of the bile-ducts is the form of fever entitled by Charcot¹⁹⁷ 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.

¹⁹⁷ Leçons sur les Maladies du Foie, etc., p. 178 et seq.

¹⁹⁸ Cyr, Traité de l'Affection calculeuse du Foie, p. 193.

¹⁹⁹ Deutsches Archiv für klin. Medicin, vol. xxxiv. p. 529.

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 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. Wagner²⁰¹ 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

²⁰¹ Deutsches Archiv für klinische Medicin, Band xxxiv. p. 531, 1884.

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 Flint²⁰³ 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.

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 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 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 Ransohoff²⁰⁵ 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 Harley²⁰⁶ 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.

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

²⁰⁵ Lancet and Clinic, 1884.

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 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 instance²⁰⁷ 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.

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.

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.

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.

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.

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 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.

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 Bradbury²¹⁰ 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 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, Bristowe²¹¹ reports a case in which pylephlebitis resulted from an ulcer of the stomach, the neighboring veins becoming implicated and the usual results following.

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

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 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.

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 the migration of the embryo from the intestinal canal. As Davaine²¹² 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 Cobbold²¹³ 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.

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

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

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.

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.

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 Virchow²¹⁶ 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 cavities²¹⁷ are sacs of echinococci, but they depart widely from the typical form, well-defined scolices being seldom encountered.

²¹⁶ Archiv für Anat., Virchow, vol. xi. p. 80.

²¹⁷ Carrière, quoted by Davaine, op. cit., p. 961.

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

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 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 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.

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, Hjaltelin²¹⁹ 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

²¹⁹ Davaine, op. cit., p. 605.

²²⁰ The Medical Times and Gazette, August, 1873, p. 164.

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 authorities²²² 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 There is no good reason for this method of treatment now, and it seems to have been discontinued.

²²² Transactions of the Clinical Society, loc. cit.

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 Pavy²²⁴ the extract of fern was mixed with a solution of potassa.

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.

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 Althaus²²⁶ 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 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.

²²⁶ On the Electrolytic Treatment of Tumors, etc., London, 1867.

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.

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 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.

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

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.

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.

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 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 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 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, 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 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.

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 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.

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.