Chapter V: Parasites of the Liver (2)

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

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

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

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

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

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

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

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

Acute Secondary Pancreatitis.

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

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

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

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

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

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

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

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

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

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

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

Chronic Interstitial Pancreatitis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

MORBID GROWTHS OF THE PANCREAS.

Carcinoma.

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

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

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

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

[Footnote 3: _Transactions of the Pathological Society of Philadelphia_, vol. ix. 13.]

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Sarcoma and Tubercle of the Pancreas.

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

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

DEGENERATIONS OF THE PANCREAS.

Fatty Disease of the Pancreas.

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

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

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

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

Albuminoid Degeneration of the Pancreas.

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

{1129} Hemorrhages into the Pancreas.

Hemorrhages into the pancreas may be divided into three classes.

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

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

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

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

There are no indications for treatment.

OBSTRUCTION OF THE PANCREATIC DUCT.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

[Footnote 4: _New York Medical Record_, Jan. 14, 1882.]

{1132}

PERITONITIS.

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

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

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

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

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

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

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

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

The references are not given by Chomel, but they are probably these: Laennec, _Histoire des Inflammations du Peritoine_, 1804; and Gasc, _Dictionnaire des Sciences Méd._, p. 490, 1809.

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

Acute Diffuse Peritonitis.

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

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

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

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

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

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

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

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

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

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

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