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.
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.
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.
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.
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.
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.
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.
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.
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).
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.
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.