Chapter XXII: Part 22

A liquid effusion more or less deeply tinged with red is usually found in the abdominal cavity.

_Symptoms_ are those of a wasting disease, with some icterus, sometimes digestive disorder, and a marked enlargement of the liver. The last feature can be easily diagnosed by palpation and percussion. If an examination through the rectum detects the enlargement and irregular rounded swellings of the surface of the liver or spleen, or the existence of rounded tumors in the mesentery or sublumbar region, this will be corroborative. The precise nature of the neoplasms can only be ascertained after death.

_Melanoma._ Melanosis of the liver is comparatively frequent, especially in gray horses, and above all when they are aging and passing from dark gray to white. In many cases a more certain diagnosis can be made than in sarcoma for the reason that primary melanotic neoplasms are especially likely to occur on or near the naturally dark portions of the skin, as beneath the tail, around the anus or vulva, in the perineum, sheath, eyelids, axilla, etc. The extent of the disease is likely to be striking, the liver, next to the spleen, being the greatest internal centre for melanosis. The whole organ may be infiltrated so that in the end its outer surface is completely hidden by melanotic deposit. The surface deposits tend to project in more or less rounded, smooth masses of varying size according to the age of the deposit and the rapidity of its growth. Individual deposits may vary in size from a pea to a mass of 40 or 50 lbs. They are moderately firm, and resistant, and maintain a globular or ovoid outline. The color of the melanotic deposits is a deep black with a violet or bluish tint. If the pigmentary deposit is in its early stage it may be of a dark gray. The deposits are firmer than the intervening liver tissue and rarely soften or suppurate.

Melanosis in the horse is not always the malignant disease that it shows itself to be in man, and extensive deposits may take place externally and considerable formations in the liver and other internal organs without serious impairment of the general health. It is only in very advanced conditions of melanosis of the liver that appreciable hepatic disorder is observed. If, however, there is marked enlargement of the liver, in a white or gray horse, which shows melanotic tumors on the surface, hepatic melanosis may be inferred.

_Lymphadenoma. Adenoid Tumor._ Lienaux describes cases of this kind in which the liver was mottled by white points which presented the microscopical character of adenoid tissue, cells enclosing a follicle and a rich investing network of capillaries.

_Angioma._ These are rare in the horse’s liver, but have been described by Blanc and Trasbot as multiple, spongy tumors on the anterior of the middle lobe, and to a less extent in the right and left, of a blackish brown color, soft and fluctuating. The largest mass was the size of an apple, and on section they were found to be composed of vascular or erectile tissue. The tendency is to rupture and extensive extravasation of blood (30 to 40 lbs.) into the peritoneum.

_Carcinoma. Epithelioma._ These forms of malignant disease are not uncommon in the liver as secondary deposits, the primary lesions being found in the spleen, stomach, intestine, or pancreas, or more distant still, in the lungs. The grafting or colonization of the cancer in the liver depends on the transmission of its elements through the vena portæ in the one case, and through the pulmonary veins, the left heart and hepatic artery in the other.

_Lesions._ The liver may be greatly enlarged, weighing twenty-seven pounds (Benjamin) to forty-three pounds (Chauveau), hard, firm, and studded with firm nodules of varying sizes. These stand out from the surface, giving an irregular nodular appearance, and are scattered through its substance where, on section, they appear as gray or white fibrous, resistant, spheroidal masses shading off to a reddish tinge in their outer layers. Microscopically these consist of a more or less abundant fibrous stroma, enclosing, communicating alveoli filled with cells of various shapes and sizes, with large nuclei (often multiple) which stain deeply in pigments. The relative amount of fibrous stroma and cells determines the consistency of the mass, and whether it approximates to the hard cancer or the soft. In the horse’s liver they are usually hard, and, on scraping off the cut surface, yield only a limited quantity of cancer juice. In the epithelial form, which embraces nearly all that have originated from primary malignant growth in the walls of the intestine, the epithelioid cells, flattened, cubical, polyhedral, etc., are arranged in spheroidal masses or cylindrical extensions, which infiltrate the tissues more or less. These seem in some cases to commence in the radical bile ducts (Martin), and in others in the minor coats of the larger biliary ducts.

As the disease advances a brownish liquid effusion is found in the abdomen, and nodular masses formed on the surface of the peritoneum.

_Symptoms._ As in other tumors of the liver these are obscure. As the disease advances there may be œdema of the legs and sheath, indications of ascites, stiff movements, icterus, occasional colics, tympanies, and diarrhœa. Nervous symptoms may also appear, such as dullness, stupor, coma, vertigo and spasms. Emaciation goes on rapidly and death soon supervenes.

TUMORS OF THE LIVER IN CATTLE.

_Sarcoma._ Round or spindle shaped celled sarcomata have been described by Sodero and Cadeac, leading in one case to perforation of the vena portæ and death by hæmorrhage into the peritoneum.

_Adenoma._ Martin records a case of a hepatic tumor formed of adenoid tissue which had extended into the vena portæ, and microscopically presented a cylindroid character. In the advanced stages it caused some jaundice, digestive disorder, obstinate constipation, progressive and extreme emaciation, and weakness which kept the animal constantly in a recumbent position.

_Angioma._ These are rarely seen in the young but are comparatively common in old cows as they are in aged men. They form masses of a dark red color and very variable size, and have a limiting sac of connective tissue or merge into the adjacent hepatic structure. Microscopically they consist of a series of irregular lacunæ filled with liquid blood, blood clots, or leucocytes, and communicating with small blood vessels in the walls and partitions. They are believed to be formed by dilatation of the liver capillaries with subsequent thickening of their distended walls, and atrophy of the nearest liver cells. Cases of the kind have been recorded by Kitt, Martin, McFadyean, Saake, Van der Sluys, Korevaar and others. Though often seen in abattoirs, they seem to have little effect on the general health, and no special symptoms have been noted as indicating their existence.

_Congenital Cysts._ These are found on the anterior surface or lower border of the liver in young calves. They have no connection with the blood vessels, nor biliary canals, contain no head of larval tænia, and do not constantly show the presence of any particular bacterium. These walls are thin and their contents alkaline, with sometimes slight blood extravasation, or a yellowish deposit in which cocci have been found. Unless connected with cirrhosis or other serious disease of the hepatic tissue, their presence seems to have no pathological significance.

_Carcinoma._ This has been recorded in the liver of cattle by Gurlt, Brückmüller, Kitt and others. From the walls of the gall bladder it grows in pyriform masses, and on the surface and in the interior of the liver, it may appear as hard, cancerous masses of all sizes.

_Epithelioma._ This has been described by Kitt, Martin, Blanc, Leblanc, Morot, Cadeac, and Besnoit. It appears in masses varying in size from a millet seed up, bulging from the surface of the organ or deeply hidden in its substance, and stained yellow or green with bile. The liver is usually enlarged, amounting to even 34 pounds (Cadeac). The formation commencing in the acini invades all surrounding parts causing compression and atrophy of the liver cells, and the formation of nests of epithelioid cells often with multiple nuclei and nucleoli. Cirrhosis is not uncommon, and fatty and other degenerations. Microbic invasion and necrobiosis are also common.

NEOPLASMS IN THE SHEEP’S LIVER.

_Adenoma_ has been met with by McFadyean, Johne, Kitt and Bollinger. They hung as pediculated tumors from the surface of the liver, and were in part wedged into its substance displacing the hepatic tissue and vessels. In general they consisted of a dense fibrous stroma with cylindroid and biliary cells in great abundance, sometimes arranged in tubular form. Specimens described by Kitt and Bollinger attained to the size of a man’s head and were stained of a deep green color.

_Carcinoma._ Casper reports a case of hepatic cancer in the sheep secondary to cancer of the mesentery.

NEOPLASMS IN THE DOG’S LIVER.

_Lipoma._ Trasbot describes two fatty tumors in the liver of a bitch, one of them as large as an infant’s head. It had a yellowish white color, and had taken the place of the proper hepatic tissue.

_Malignant Tumors._ These are rather common. _Sarcomatous_ masses with round and fusiform cells in a fibrous stroma; _encephaloid_ with a delicate stroma and large alveoli filled with cells, and having a soft brainlike consistency; _carcinoma_ with dense and thick fibrous stroma and nests of cells in comparatively small numbers; and _epithelioma_ with flattened, cylindroid or other epithelial cells in masses often affecting a tubular aggregation, are seen in different cases. Sometimes apparently primary, they can more commonly be traced to pre-existing centres of the same formation on the course of the portal vein or elsewhere.

_Symptoms._ A gradual wasting and emaciation with a yellowish pallor of the mucous membranes are characteristic. Trasbot gives the excessive atrophy of the temporal and masseter muscles as pathognomonic. Ascites is a usual complication. Enlargement of the liver, as shown by percussion of the right hypochondrium, and, in case of flaccid abdomen, by manipulation, and attendant signs of tenderness are corroborative. Variability or loss of appetite, and vomiting is not uncommon, and in case of primary or secondary deposits in other organs in the abdomen, thorax or elsewhere, the symptoms resulting from functional derangement of such organ may be found. Treatment is hopeless.

CALCAREOUS NODULES AND DEGENERATIONS OF THE LIVER.

Calcified roundish nodules, in groups, under capsule. Mostly in
solipeds. Theories of origin: parasites, microbes, emboli, omphalitis,
intestinal disease, biliary obstructions. Calcification of liver with
large abdominal aneurisms. Cszoker’s case, Diagnosis and specific
treatment impossible.

In the domestic animals in general the liver may become the seat of imperfectly spherical nodules of a white, yellow or brownish white color, varying in size from a millet seed to a pea or hazel nut, and of a gritty consistency and feeling, from the deposition of earthy salts. These may be seen in groups under the proper capsule, the adjacent hepatic tissue being healthy, or atrophied, sclerosed or pigmented. These lesions have been found most abundantly in solipeds.

_Pathogenesis._ The most varied doctrines have been advanced as to the origin of these lesions. They have been attributed to the previous presence in the liver of linguatula, echinococcus, cœnurus, oxyurus, distoma, and other parasites (Cadeac, Mazanti, Olt, Ostertag, Gripp, Leuckart, Ratz), to glanders, to microbian attacks (Dieckerhoff), to minute embolic infarcts in omphalitis in the foal, or intestinal disease in the adult (Kitt), and to obstructions by the eggs of distomata in the biliary ducts (Galli-Vallerio). It is not improbable that the lesion may be due to any one of these in a specific case, and this may be ascertained by the existence of certain definite features and conditions. Linguatula, echinococcus and cœnurus can only be suspected in districts where these prevail, and a careful examination of the central mass of the nodule should reveal the presence of the indestructible hooklets, as certified for given cases by Olt, Ostertag and Gripp. In case of nematoid worms or distomata, the eggs may possibly be found as in the cases of Villach and Ratz, or the embryos (Mazanti). Or there may be traces of channels formerly hollowed out by the worms in the vicinity of the nodules, as seen by Leuckart. Coincident tumors of the intestinal mucosa from larval nematodes, or aneurism or emboli in the anterior mesenteric artery would corroborate this conclusion. If distomata had started the lesions, the distension of the gall ducts and the thickening of their walls would be likely to indicate their former presence. Glander nodules might be suspected from the absence of a distinct rounded or oval outline, from the lack of a distinct, clear line of demarcation between the nodule and the adjacent liver tissue, and by the manifestation in the periphery of the nodule and around it of free cell proliferation, showing the mode of progression by the invasion of new tissue. If still active, the bacilli should be discoverable in stained scrapings or sections. There should also be distinct indications of the lesions of glanders in the lymph glands of the portal fissure, of the mediastinum, of the submaxillary region and of other parts.

Heiss records an interesting case of general calcification of the horse’s liver, with large aneurism of the abdominal aorta, mesenteric and renal arteries. The liver was thirty-two pounds, puckered on the surface and showed calcic degeneration of the walls of the vessels and hepatic tissue, to such an extent that when the organ was dried it did not add materially to its hardness. Microscopically the diseased centres indicated minute blood clots (thrombi), with fibrinous development and cretifaction. The lesions in this case were attributed to multiple emboli in connection with the aneurism. It might suggest further, microbian infection of both the aneurismal and hepatic vessels. In another case of extensive cretifaction of the horse’s liver reported by Cszoker, the calcified masses tended to assume rounded forms like tubercle, and had a clear glistening surface.

These lesions are mainly interesting in a pathological sense, and unless they are very extensive do not give rise to appreciable symptoms.

_Treatment_ could only be prophylactic and directed to the removal of the special conditions, in which the calcification originated in a given locality.

ACTINOMYCOSIS OF THE LIVER.

On damp infested soil, in cattle and swine. Round tumors, hard surface, soft centre, fibrous sac, club-shaped cells in tufts. Symptoms of liver disorder. Coincident external actinomycosis. Treatment: potassium iodide.

In damp soils where actinomyces are present in the soil and vegetation, it is not uncommon to find the characteristic growths in the liver of cattle and swine. Rasmussen saw twenty-two cases of hepatic actinomycosis in one year (1890) and in a number of cases he has found the liver, spleen, peritoneum and intestine simultaneously affected. Jensen who has also recorded hepatic cases, found tumors extending from the liver to the diaphragm. He describes them as rounded masses, of different sizes, enclosed in a fibrous envelope of variable thickness, hard and resistant at the surface and somewhat softened toward the centre. Microscopic examination detects the club-shaped cells arranged in tufts and radiating from a common centre.

_Symptoms_ are only the general indications of hepatic disease differing according to the size, and position of the morbid product and its interference with normal functions. When, however, superficial actinomycosis is found these symptoms may be fairly attributed to the existence of similar products in the liver.

_Treatment_ consists in the administration of potassium iodide in full doses, daily for a week, followed by a laxative, and then, after an interval of two days, repeat the treatment for a second week, and so for a third, fourth and fifth until the microbe has been destroyed.

PARASITES OF THE LIVER.

Lying as it does in the channel of the blood charged with the products of absorption from the intestine, the liver is especially liable to parasites. Among protozoa are: Monocercomonas hepatica (pigeon), saccharomyces guttulatus (rabbit), eimeria falciformis (rabbit), coccidium oviforme (rabbit, pig, dog). Among the lower cryptogams are actinomyces (ox, pig). Of the tapeworm family are: Cysticercus tenuicollis (ruminants, pig), c. pisiformis (rabbit), c. cellulosa (dog, pig), echinococcus veterinorum (animals, man), tænia fimbriata (sheep, deer), and an undetermined cœnurus (cat). Of trematodes are: Distoma hepatica (herbivora, man), distoma lanceolatum (herbivora, man), distoma giganteum, or Americanum (cattle), d. truncatum, d. conjunctum, d. campanulatum (dog), amphistoma explanatum (ox). Of nematodes are: Stephanurus dentatus, ascaris suis, oesophagostoma dentatum (pig), sclerostoma equinum, ascaris megalocephala (horse), ascaris bovis (ox), oesophagostoma columbiana (in ruminants), filaria hepatica, enstrongylus gigas, ascaris marginata (dog), ollulanus tricuspis, ascaris mystax (cat). (See Parasites).

DISEASES OF THE PANCREAS.

Obscure. Shown only by digestion or hepatic disorder. Excess of fat in
stools suggests suppression of secretion. Intestinal fermentations.
Suspension of glycogenesis and consequent emaciation, stunting or
poisoning. Pancreatic calculus and icterus.

Diseases of the pancreas are even more obscure than those of the liver. Situated on the course of the duodenum, beneath the lumbar vertebræ and their right transverse processes, and separated from the lateral walls and floor of the abdomen by the great mass of the intestines, it is not open to manipulation or satisfactory percussion, and its secretions being used up in the function of digestion, so that they cannot be perceived and tested externally like the secretions of the kidneys. Beside the general constitutional disorder therefore, we must look rather to the derangements of the digestive functions, to the abnormal condition of the fæces, and to the alterations in subordinate functions like the glycogenic action of the liver, for indications of an unhealthy state of the pancreas. The suppression of the pancreatic secretion has long been associated with the occurrence of fat in the stools, yet this may result from the lack of bile which has important functions to fulfill in emulsionizing fat, and in securing its endosmosis. On the other hand the lack of pancreatic juice may hinder the complete digestion of the albuminoids, and favor their fermentation and the occurrence of tympanies, congestions, abnormal secretions, etc., which may be easily attributed to another origin. Then again the dependence of the liver on the pancreas for its stimulus to glycogenesis, would suggest a series of disturbances from the abundance of the unused food principles, from the hindrance to nutrition and growth, and perhaps from the toxic action of the hepatic products. Once more, through the common excretory duct, infection of the pancreas may extend to and involve the liver, and blocking of the common duct by pancreatic parasites, or calculi, may stop the flow of bile and cause jaundice or other icteric disorder. And yet, it is rarely the case that pancreatic disorder is successfully diagnosed, and it is too often only at the post mortem examination that the actual lesions are revealed.

CATARRHAL PANCREATITIS.

Probable causation by parasites, calculi, irritants, microbes.
Lesions: mucosa reddened, thickened, ducts dilated, epithelium fatty,
granular, desquamating, pus, connective tissue indurated.
Interdependence of pancreatitis and hepatitis in horse, sheep and
goat. Liver lesions. Symptoms: loss of vigor, endurance, appetite, and
condition. Icterus, costiveness, fœtid, fatty stools, percussion
tenderness—right side. Treatment: antithermics, eliminants,
antiseptics, derivatives, alkalies, salicylates, ether.

_Causes._ We know little of the causes of this affection, but it may be inferred that parasites, calculi and other irritants, will produce in this as in other mucosæ a mucopurulent inflammation. Then again the presence of pus suggests the coöperation of pus microbes as in the infective catarrhal icterus. The blocking of the common gall and pancreatic duct, by gall stones or biliary products, will entail arrest of the discharge of pancreatic juice, and a consequent pancreatitis, just as blocking with pancreatic products will cause hepatitis and icterus.

_Lesions._ The mucosa of the pancreatic ducts is reddened, congested and thickened and their lumen blocked by a white, granular matter, containing pus globules, fibrine filaments, and granular, ciliated epithelium. The blocked ducts become dilated, and their walls thickened, the epithelium is desquamated to a greater or less extent, and the raw exposed surface may present ulcers or granulations. The pancreatic cells undergo fatty degeneration and the connective tissue becomes steadily indurated (sclerosis). These lesions were especially noted by Megnin and Nocard in a case of pancreatitis in the horse.

In the horse, sheep and goat, which have a common outlet for the bile and pancreatic juice, the blocking of the latter and the arrest of the bile almost of necessity causes hepatitis, and infection in the one gland is directly transferred to the other so that pancreatitis and hepatitis are mutually causative of each other. In the ox, pig, dog and cat, in which the bile and pancreatic juice are poured into the duodenum through separate ducts and orifices, this mutual pathogenic action is not so certain.

When the liver is implicated, there is catarrh and dilatation of the bile ducts, fatty degeneration commencing in the centre of the acini, pigmentation appearing at their periphery, and sclerosis of the organ follows.

_Symptoms._ In Nocard’s equine case there was progressive loss of spirit, energy, and endurance; appetite was poor and eating listless; after two weeks jaundice set in, the visible mucosæ and skin showing a yellow tinge, and the scanty urine becoming brownish yellow; the bowels became costive the fæces being formed of small hard discolored balls, but no excess of fatty matter is recorded. Emaciation advanced rapidly, the most marked wasting being in the muscles of the back, loins and croup. Death ensued at the end of two months from the commencement of the illness. In man sudden, violent colic, with nausea, tympany and collapse are prominent symptoms.

_Diagnosis_ is more satisfactory when with digestive disorder, tardily developing icterus, and rapid emaciation, there is an excess of fat in the ill-smelling fæces. Pain on percussion of the right hypochondrium would be an additional feature.

_Treatment_ can rarely be adopted because of the uncertainty of the diagnosis. It would proceed on general principles, antithermics, eliminants, antiseptics, and counter-irritants being resorted to as the conditions seem to demand. Alkaline laxatives and diuretics, salicylates of soda or potash, and guarded doses of sulphuric ether to solicit the action of the pancreas, might be resorted to. The disorder of the liver would require attention along the lines indicated under catarrh of that organ.

INTERSTITIAL PANCREATITIS.

Causes: paresis, marasmus, septic infection, blood diseases. Lesions:
connective tissue in excess—pancreas and liver; catarrhal
complications; calcic points; congestion and petechiæ in septic
infection. Areas of fat necrosis in the pancreas and abdominal adipose
tissue. Stearates of lime. Calcic foci in animals. Symptoms: obscure.
Treatment.

This is especially liable to accompany paretic and wasting diseases, septic infection, and diseases of the blood. Radionow examined the pancreas in animals that had suffered from chronic paralysis, gastro-intestinal catarrh, hepatic catarrh, chronic anæmia and marasmus, and found fatty degeneration of the epithelium, with atrophy and pigmentary degeneration of the glandular epithelium. The fibrous tissue of the gland was in excess in the pancreas and in the liver (sclerosis), and mucous cysts were found.

Siedamgrotzky found a chronic interstitial pancreatitis connected with alopecia, œdema and leucocythæmia. The pancreas was indurated, fibrous, resisting the edge of the knife and sprinkled with gritty particles. Much of the glandular tissue had been destroyed, and the ducts were filled with a dense, grayish, grumous mucus.

Kirilow and Stalnikow have found interstitial pancreatitis marked by congestion and ecchymosis, with intervening anæmic areas, in animals injected with septic matter. There was increased secretion in the early stages.

A marked feature of pancreatitis in man is the occurrence in the interlobular tissue of the gland, the omentum, mesentery and abdominal fatty tissue generally, of circumscribed areas of fat necrosis, each varying in size from a pin’s head upward even to a hen’s egg. On section these show a soft tallowy consistency and Langerhans has shown that they are composed of lime and fatty acids in combination. When lime is in excess they become gritty. According to Osler they may be dependent on some other primary affection (Bright’s disease). The partially calcified concretions found in the pancreatic ducts, and the yellowish white, gritty areas, which represent the degenerate lobules in animals (Seidamgrotzky) are suggestive of a similar morbid condition of the pancreas or it may be of some distant organ. Of late years a number of cases have been recorded in man and a very high mortality noted.

The _symptoms_ in the lower animals are very obscure, and an accurate diagnosis is looked upon as almost impossible. They are essentially the same as given above under catarrhal pancreatitis.

_Treatment_ too has the same narrow limitations.

PANCREATIC ABSCESS, SUPPURATIVE PANCREATITIS.

A complication of strangles or purulent infection. Symptoms: Colics,
chill, tender right hypochondrium, emaciation, fatty stools.
Treatment: Constitutional.

Reimers has reported several cases of pancreatic abscess, as a phase of irregular strangles (rhinoadenitis). In one case multiple abscesses with an aggregate capacity of 2½ quarts were found, and some of the pus had escaped by rupture into the peritoneum and produced infective inflammation. The abscesses had destroyed the greater portion of the gland, only a few isolated lobules being left.

Galland found an abscess as big as a walnut in the pancreas of a horse which had multiple tumors in the abdomen.

_Symptoms._ Colics occur from the local phlegmon, and it may be from its pressure on the duodenum so as to obstruct it, and this appearing in the course of strangles would indicate a forming abdominal abscess. Staring coat or shivering may coincide. Tenderness of the abdominal walls has been noticed by Reimers, together with a partial loss of appetite and a characteristically rapid emaciation. Fatty stools, if present, would be almost the only pathognomonic symptom.

_Prognosis_ is that the abscess will open into the abdomen, and cause fatal infective peritonitis. It is only as an exceptional occurrence that its rupture into the duodenum or colon can be hoped for, yet in such a case recovery is possible.

_Treatment._ Little can be done. It would be well to treat the constitutional symptoms, and await results.

FOREIGN BODIES IN THE PANCREAS.

Brückmüller has noticed needles and other sharp objects in the pancreas of the dog, determining abscess and the formation of a thick, greenish pus in the adjacent glandular follicles. Goubaux once found a fragment of straw in the pancreatic duct of the horse. Such conditions are not likely to be diagnosed, but if this could be done laparotomy might be permissible in the dog for the removal of the foreign body.

PANCREATIC CALCULI.

Mostly in cattle from over feeding, dry feeding, inactivity. Small.
Multiple. Round, angular, lobulated. Nucleus. Composition. Dilated
ducts. Atrophied or sclerosed glandular tissue. Prevention: succulent
food, water at will, open air life, correction of local catarrh.

Pancreatic like biliary calculi have been found especially in cattle. They appear to be predisposed by their stimulating, forcing feeding, by their quiet life apart from all causes of excitement and especially by the combined effect of dry feeding and prolonged confinement in the stall through the long winter.

The calculi are usually small but numerous, Jungers having found 36 weighing 38 grammes. Bär has found a mass with an aggregate weight of 23 grammes.

The form of the calculus varies; many are angular from mutual attrition in the large ducts; others from the smaller ducts are rounded; those from the glandular follicles may be even lobulated, in keeping with the divisions of the cavity. The color is white and each shows a distinct central nucleus of epithelial, mucus, or other origin. Their specific gravity is 2.397 (Fürstenberg), and their composition 92 per cent. calcium carbonate, 4 per cent. magnesia, and traces of calcium phosphate (Gurlt).

The pancreatic ducts are as a rule greatly dilated and thickened (in man they form enormous cysts, Senn, Osler), and the glandular tissue is atrophied, indurated (sclerosed), and of a brownish yellow color.

_Treatment_ of such cases would be unsatisfactory. By way of prevention succulent food, abundance of pure water, and the correction of any infective catarrhal affection of the duodenum, or of the bile or pancreatic ducts would be specially indicated. Free exercise in the open air would be desirable.

PANCREATIC NEOPLASMS. TUMORS.

Often malignant, and secondary. Melanoma in white horse. Carcinoma in
mare and dog. Epithelioma. Debility, icterus, abdominal swelling,
emaciation. Treatment: laparotomy, or potassium iodide.

Tumors of the pancreas are quite frequently malignant, and show a preference for the head of the organ. They may be primary but are more frequently secondary.

In gray horses melanotic tumors are found, in connection with similar formations externally, and especially as age advances. Brückmüller found them of varying size, from a pea to a hazel nut, scattered through the pancreas and adjacent tissues.

Gamgee records a carcinoma of the pancreas of a mare.

Carcinoma is more frequent in this organ in dogs, the neoplasm having an irregular form, an imperfect line of delimitation from surrounding parts and a hard, fibrous stroma enclosing caseous centers, undergoing fatty degeneration.

Nocard reports an epithelial tumor of the head of the pancreas in a bitch. The animal which had been ill for six weeks was debilitated, emaciated, and icteric with a marked abdominal swelling. It died two weeks later, and necropsy revealed a whitish sublumbar tumor, the size of a large apple, with irregular rounded projections. This pressed on the posterior vena cava, surrounded the vena portæ and gall duct and completely closed the latter. Microscopic examination showed it to be an epithelioma. The liver was undergoing cirrhosis.

_Treatment_, usually hopeless, would be by laparotomy. If actinomycosis were present give potassium iodide.

DISEASES OF THE SPLEEN.

No guidance through palpation or secretion. Leukæmia. Lymphadenoma.
Spleen a favorite culture ground for microbes. Congestions,
engorgements, ruptures. Safety valve to portal system and liver.
Rhythmic splenic contractions under reflex action.

The spleen even more than the pancreas is so deeply seated and so surrounded by other organs, that its diseases are not readily appreciable by physical examination, while the absence of any special secretion excludes the possibility of diagnostic deductions through this channel. Even the relation of the condition of the organ to the number of the leucocytes and red globules fails to afford trustworthy indications of disease, since leucocytes originate in other tissues as well as the spleen, and the destruction of red globules may take place elsewhere. Yet an excess of eosinophile leucocytes in the blood suggests hypertrophy or disease of the spleen, and an excess of leucocytes in general is somewhat less suggestive of disease of this organ (see Leucocythemia). If adenoma is further shown, in enlargement of lymphatic glands elsewhere there is the stronger reason to infer disease of the spleen.

The physiological relation of the spleen to the blood especially predisposes it to diseases in which the blood is involved. The termination of splenic capillaries, in the pulp cavities, so that the blood is poured into these spaces and delayed there, opens the way, not only for the increase of the leucocytes, and the disintegration of red globules, but for the multiplication of microörganisms which may be present in the blood, and for a poisoning (local and general) with their toxins. Hence we explain the congestions, sanguineous engorgements and ruptures of the spleen in certain microbian diseases (anthrax, Southern cattle fever, septicæmia, etc.)

We should further bear in mind that the spleen is in a sense a safety valve for the blood of the portal vein, when supplied in excess during digestion. In this way it protects the liver against sudden and dangerous engorgements, but it is itself subjected to extreme alternations of vascular plenitude and relative deficiency. This may be held to take place largely under the influence of the varying force of the blood pressure in the portal vein, but according to the observations of Roy on dogs and cats, it is also powerfully influenced by muscular and nervous action. He found rhythmic contractions of the organ due to the muscles contained in the capsule and trabeculæ, repeating themselves sixty times per hour, and which might be compared to tardy pulsations. He further found that electric stimulation of the central end of a cut sensory nerve, of the medulla oblongata, or of the peripheral ends of both splanchnics and both vagi caused a rapid contraction of the spleen. The spleen may thus be looked on not only as a temporary store-house for the rich and abundant blood of the portal system of veins during active digestion, but also as a pulsating organ acting under the control of nerve centres in the medulla. That the various ascertained normal functions of this viscus may be vicariously performed by others, as shown in animals from which it has been completely extirpated, does not contradict the occurrence of actual disease in the organ, nor the baleful influence of certain of its diseases on the system at large.

ANÆMIA OF THE SPLEEN.

General anæmia, debility, wasting diseases, starvation, hæmorrhage,
stimulus to formation of red globules, asphyxia, electricity, cold,
quinine, eucalyptus, ergot. Symptoms: lack of eosinophile leucocytes
in the blood of a debilitated subject may lead to suspicion.
Treatment: tonic, light, sunshine, pure air, exercise, nutritive food,
iron, bitters.

In cases of general anæmia the spleen is liable to be small, shrunken, wrinkled, and when cut the surface is drier and lighter colored than in the normal condition. This condition may be seen after old standing debilitating diseases, but is common in animals that have been reduced by starvation, just as the opposite condition of hyperæmia and enlargement comes of abundance of rich food and an active digestion. It may shrink temporarily as the result of profuse hemorrhage, but Bizzozero and Salvioli found that several days after such loss of blood it became enlarged and its parenchyma contained many red nucleated hæmatoblasts. The result of hemorrhage is therefore to stimulate the organ to enlargement and to the resumption of its embryonic function of producing red blood globules. Contraction of the spleen further occurs under asphyxia, the deoxidized blood being supposed to operate through the medulla oblongata. As already noted the spleen shrinks under stimulation of the central end of a sensory nerve (vagus, sciatic). An induced current of electricity applied to the skin over the spleen causes marked contraction (Botkin). Cold, quinine, eucalyptus, ergot and other agents also induce contraction. In the normal condition there is an inverse ratio between the bulk of the spleen and the liver, the enlargement of the one entailing a diminution of the other, but in certain diseased states, such as anthrax, ague, etc., both are liable to enlargement at the same time.

_Symptoms_ of splenic anæmia are wanting, through a lack of eosinophile leucocytes, in the blood of a starved or otherwise debilitated animal, may lead to suspicion of the condition.

The _treatment_ of such a case would be addressed rather to the general debility which induced the splenic contraction than to the contraction itself. Light, sunshine, pure air, exercise, grooming, nourishing food and the avoidance of all debilitating morbid conditions would indicate the principles of therapeutic management.

HYPERÆMIA—CONGESTION OF THE SPLEEN.

Four hours after full meal in splenic diastole. In well fed, high
conditioned. From obstruction of splenic or portal vein or vena cava,
heart, liver, or pulmonary disease, inhibition from encephalon acting
through splanchnics or vagi, microbes, ptomaines, toxins, paresis,
albuminoid diet. Spleen may be seven times its normal weight. Lesions:
simple blood engorgement: proliferation of pulp cells: increased
friability; rupture; dark color; hyperplasia of trabeculæ—hypertrophy.
Symptoms: none; or colic; palpation in ruminants; tenderness.
Treatment: directed against the causative disease; quinine,
cinchonine, eucalyptus, ergot, cold douche, electricity, puncture.

Considerable hyperæmia of this organ takes place physiologically in connection with active digestion in the first four or five hours after an abundant meal, and especially at intervals of a minute, during what may be called the diastole of the viscus. The supply of blood is also much greater in the well fed animal, than in the emaciated and impoverished one.

_Pathological hyperæmias_ of a _passive_ kind may occur as the result of obstructions in the veins leading from the spleen, such as the splenic veins, the posterior vena cava, or that part of the portal vein comprised between its junction with the splenic and the liver. Diseases of the right heart or its valves, of the lungs (emphysema), or of the liver which hinder the onward flow of blood and increase the blood tension in the vena cava or portal vein have a similar action. Perhaps we should include inhibition of the nerves (splanchnic, vagi) and nerve centres (medulla oblongata, cerebral cortex) which preside over the contraction of the splenic vascular walls, and of the capsular and trabecular muscles. There is reason to believe that the ptomaines and toxins of several microbian diseases, operate through these centres, while other such microbes and toxins operate directly on the spleen itself.

_Active congestions_ of the spleen are most commonly associated with microbian diseases and may be attributed partly as above stated to the action of the toxic products on the contraction nerve centres, and on the splenic vessels and parenchyma, but also in no small degree on the active proliferation of the germs themselves in the splenic pulp, and of the splenic cells. Among the most notable instances of this kind are, _in man_, malarious, yellow and typhoid fevers, and, _in animals_, anthrax, and Southern cattle fever. In most febrile diseases, however, there is a tendency in this direction, which may be fairly attributed to the paresis of the organ and the delay of the blood in its pulp channels and spaces with the consequent local increase of microbes and toxins. The microörganisms can usually be found abundantly in such cases, in the liquid of the pulp, and in the interior of the leucocytes and other cells that go to make up its solid constituents.

It has been long recognized by veterinarians that acute congestion often arises in connection with a sudden transition from a poor or insufficient diet to an abundant and nutritious one and especially to one that is rich in albuminoids (beans, peas, vetches, lucerne, sainfoin, clover, trefoil, in the fresh or preserved condition). If these are not in themselves the direct causes of acute and fatal engorgements of the spleen, they at least contribute in no small degree to the overdistension of the pulp spaces, the paresis of the organ and its successful invasion by pathogenic microbes.

The acute congestion attendant on specific microbian infection may be estimated by the increase in weight of the spleen. In the Southern Cattle fever this organ, which is normally 1.45 ℔., is habitually 2 to 5 ℔s., and may reach 8 or 10 ℔s. and in anthrax an equal increase may be noted.

_Lesions._ In such cases the organ may appear as if there were a simple blood engorgement, and this is largely the case in the early stages, but with the persistence of the disease there occurs an active proliferation of the splenic cells and especially those of the pulp. With the hyperæmia the consistency of the organ is diminished, and still more so with the cell hyperplasia, so much so that in extreme cases rupture may ensue. The color is always darker (purple or blue), but this is only in part due to the abundance of blood and in part to the thinness of the splenic capsule. If the condition persists a hyperplasia of the capsule and trabeculæ ensues, and the condition becomes essentially one of hypertrophy.

_Symptoms._ In the slighter congestions there are no appreciable symptoms. In the more severe there may be more or less violent colic, but this is usually marked to some extent by the profound depression attendant on the specific fever which is the cause of the congestion. Palpation of the spleen is impossible in the horse. In ruminants it may sometimes be felt along the upper border of the rumen just behind the last rib on the left side. It is soft and yielding retaining the indentation of the finger. If manipulation produces signs of pain it is all the more significant.

_Treatment._ As a rule this is the treatment of the fever which determines the hyperæmia. Apart from this, laxatives, quinia other alkaloids of cinchona bark, eucalyptus, a current of cold water directed to the region of the spleen, or induction currents of electricity to the same region are also decided stimulants to contraction. Ergot has been used with alleged advantage. In cattle acupuncture of the spleen has been put in practice in anthrax.

CHRONIC CONGESTION OF THE SPLEEN. HYPERTROPHY.

Hypertrophy from chronic congestion, over feeding, hepatic cirrhosis.
In _horse_: from mechanical obstruction in heart, lungs, posterior
cava, splenic veins, angioma, from glanders or tubercle in lungs,
chronic splenic congestion, disease of splenic plexus. Lesions:
increase enormous; mainly of pulp, or largely of fibrous framework.
Special neoplasms. Symptoms: excess of leucocytes in blood,
eosinophile cells, weakness, anæmia, emaciation, bleeding from mucosæ,
stretching, right hypochondriac tenderness, stiff gait, ascites,
colic, disorder of the bowels, rectal exploration. Treatment: is that
of primary disease; not encouraging; quiniae, eucalyptus, saline
laxatives, open air, sunshine, electricity. In _cattle_ is habitually
enlarged in Texas fever area. In lymphadenoma increase mainly of
fibrous framework and Paccinian bodies, and of adjacent lymph glands.
Symptoms: leukæmia, employ palpation, percussion, rectal exploration.
Treatment as in the horse. In _swine_: from high feeding, leukæmia,
lymphadenoma, tuberculosis, neoplasms, liver, heart and lung disease.
Lesions: great increase of Paccinian bodies, fibrous capsule and
trabeculæ. In _dog_: from traumas, leukæmia and lymphadenoma. Enlarged
Paccinian bodies and adjacent lymph glands. Symptoms: leukæmia, many
eosinophile cells, abdominal enlargement, palpation, icterus.
Treatment: as for large animals.

A continuation of passive congestion from the causes enumerated above, leads to permanent increase of the fibrous reticulum and connective tissue and increase of the splenic pulp. Even the stimulus of a rich and abundant alimentation increases the size of the whole organ, the amount of pulp and the number and development of the Paccinian bodies. Apart from disease the spleens of well fed cattle or horses are always decidedly heavier than those of the starved or debilitated. Of mechanical causes the most potent is cirrhosis of the liver or some other obstacle to the free passage of blood through that organ. The most common causes are, however, the continuous operation of those specific poisons which determine the acute hyperæmias.

SPLENIC HYPERTROPHY IN HORSES.

_Causes._ It occurs as the result of mechanical obstruction of the posterior vena cava as noticed by Varnell, from obstruction in the splenic artery or veins by Ellenberger and Schütz, as the result of an angioma by Martin, as the result of the morbid hyperplasias in specific diseases—glanders, tuberculosis—taking place in the spleen or lungs and thus directly or indirectly causing chronic congestion of the spleen (Morot, Leisering, Nocard, Varnell) and again as the result of innervation, in disease of the splenic plexus of nerves (Varnell).

_Lesions._ The increase in size may be enormous (42 lbs. (Bouret and Druille), 92 lbs. (Cunningham), and over 100 lbs. (Girard)). The consistency is varied. There may be such a redundancy of blood and splenic pulp that the capsule is distended to its utmost or even ruptured (Peuch). In other cases the splenic veins have given way and the blood has poured out into the abdomen with fatal result (Crafts, Cunningham, Reis). In other cases the spleen is enlarged, unevenly swollen and indurated by the formation of angioma (Jacob), lymphadenoma, glander or tuberculous nodules. In still others the capsule and fibrous framework are greatly thickened and the substance of the organ has assumed the consistency of the hepatized lung (Rodet).

_Symptoms._ These are suggestive rather than diagnostic. Most prominent is the condition of the blood with excess of leucocytes and especially of the eosinophile cells. Weakness, emaciation, feebleness of pulse, bloodlessness, bleeding from the nose or other natural passages, are attendant symptoms. In cases of extreme hypertrophy distension of the abdomen is marked and even the enlarged spleen may be made out by palpation, there may be special tenderness and dullness on percussion. Even partial sweats over the region of the spleen (Cadeac), and stretching with the fore feet far in advance (Welsby) have been noted as symptoms. In such conditions the animal walks stiffly, groans in turning, or when suddenly started and is with difficulty urged beyond a walk. There may be ascites, signs of colic, or irregularity of the bowels. Rectal exploration may reveal the hypertrophy.

_Treatment_ is usually the treatment of the primary disease. In glanders, tuberculosis, lymphadenoma, or leucocythemia there is little to hope for. Nor is there much in hepatic cirrhosis, obstruction of the vena cava or valvular disease of the heart. In simple hypertrophy we may resort to quinia or other bitters, eucalyptus, saline laxatives, exercise in the open air and sunshine, and local currents of electricity.

SPLENIC HYPERTROPHY IN RUMINANTS.

A moderate hypertrophy is the rule in the case of cattle which have passed through the Southern cattle fever, but have continued to live within the area of its prevalence. Gamgee’s observations in 1868 were very conclusive on this point. In over 1,000 western cattle the average weight of the spleen was 1.45 ℔., in 441 Cherokee (Indian Territory) cattle the average was 2.34 ℔s., and in 262 Texas cattle the average was 2.66 ℔s. All these animals were killed for beef, in what was considered to be perfect health. The difference relative to the weight of the entire animal is even greater than is indicated above, for at that date even more than at present, the Texas steer was a small and thin animal in comparison with the portly western bullock.

In lymphadenoma the organ may weigh 24 ℔s. (Tannenhauser); in simple hypertrophy it has been found to weigh 37 ℔s. (Koch). There was usually a marked increase in the size and number of the Paccinian bodies, and hyperplasia of the fibrous reticulum, while the pulp might be deficient and the cut surface rather dry. The adjacent lymph glands are usually enlarged.

_Symptoms._ Unless in the case of excessive increase, no symptom is usually observable, apart from leucocythæmia. With enormous hypertrophy the enlarged organ may be recognized by palpation, percussion, and perhaps rectal exploration.

_Treatment_ is unsatisfactory apart from the control and arrest of the primary diseases. For simple hypertrophy, bitters, laxatives and electricity may be tried.

SPLENIC HYPERTROPHY IN SWINE.

_Causes._ This disease appears to be rather frequent in pigs, in connection with high feeding, and more particularly with leucocythæmia and lymphadenoma. It is further a complication of tuberculosis and of neoplasms located in the spleen, and of hepatic, cardiac and pulmonary disorder.

_Lesions._ In leucocythæmia there is general enlargement of the spleen, and especially of the Paccinian bodies which may attain the size of a pea (Leisering, Fürstenberg, Bollinger, Siedamgrotzky, Röll, Ellinger). The total weight of the organ may attain to 5 lbs. (Mathieu), or 13 lbs. (Goubaux). In a remarkable case recorded by Zell, the organ measured 30 inches in its longest circumference and 20 inches in its shortest. It had an enormous thickening of the capsule and trabeculæ which enclosed softened contents in a state of fatty degeneration.

_Symptoms_ are wanting, as most of the observed cases were only discovered after the animal had been killed for pork.

SPLENIC HYPERTROPHY IN THE DOG.

This condition has been less frequently seen in dogs, the recognizable causes having been traumatism (Notz), and leucocythæmia (Zahn, Forestier, La Forgue, Nocard). Lymphadenoma is another complication (Nocard, Leblanc, Siedamgrotzky, Bruckmüller). The spleen has been found to weigh 2 lbs., (Bollinger, Siedamgrotzky). As in other animals the enlargement of the Paccinian bodies has been a marked feature. In other cases the splenic lymph glands are enlarged.

The _symptoms_ are obscure as in other animals. Yet the presence of white cell blood, with a predominance of eosinophile cells, enlargement of the abdomen, and the detection of a large solid body in the left hypochondrium which proves tender to the touch may prove more satisfactory than in other animals. In certain cases it has obstructed the biliary duct by pressure and entailed hepatic disorder and jaundice.

The _treatment_ would not differ from that of the larger animals.

Siedamgrotzky has also observed splenic hypertrophy in the cat in connection with leucocythæmia.

SPLENITIS. PERISPLENITIS.

Causes: extension from adjacent inflammations, penetrating bodies,
contusions, lacerations, infections, over exertion, cold, damp, over
feeding. Symptoms: those of primary disease, visible traumas, chill,
fever, swelling, flatness of percussion sound, absence of crepitation,
anorexia, vomiting, constipation, diarrhœa. Prognosis usually good.
Treatment: castor oil, enemata, cold douche, electricity, phlebotomy,
in infective cases quinine, salol, salicylates, iodides.

No accurate border line can be drawn between splenic hyperæmia and hypertrophy on the one hand and inflammation of the spleen on the other. It is, however, not difficult to assign to inflammatory action all cases that tend to suppuration and abscess. Also in perisplenitis with adhesions to adjacent parts like the liver, stomach, intestine, kidney or abdominal wall inflammation cannot be doubted.

_Causes._ Extension from the disease of adjacent parts—perihepatitis, perinephritis, peritonitis, enteritis—is a distinctly appreciable cause, as are also penetration of the spleen by foreign bodies, contusions, lacerations and infections of the organ. Cruzel, who claims an extensive acquaintance with the disease in working oxen, attributes many cases to violent exertions, overdriving, cold and damp weather, and an overstimulating alimentation. As inflammation may supervene on hyperæmia and hypertrophy we must accept the various causes of these conditions as factors in producing inflammation.

_Symptoms._ Most observations of inflammation of the spleen and its results have been made only post mortem, so that we must allow that the simple forms occur and undergo resolution without obvious symptoms. In the perisplenitis supervening on another disease also in infective cases there will be the antecedent symptoms of such primary diseases. In those resulting from traumatic injury, bruises, swellings or wounds, cutaneous or subcutaneous, there will often be suggestive features. In the more purely idiopathic cases symptoms are only shown when the lesions are extensive and acute. In oxen, Cruzel has noted the initial chill, followed by disturbance of the respiration, more or less hyperthermia, and a swelling of the left flank and hypochondrium in the absence of tympany of the rumen. The nature of this swelling is the most characteristic feature, as it gives a flat instead of a drumlike sound on percussion, and does not bulge outward and downward over the whole left side of the abdomen, pit on pressure, nor crepitate uniformly all over from fermentation, as in overloading of the stomach.

If abscess should form, chills and high febrile reaction are marked symptoms. In vomiting animals, anorexia, nausea, vomiting, constipation, and even diarrhœa may appear.

_Prognosis._ Unless in extreme cases and those due to traumatism or infection, the result of splenitis is usually favorable.

_Treatment_ would consist in depletion from the portal system and spleen by rectal injections, and laxatives which like castor oil, will operate without extensive absorption. Cold water or ice applied to the left flank and induction currents of electricity may also be resorted to. General blood-letting is strongly advised by Cruzel, and Friedberger and Fröhner. In infective cases quinia, salicylates, salol, and the sulphites, or iodides would be indicated.

HÆMORRHAGIC INFARCTION OF THE SPLEEN.

In congestive conditions. Absence of free capillary anastomosis and
contraction, absence of valves in splenic veins. Embolism of splenic
artery. Clots in pulp spaces. Wedge shaped infarcts, first black,
later yellow, later caseated, or cicatrized. Abscess. Prognosis good
in non-infective forms. Treatment as for hyperæmia, or infection, or
both.

This condition appears in hyperæmia, hypertrophy, splenitis, and splenic infection and largely because the structure and circulation in the organ conduce to such trouble. The splenic arteries terminate in open vascular spaces filled with splenic pulp and where all trace of a freely anastomosing capillary network is lost. The splenic veins in the same manner originate from these open vascular spaces. There is, therefore, an absence of the free communication of capillary network, which virtually acts as a safety valve in other vascular tissues, and the vascular cavities connected with each terminal artery are independent of those belonging to another, and find no way of ready relief when they become over distended, or when there occurs obstruction (thrombosis) of their afferent or efferent vessels. From blocking of arteries or veins there is at once produced a wedge shaped area of stagnation which cannot be relieved through any collateral circulation. Again the splenic veins, being destitute of valves, offer no obstacle to the reflux of blood into such vascular spaces whenever the further access of blood has been arrested by the blocking of the artery. The blocking may occur in the afferent artery through embolism by clots carried from the lungs or left heart, or formed within the vessel by the colonization of microbes on its walls. Even more likely is the formation of coagula in the vascular spaces themselves as the result of the introduction of pus, or septicæmic microbes, which are long detained and have ample time for multiplication in these cavities. In either case the result is obstruction to the sanguineous current, the filtering of blood backward from the veins and the engorgement of the cavity with blood. The plugs consist of fibrinous matter enclosing colonies of micrococci, and the result is not only black infarction of the spleen, but a subsequent general infection of the system at large.

The wedgeshaped infarcts are usually situated at the surface of the organ, the base turned outward and forming a dark projection on the surface, and the apex turned inward. The aggregation of two or three in one group may considerably alter the outline. If recent they are of a dark red color. Later from absorption of the coloring matter and fatty degeneration of the mass they assume a pale yellow hue and the swelling flattens or disappears. Later still through complete fatty degeneration they may be transformed into caseated masses, or through organization into fibrous tissue they may form thick white cicatrices. If pus cocci are present suppuration and abscess may be the outcome.