Physiologically after a meal is hyperæmic, and may increase one-third. Rich feed and temporary idleness may cause morbid congestion. Other causes are: ptomaines and toxins in spoiled food, hepatic irritants, damp, hot, tropical climates, warm, damp, buildings, overfeeding, dilated right heart, insufficiency of tricuspid valve, pulmonary emphysema or congestion. Absence of valve between the right heart and hepatic veins, slow hepatic circulation, dilatability of hepatic vascular system, compression of lung by false membranes, œdema, hepatization, infarction, hydrothorax. In horse: special causes: spoiled fodders, carminatives, volatile oils, work in hot sun, vaso-dilatation in heat and atony, falls, kicks, goring, blows; passive forms from obstacles to the circulation. Lesions: Hepatic enlargement to 20 or 30 pounds, and dark red color, darker spots of extravasation, hepatic vein congestion in centre, and portal vein congestion in periphery of acinus, softening, granular, fatty, nuclei disappear from hepatic cells, nutmeg liver, cirrhosis. Symptoms: general febrile symptoms, great prostration, drowsiness, slight colics, arched loins, trembling or jerking, lies on right side, percussion on last ribs painful, slight icterus and increased urination and urea. In passive cases, less icterus and kidney trouble; tends to intestinal catarrh and ascites. Prevention: good hygiene, moderate laxative ration, cool air, exercise. Treatment: green or laxative foods, salines, derivatives, water at will, always before morning feed. In dog: overfeeding, indolence: pulmonary and circulatory troubles. Lesions: nutmeg liver, degeneration, cirrhosis. Symptoms: pampered idleness, obesity, pulmonary or cardiac disease, intestinal catarrh, piles, ascites, slight icterus, percussion tenderness of right hypochondrium, lying on right side, increase of percussion flatness. Treatment: saline purgatives or laxatives, antiseptics, restricted laxative diet, open air exercise, derivatives, etc.
Physiologically the liver undergoes hyperæmia in connection with an abundant meal and active digestion. Within the limits of health it may increase one-third in bulk and weight. When this hyperæmia attends on temporary idleness and rich feeding it may overstep the limits of health and become pathological. Other causes of pathological congestion are, tainted food rich in ptomaines and toxins, food injured by cryptogams, and food that contains principles irritating to the liver. It is especially common in swampy regions in tropical or semi-tropical latitudes, and where the warm air is surcharged with moisture. Hot, close, damp stables, with overfeeding and lack of exercise in the pampered horse or dog, or under the forcing system of feeding for exhibition, or for the butcher, acts in a similar manner. Dilatation of the right heart, or imperfection of the tricuspid valve is a direct cause of mechanical congestion and emphysema, congestion or other obstruction in the lungs has a similar effect. In short the absence of valves between the right heart and the hepatic veins determines a passive congestion of the liver whenever there is any serious hindrance to the passage of blood through the right heart and lungs. The tardy circulation through the liver (5 mm. per second) also predisposes to congestion. The great development of the circulatory system in the liver, and its dilatability predisposes it to such congestions in a pre-eminent degree. For the same reason the liver suffers in the horse that is attacked with pulmonary congestion, whether as the result of overwork or of heat congestion. It will also suffer from compression of the lungs by false membranes or hydrothorax, or obstruction, by œdema, hepatization or infarction. The toxic matters produced in infectious diseases, and especially those affecting the intestinal canal and its connections, are arrested in the liver and contribute to hyperæmia.
Causes. Beside the general causes above mentioned, may be specially named, musty, decomposed, and irritant fodders: those which like green legumes, are easily fermented; and those which contain stimulating volatile oils or carminative principles. They are also especially exposed to such causes as severe and prolonged work under a hot sun, the nervous atony which causes vaso-dilatation in a hot climate, and such traumatisms as come from falls, kicks, goring, and blows by shafts, poles and clubs. These especially induce active congestion. The passive forms come mainly from obstruction in the lungs, or heart (dilatation, right valvular insufficiency, pericarditis, hydropericardium, myocarditis, fatty degeneration, endocarditis), or in the posterior vena cava.
Lesions. The congested liver is enlarged and deeply colored with blood. The weight of twenty to thirty pounds is often attained. While the color is of a deep red throughout, there are spots of a still darker hue indicating the seat of subcapsular or deeper seated hemorrhages. The color varies according as the congestion is passive or active. In the former the coloration is deeper in the centre of the acinus (nutmeg liver) indicating congestion of the hepatic veins, while in the latter the periphery of the acinus may be most deeply stained implying congestion of the portal vein. The consistency of the organ is diminished, and the more acute the attack the greater the friability. In such cases there is a parboiled appearance indicating granular and commencing fatty degeneration. Under the microscope the relative distension of the intralobular, and interlobular veins and the hepatic capillaries becomes more distinctly marked and the presence of pigment and fatty granules and the lack of protoplasm and nuclei in the hepatic cells indicate their progressive changes. When the peripheral cells are pale from fatty granules the contrast between the light margin and dark centre of the acinus, makes the mottled or nutmeg aspect of the liver much more pronounced.
In old standing cases of passive congestion the liver may be the seat of fibroid degeneration, extending from the capsule inward in bands or trabeculæ, and giving to the organ a firm resistant character (sclerosis, cirrhosis).
Symptoms. The symptoms are general and suggestive rather than pathognomonic. There are dullness, prostration, unsteady walk, pendent head, with occasional jerking, semi-closed eyes, redness of the conjunctiva, slight colicy pains, arching of the loins, muscular tremblings and decubitus on the left side rather than the right. The more definite symptoms are tenderness on percussion with the closed fist over the last ribs (the liver) especially on the right side, increase of the area of hepatic percussion dullness (which may be rendered valueless by a loaded colon), the presence of a slight icterus in the conjunctiva and urine, and an increase of the urine secreted and an excess of the contained urea.
In passive cases however the obstruction to the escape of blood from the liver prevents the development of icteric symptoms, of uræmia and of polyuria. In all such cases however there follows a general congestion of the portal system and if it persists for any length of time gastro-intestinal congestion and catarrh and even ascites may develop.
In all cases alike the history of the attack will help towards a satisfactory diagnosis.
Prevention. A rational hygiene embracing daily work or exercise, moderate laxative diet, green food in its season, pure cool air are important precautions.
Treatment. A moderate supply of green or laxative food, the withholding for the time of grain, and especially of maize, wheat or buckwheat, saline laxatives daily, and a stimulating embrocation or blister to the tender hypochondrium are the most important measures. Exercise in a box stall, or still better in a yard or paddock in the intervals between more systematic work forms an important adjunct to medicine. As a laxative sulphate of soda is to be preferred at first in a full cathartic dose and later in a daily amount sufficient to relax the bowels. Given in a bucket of water every morning before the first meal a very small dose will be effective.
Active congestion is very rare excepting in over-fed and indolent family pets. Passive congestion induced by diseases of the lungs and heart is however far from uncommon.
Lesions. True to their origin these usually appear as the spotted nutmeg liver with the deep congestion in the centre of the acini. For the same reason the fibroid degenerations shown in chronic cases, show the firm fibroid neoplasm chiefly around the hepatic veins. Granular, fatty and pigmentary degeneration of the cells are found as in the solipeds.
Symptoms. These are as obscure as in the horse. There is always a history of a sluggish, gourmandizing life, and in the early stages, a manifestation of embonpoint which suggests a torpid liver. Further suggestions may also be obtained from coexisting diseases of the lungs, or heart, from gastro-intestinal catarrh, from piles, or ascites. Then there is at times a slight icterus of the conjunctiva and urine. Finally tenderness on percussion on the right hypochondrium, decubitus on the left side, and an increased area of dullness on percussion may afford useful hints for diagnosis.
Treatment. In the rare cases due to infection from the intestine, an active saline purgative followed by antiseptics (salol, naphthalin, naphthol, etc.,) daily will be of value. It is also desirable to keep up the action of the bowels by morning doses of salines. In cases consequent on chest disease attention must be given to such primary trouble. In all cases a restricted laxative diet, and graduated but increasing exercise in the open air are demanded.
Causes: Mechanical injuries, falls, blows, kicks, degenerations, amyloid, fatty, granular, congestion, neoplasms, glanders, tuberculous, myomatous, microbian infection. In the horse, disease of liver, heart, lungs, hepatic artery, portal vein, degenerations following overfeeding, idleness, foreign bodies, arsenic, phosphorus, parasites, violent movements in colic, running, draught, leaping. In the dog, pampering and traumatism. In cattle forced feeding, emaciation, microbian infection. In birds, tubercle, tæniasis, microbian infection. Lesions: extravasation, intracapsular, or through capsule into the peritoneal cavity. The extravasation bulges of a deep black, covering a dark softened, pulpy, hepatic tissue, with light colored fatty tissue around. Clots may be stratified from successive bleedings. Liver usually enlarged. Symptoms: onset sudden, or preceded by stiffness, soreness and other signs of hepatic trouble. Extensive rupture, entails weakness, unsteady gait, perspiration, pallor of mucosæ, small weak rapid pulse, palpitations, dilated pupils, rolling eyes, amaurosis, tremors, convulsion in case of survival, coldness, œdemas. Death in five hours to five days. Risk of relapse in recovering cases. Treatment: rather hopeless, rest, laxative, ergot, ferric chloride, tannic acid, witch hazel, cold water, snow or ice to right side. In meat producing animals fatten.
Causes. Hemorrhage and rupture of the liver are closely correlated to each other, the accumulation of extravasated blood in the parenchyma in the one case leading to over distension of the capsule, and the laceration of this capsule and of the adjacent substance of the liver occurring in the other as a mere extension of the first. They usually occur as the direct result of mechanical injury (falls, blows, kicks) acting on a liver already softened and friable through disease. These predisposing degenerations may be amyloid (Caparini, Johne, Rabe), fatty (Julien, Gowing, Adam, Siedamgrotzky), granular softening, hepatitis or congestion (Zundel), glander neoplasms (Mathis), tubercles, angiomata (Trasbot), microbian infection (Stubbe), tumors (Brückmüller).
In the horse predisposing conditions may be found in diseases of the liver, heart or lungs, in embolism of the hepatic artery (Wright), in obstruction of the portal vein (Pierre), in infarction of the liver, in degeneration with softening, in sarcomatous, melanotic, glanderous or cancerous deposits in its substance, in degenerations consequent on over feeding, idleness, congestions, on the penetration of husks of grains into the liver substance, on arsenical or phosphorus poisoning. The presence of flukes, echinococci and other parasites may also cause congestion and softening. To the immediate or traumatic causes above named may be added the violent movements attendant on a severe attack of colic, and violent exertions in running, draught, leaping, etc. (Friend).
In the dog we must recognize all the pampering conditions which predispose to congestion and degeneration, together with more direct operation of kicks, blows, falls, fights, over exertion, etc.
In cattle a forcing regimen is especially predisposing, and yet the loss of vigor resulting from a diametrically opposite treatment, must be accepted as an occasional cause. Stubbe found in emaciated cows miliary hemorrhagic infarcts of a dark red color which gradually extended to an inch or more in diameter. These he traced to microbian infection coming by way of the chronic intestinal lesions which are common in old cows. The final result of such infarctions was loss of hepatic substance and the formation of cicatricial tissue with a marked depression on the surface of the organ.
In birds fatal hepatic hemorrhages occur in connection with local tubercle (Cadiot), tæniasis of the liver, or microbian infection.
Lesions. The hemorrhage may take place into the substance of the liver only, or the capsule may be lacerated so that the blood escapes into the peritoneal cavity in considerable quantity.
In the horse it usually occurs in the right or middle lobe, rarely in the left. There may be one or more hemorrhagic effusions varying in size from a cherry to a duck’s egg, or even an infants’ head (Lorge). This projects from the surface of the organ and its deep black contrasts strongly with the white of the adjacent capsule. When laid open the hepatic tissue is seen to be softened and pulpy, and its dark color forms a striking contrast with any surrounding fatty liver. Any form of degeneration may be revealed on microscopic or chemical examination. Not unfrequently small clots of blood form under the capsule raising it in the form of little sacs. Such clots are usually stratified indicating a succession of small hemorrhages.
When the capsule is torn, the lesion may extend from one surface of the organ to the other, and the edges, smooth, uneven or fringed, are united together by a blood clot.
In case of hemorrhagic infarcts the lesion usually has a distinctly conical outline corresponding to the vascular distribution. These are especially characteristic of cases supervening on heart disease.
The volume of the liver is usually increased and the weight may reach 30 lbs. (Schmeltz), 34 lbs. (Lorge), or even 66 lbs. (Trasbot).
In other domestic animals analogous lesions are found modified largely according to the size of the subject.
Symptoms. These may develop instantaneously without any marked premonitory indication. In other cases tenderness on percussion over the liver, stiffness or groaning under sudden movements or turning, arching of the back, hanging of the head, slowness in rising, costiveness, slight transient colics, and even icterus may have been detected on close observation. The symptoms of actual rupture are essentially those of internal hemorrhage. The animal becomes weak, or unsteady upon its limbs, perspires, arches the back, and shows a marked pallor of the visible mucosæ. The pulse is small, thready, weak and accelerated, and the heart beats violent or palpitating. The percussion dullness over the liver is extended (Weber), the loins become insensible to pinching, and there may be some distension of the abdomen. Dilatation of the pupils, retraction or rolling of the eyes, amaurosis, tremors of the muscles of the neck, lying down, or falling, and general convulsions may precede death. This may occur in a few hours or it may be delayed if the lesions are restricted. In case of survival, coldness and œdema of the extremities and sheath have been observed. The lesser hemorrhages may terminate in recovery if there is no attendant incurable disease. In anthrax, glanders, cancer, tuberculosis, septicæmia, etc., a favorable issue is not to be looked for.
Duration. Termination. In severe cases a fatal issue may be expected in from five hours to five days. In the milder cases which make a temporary recovery there is great danger of a second hemorrhage from the new vessels in the tissue undergoing organization or from the adjacent degenerate liver tissue. The course of the affection may be altered by such complications as arthritis (Dieckerhoff), pneumonia, pulmonary thrombosis (Leblanc), enteritis or peritonitis (Cadeac).
Treatment is usually of no avail. Rest, and the administration of laxatives and hæmostatics, have been especially recommended. Of the latter, ergot by the mouth or ergotin subcutem, tends to contraction of the blood-vessels and to check the flow. Ferric chloride is also used, though apt to interfere with hepatic function. Tannic acid, hamamelis, and other astringents may be used instead. Cold water, snow or ice applied to the right hypochondrium may act as a check to the hemorrhage. Unless in purely traumatic cases in an otherwise healthy liver, a recovery is at best temporary, and the already degenerate liver is liable to relapse at any moment. In horses and dogs, therefore, recovery is by no means an unmixed good. Meat producing animals that recover should be prepared for the butcher.
Forms of hepatitis: Parenchymatous hepatitis. Definition: Degeneration of hepatic cells. Relation to enteritis and nephritis. In horse—causes:—as in congestion, pampering, spoiled fodder, malt, inundated meadows, chill, overfeeding, hot moist climate, hæmoglobinæmia, infection. In cattle—causes:—forcing ration, hot weather, overwork, infection. In dog—causes:—infection from alimentary canal. Lesions: Enlarged, softened liver, round edges, a week later yellow atrophy, granular on section, bloodless. Acini with indefinite margins, cells granular, nuclei lost. In dog centres of softening. Symptoms:—in horse: Attack sudden, rigor, fever, dullness, prostration, yellowish red mucosæ, unsteady gait, slight colic, anorexia, urine decreased, glairy, brownish red, groaning in defecation, excited circulation and breathing, increased icterus by third day, fœtid, colorless diarrhœa. Diagnosis: Coincidence of fever, prostration, icterus, painful defecation, fœtid diarrhœa, light color of stools, tenderness and flatness on percussing hepatic area. From influenza by absence of watering eyes and contagion. Prognosis in horse: Very grave unless urine is free. Treatment in horse: Portal depletion, calomel, ipecacuan, salines, diuretics, fomentation of loins, antiseptics, derivatives, mineral acids, bitters. Careful laxative diet in convalescence. Symptoms in cattle: Slower onset, anorexia, dullness, depression, drivelling saliva, grinding teeth, icterus, constipation, later fœtid diarrhœa, pale colored stools, recumbency, groans on rising, arching back, tender right hypochondrium, fever. Prognosis grave. Death in five to six days. Treatment as in horse: Only saline laxatives. Symptoms in dog: Muscular tremors, staring coat, hyperthermia, icterus, fœtid breath, ventral decubitus, extreme prostration, anorexia, tender right hypochondrium, diminished urine, death in two or three days. Treatment in dog: Calomel and jalap, diuretics, laxatives, derivatives, germicides, in convalescence, mineral acids, bitters, careful diet.
The different forms of inflammation of the liver are distinguished according as they affect, especially the hepatic cells and tissue of the acini (parenchymatous), as they result in suppuration (suppurative, catarrhal, abscess), as they cause necrobiosis in nodular masses (infectious or necrotic), as they lead to fibroid thickening under the peritoneum and proper capsule (perihepatitis); or as they cause general fibroid induration of the organ by increase of its connective tissue (cirrhosis).
The characteristic morbid lesion in this disease is the degeneration of the liver cells, loss of their protoplasm and nuclei and of their normal functions. It may be circumscribed to limited areas, or may affect the liver, generally. As the hepatic functions, are so intimately related to those of the bowels and kidney, the affection is usually accompanied by inflammations of these organs as well.
Causes in horses. The same general causes which produce congestion, may also determine the further morbid stage of inflammation. Cadeac mentions a case which developed in a horse kept alone and idle in the stable. He makes no mention of condition, food, cleanliness nor ventilation. Haubner and Franzen have traced it to a diet of malt or of hay harvested from inundated meadows. Zundel records a case following exposure to extreme cold. More commonly the disease is secondary to the overtaxing of the liver, by heavy feeding in warm moist climates, or in hæmoglobinæmia, or to the arrest of the micro-organisms of the food, or of infectious diseases.
Causes in Cattle. These suffer rarely, but from essentially the same conditions. It has followed aphthous fever (Eletti), and arisen under a forcing ration, in hot weather (Callot, Cruzel), or under overwork (Cruzel).
Causes in Dogs. Most cases result from infection by way of the stomach and intestines, or by the transfer to the liver of the ptomaines and toxins of such infections. It is thus related in its origin to catarrhal jaundice and hyperæmia.
Lesions. In the earliest stage with albuminoid exudation into its substance the liver may be greatly enlarged, its sharp edges rounded, and its consistency softened. After a week’s illness atrophy may have set in and the organ appears shrunken and of ocherous yellow. In the early stages there may be sanguineous engorgement, the cut surface may bleed freely, and small extravasations may show throughout the liver substance, later the clay yellow hue, the granular aspect and the absence of blood on the cut surface are characteristic. The margins of the adjacent acini are indefinite or lost, and under the microscope the hepatic cells are charged with granules (albuminoid, fatty and pigmentary), while the nuclei are no longer demonstrable.
In cattle the liver may be double the normal size and at first of a deep purple red, which may change later to the earthy yellow.
In dogs the liver is tumid and yellow, and marked by small pea-like centres of softening. There is marked softening and the microscope reveals the characteristic degeneration of the hepatic cells.
Symptoms in the Horse. These resemble those of congestion rendered more intense and therefore somewhat less obscure. The attack is usually sudden, there may be rigor followed by hyperthermia, dullness, pendent head, drooping eyelids, injected conjunctiva with a yellowish tinge, unsteady gait and slight indications of colic. There is anorexia, partial suppression of urine, and what is passed is thick, glairy and brownish red, fæces are passed with pain, and groaning, probably from compression of the liver, the heart beats violently, while the pulse is small, breathing accelerated and perspiration abundant. The temperature rises (101° to 106°) and remains high throughout unless lowered through biliary intoxication. Percussion over the liver and especially on the right side shows increased area of dullness and marked tenderness. On the second or third day the icterus usually increases, and a slight fœtid diarrhœa may set in with marked fœtor of the pale or colorless discharges. The jaundice is not, however, a criterion of the danger, as it may become less marked or entirely disappear because of the extensive degeneration of the hepatic cells and the arrest of the formation of bile.
Diagnosis in the horse. The disease is recognized by the coincidence of fever, with great depression, icterus, painful defecation, constipation followed by a fœtid diarrhœa with lack of color in the stools and by increased area of dullness and tenderness in the region of the liver and especially on the right side. From influenza which it resembles in many respects, it is distinguished by the absence of watery discharge from the eyes, and by the entire absence of all indication of contagion. The cases occur one at a time.
Prognosis in the horse. The disease is exceedingly fatal. When the kidneys remain active, the poisons are eliminated and there may be hope of recovery, but when urine is suppressed an early death by poisoning is to be expected.
Treatment in the horse. A most important indication is to secure depletion from the portal system. Calomel 1 dr., aloes 4 drs., ipecacuan 1 dr. may be given in bolus, and followed by small daily doses of sulphate and nitrate of soda with bitters, with or without the ipecacuan. Action on the kidneys is essential to secure elimination of the poisons which threaten a fatal poisoning if retained. To favor the same action fomentations may be applied to the loins. The frequent presence of pathogenic microörganisms either in the bowels or liver suggests the use of germicides (salol, salicylic acid, salicylate of soda, naphthalin, naphthol, beta-naphthol, etc.) as in catarrhal jaundice. Sinapisms or blisters applied to the right side of the chest and over the short ribs may be useful, and after the subsidence of the more violent symptoms, dilute mineral acids and especially nitro-muriatic acid may be resorted to in combination with diuretics and bitters.
When appetite returns succulent, laxative, non-stimulating food in small quantity should be given. Wheat bran mashes, carrots, turnips, potatoes, apples, fresh grass, ensilage may be adduced as examples. Throughout the disease the ingestion of an abundance of pure water should be encouraged.
Symptoms in the ox. These may appear more tardily than in the horse, loss of appetite, staring coat, dullness, pendent head and ears, unsteady movements, rigors, drivelling of saliva from the mouth and grinding the teeth are usually noted. To these are added the more diagnostic symptoms of slight (or severe) jaundice, constipation followed by a fœtid light colored diarrhœa, a strong disposition to remain recumbent, marked suffering attendant on rising, arching of the back when up, and tenderness on percussion over the right hypochondrium. The temperature gradually rises, though more slowly than in the horse, and may again descend under a profound poisoning.
Course. The disease reaches its acme in four to six days, and generally has a fatal issue.
Treatment, is on the same lines as for the horse only as a purgative, sulphate of soda may advantageously replace the aloes.
Symptoms in the dog. The symptoms are those of congestion in an exaggerated form. There are muscular tremors, erection of the hair, followed by rising temperature up to 105° or 106°, an icteric hue of the mucosæ, the pulse is accelerated, strong, irregular, respiration rapid, panting, fœtid breath, ventral decubitus, and prostration extreme. Appetite is completely lost, the bowels become relaxed, the stools fœtid, the right hypochondrium painful on pressure or percussion, and the urine greatly reduced and icteric or suppressed. This feature of urinary suppression, determines a rapid poisoning and death in two or three days.
Treatment must follow the same lines as in other animals, a purgative of calomel and jalap, followed by diuretics, laxatives, derivatives, and above all germicides. In case of survival mineral acids, aqua regia, bitters, and a carefully regulated diet will be in order.
Causes in horse: pyæmia, omphalitis, thrombosis, infection, biliary calculi, concretions or parasites, foreign bodies, hot, damp climates, strangles, brustseuche, glanders, endocarditis. Lesions in horse: from parasites and mechanical irritants, pea-like or hazelnut; embolic abscess, pin head to hen’s egg; infection from strangles, foreign bodies, etc., may be of large size, and burst into adjacent organs, the peritoneum or externally. Symptoms in horse: of pre-existent malady, remitting fever, successive chills, intermittent icterus, hypochondriac tenderness. Spontaneous recovery, aspiration, opening, antiseptics locally and generally. Lesions in ruminants; secondary multiple abscesses, bean-like or (with foreign body) very large, may extend into adjacent parts. Symptoms in cattle: fever, chills, jaundice, tympany, diarrhœa, dysentery, wasting, tender right hypochondrium. Treatment: as in horse. Causes in dog: foreign bodies, tumors, infections, blows, traumas. Lesions: traumatic abscesses, single, large, infectious abscesses multiple, small. Former fœtid. Symptoms in dog: hepatic congestion or colic, then chills, prostration, irritability, tenderness of right hypochondrium, nausea, vomiting. Treatment in dog: antiseptic aspiration, laparotomy.
Causes in the Horse. Hepatic abscess arises from a great many primary morbid conditions. As a secondary abscess it is seen in the different forms of pyæmia and especially in suppurative omphalitis in young animals. It may start in thrombosis determined by clots or septic matters carried from a distance through the portal vein or hepatic artery, in biliary calculi or concretions, in parasites introduced from the duodenum, in barbs or husks of the cereals that have penetrated through the biliary ducts, or in bacteria or their toxins which have been carried from the bowels, spleen or pancreas. The government veterinarians have found it a comparatively common lesion in the hot damp climate of Hindoostan, and a similar frequency has been noticed in west Africa. Among general affections it is liable to occur in strangles, contagious pneumonia, glanders, endocarditis of the left heart and phlebitis with the formation of thrombi in the lungs. In the two last named disorders, the affection takes place by the simple transference of detached clots to the liver to block its arteries or capillaries. Or it may be that micro-organisms are transferred in the same way. With modern views of suppuration the presence of the pyogenic organisms must be conceded.
Lesions in the horse. Cadeac distinguishes the different types of hepatic abscess as: 1st biliary abscess in which suppuration commences in the interior of the biliary ducts and usually from parasites or mechanical irritants introduced or from calculi or concretions formed within them: these rare abscesses contain biliary salts, pigments, and epithelium and acquire the size of a pea or hazelnut: 2d Metastatic abscesses which start in the arterial, portal, or capillary vessels, by the arrest of infecting clots, which determine a further clotting, the obstruction of the vessel, the accumulation of leucocytes and the formation of abscess of the size of a pin head or larger up to a hen’s egg, surrounded by a hæmorrhagic infarct softening in the centre: these are numerously disseminated through the liver: 3d Mechanical Abscess due to the penetration of foreign bodies or parasites: 4th Infection as in strangles. These may attain a large size, cause adhesion to adjacent organs, and rupture into the chest, the colon, stomach or peritoneum. The pus may even escape externally through the right hypochondrium.
Symptoms in the horse. These are always obscure and vary much with the source of the malady. If there has been a pre-existing hepatic malady the symptoms of that will be in evidence; if an omphalitis its existence may still be recognizable; if pulmonary or cardiac disease, that may be detected; if parasites, evidence of their existence may perchance be found; if gall stone, a previous violent hepatic colic with icterus may have occurred; and if intestinal septic disorder, there may be the testimony of intestinal troubles. The more diagnostic symptoms are a fever of a remittent type, one or several violent shivering fits, a marked jaundice which like the fever shows exacerbations, and a similar irregularity of the condition of the urine which may be successively of a dark brown, a deep yellow, and a transparent amber color. Tenderness and grunting on percussion of the right hypochondrium would be an additional aid in diagnosis.
Treatment. Death has been hitherto considered as the inevitable result, yet recoveries may ensue after rupture into the colon or through the abdominal walls. If the seat of the abscess can be ascertained its evacuation through an aspirator and the subsequent injection of an antiseptic would be appropriate. The concurrent use of antisuppurants like hyposulphite of soda, or sulphide of calcium would also be in order.
Causes in Cattle. Hepatic abscess is much more frequent in cattle, and is commonly a result of perforation by sharp pointed bodies (needles, pins, nails, wires, etc.) from the reticulum and rumen, or of parasites, or biliary calculi. Other cases are occasioned by the presence of tubercles, actinomycosis, or omphalitis.
Lesions in Cattle and Sheep. Secondary abscesses are usually multiple and disseminated through the organ, though Cadeac says they are more common in the left half. They vary in size from a bean to a pigeon’s egg, project often from the surface, and contain a viscid, creamy, yellowish or greenish pus. Abscesses dependent on foreign bodies often attain a great size, so as to contain a pint or quart of pus (Landel). They may make their way through the diaphragm, rumen, or abdominal wall leaving a thick cicatrix in the liver, or they may become slowly absorbed and dry up into a putty-like or cretaceous mass. Brusaferro found hepatic abscesses in lambs twenty to thirty days old—probably of omphalic origin.
Symptoms in Cattle are usually very obscure. Fever, shivering fits, jaundice, indigestion, diarrhœa or dysentery, emaciation, colics, tender right hypochondrium, and peritonitis may all be in evidence but the diagnosis is little better than a guess.
Treatment when possible at all would be on the same lines as for the horse.
Causes in the dog. According to Cadeac these are mostly foreign bodies (needles, pins, etc.) which have been swallowed, tumors of the liver or adjacent organs, phlebitis and thrombosis of the portal vein, pyæmia, septicæmia, and external injuries (kicks, blows, contusions, falls, etc.)
Lesions in the dog. As in the other animals traumatic abscess is usually solitary and large, secondary abscess multiple and small. The pus developed around a foreign body is reddish, greenish and fœtid, that of the metastatic abscess is usually whitish or yellowish and with a sweet odor.
Symptoms in the dog are those of hepatic congestion, or violent gall stone colic, followed by severe rigor, great depression, or irritability, and tenderness over the right hypochondrium. Nausea and vomiting is a marked symptom though not a diagnostic one.
Treatment. If the flaccid abdominal walls will allow of the locating of the abscess it should be treated by aspiration and antiseptic injections. It would even be admissible to perform laparotomy, stitch the wall of the abscess to the external wound, and empty it under due antiseptic precautions.
In ox, sheep, pig, dog, horse. Necrotic areas projecting on surface of liver. Causes: bacteria, toxins, from bowels, womb, navel. Lesions: In cattle dirty gray nodules in brownish red liver, nodules firm, granular, necrotic, elements do not stain, later leucocytes and fibro-plastic growth in periphery. In lambs the nodules are white, common to the lungs and pleura, pathogenic to rabbit. In pigs nutmeg liver, cells without nuclei, fatty, granular, pathogenic to rabbits, guinea pigs, rats and young pigs. In dog, nutmeg liver, with violet areas, and white spots, 1–2 lines, having granular, fatty cells without nuclei. Symptoms: fever, constant lying, tarry fæces, icterus, tender right hypochondrium, and those of the primary disease. Treatment: antisepsis of primary seat, and bowels, elimination by kidneys, general antisepsis, stimulants, etc. Case usually hopeless. Prevention.
This has been observed particularly in cattle, but also in sheep, pig, dog and horse. It is characterized by the formation of circumscribed areas of gangrene, becoming hard, dry, yellowish and usually slightly projecting beyond the adjacent surface. Its infected character is shown by the presence in the lesion and adjacent parts of the hepatic tissue of an abundance of bacteria, which, from the varied description, appear to differ in different cases. The cause may however be safely stated as one of the bacteria of gangrene. It is alleged with some show of reason, that the lesion may be determined by the action of toxins and ptomaines produced by bacteria in the alimentary canal and carried to the liver with the portal blood (Cadeac). The bacteria themselves commonly come from the same source, (Stubbe), but also from the uterus (Berndt), the mammæ (LeBlanc), and above all from the suppurating or septic umbilicus. McFadyean in five cases found a long slender bacillus, Hamilton in a single case in the horse found cocci, Rivolta in an infectious hepatitis in sheep found bacterium subtilis agnorum, and Semmer found the same condition in young pigs from micrococci introduced through the diseased umbilicus.
Lesions. In cattle the liver has a general brownish red, or greenish white color, and shows projecting, hard nodules of a dirty gray color more or less tinged with yellowish brown. The margins of these hard nodules are very sharply defined, and on section show a homogeneous granular surface, devoid of areas of softening or of connective tissue, and formed of the hepatic parenchyma in a state of necrobiosis. The granules and nuclear elements do not stain like those of healthy liver. As the disease advances the periphery of the nodule may be invaded by leucocytes and become the seat of a fibro-plastic hypertrophy (McFadyean) with the ultimate formation of cicatricial tissue (Stubbe).
In lambs Rivolta found the necrosed nodules standing out as white patches under the capsule of the liver, but similar lesions were met with in the lungs and pleuræ, an observation which has been confirmed by Hanbold. The affection was conveyed by inoculation to the rabbit.
In pigs Semmer found nutmeg liver, deep red or grayish yellow, hypertrophied, the hepatic cells swollen and divested of nuclei but containing fatty and pigmentary granules. It was inoculable on rabbits, guinea pigs, white rats and on young pigs.
In the dog, Courmont and Doyon found congested liver (portal congestion) with projecting patches of a deep violet color and sharply defined borders, and one to two lines in diameter, also salient white spots with distinct outlines. In the white spots the hepatic cells had lost their nuclei and were charged with fatty granules.
Symptoms. These are indications of hepatic disease. In parturient cows, Berndt noted fever (102° to 104°), anorexia, stiffness, cough, labored breathing, intense thirst, constant decubitus, and constipation followed by lowering temperature, tarry fæces and icterus. The region of the liver was very sensitive to pressure or percussion. In the other animals the symptoms appear to be largely over-shadowed by those of the primary disease, but the same general indications of jaundice, hepatic tenderness and digestive disorder are superadded.
Treatment when it can be intelligently adopted, consists largely in evacuation and antisepsis of the seat of primary infection, and of the prima viœ, and in maintaining elimination by the kidneys. In this way, as in congestion and hepatitis, the concentration of the poison is as far as possible counteracted, and an opportunity may sometimes be furnished for the recuperation of the liver cells. As a rule, however, the case is hopeless, and thus preventive measures, by cleanliness, disinfection and antisepsis of the ascertained sources of the infection are indicated.
Inflammation of capsule of liver (external and Glisson’s). Causes: Traumas, infective diseases, phlebitis of the portal vein, chill, distomatosis. Lesions: Peritonitis and inflammation of the capsule in patches, yellowish gray exudate, fibroid thickening or pus. Adhesions to adjacent objects. Thickening of trabeculæ. Symptoms, tardy respiration and circulation, tender hypochondrium, colics, diarrhœa, painful defecation, moan with expiration. Slight cases recover. Sequelæ: compression of portal vein or bile duct, gastric catarrh, piles, etc. Treatment: Salines, alkaline diuretics, mineral tonics, bitters.
This is inflammation of the external capsule of the liver and Glisson’s capsule. It may arise from direct mechanical injury, or by extension of inflammation from adjacent structures, such as the peritoneum. It may also complicate contagious pneumonia in the horse, tuberculosis in the ox, pneumoenteritis in pigs, and also phlebitis of the vena portæ (Cadeac, Morot). It may follow a chill, or distomatosis.
Lesions. These are essentially peritonitis circumscribed by the liver, and extending to the proper capsule, and its vaginal investments of the hepatic vessels. It is usually limited to certain spots which become the seats of a yellowish gray exudation, with a tendency to fibroid development and thickening, but sometimes degenerating into pus. The deposits on the outer side of the hepatic peritoneum may develop false membranes and fibrous adhesions to surrounding objects, the diaphragm, omentum, stomach or intestine. The deposits under the peritoneum lead to similar fibrous development with hypertrophy or thickening of the capsule, the trabeculæ extending thence into the liver and the vaginal sheaths of the vessels. Such areas of thickening are revealed as depressed spots or patches of a white color, and showing a firm fibrous, pearly appearance when incised. Such lesions are not uncommon in the livers of horses, cattle and swine. In the pig they may have a violet, or brownish red color, but with spots of other colors—grayish or brownish (Kitt).
Symptoms. Dopheïde, who has studied the disease in cows and to a less extent in horses, found a reduction in pulsations (26 per minute) and respirations (6 per minute) in connection with a mild peritonitis, intestinal catarrh, colicy pains and diarrhœa. The conjunctiva is pale, the pulse compressible, the respirations unequal and accompanied by a moan, and the appetite impaired or lost.
If confined to mere spots on the liver, a restoration to apparently vigorous health may take place, but if extensive it may lead to compression and obstruction of the portal vein or bile duct, or to compression and atrophy of the liver, with corresponding symptoms.
Treatment. As in other congestions of the liver, the use of salines to deplete the portal system, and of alkaline diuretics are especially indicated, to be followed by bitters and mineral acids. Sinapisms and other counter-irritants to the region of the liver are of great service. If not complicated with abscess, or microbian infection, cases of this kind will often do well.