Part 83

There is usually some œdema of the lung, larnyx and pia mater.

There are catarrhal lesions of the abomasum and entire intestinal canal with granular degeneration of the epithelium and spots and patches of arborescent congestion and hæmorrhage. The icteric tint is usually distinct.

Prognosis is always grave. Acute cases are almost always fatal. Chronic cases due to eating lupins in which the poison is relatively weak, or a very restricted amount of the more poisonous lupins, may recover. This mortality is very serious in the affected districts 5.8 per cent. of all the sheep of some districts in Pommerania perishing yearly from this affection and entailing the loss of almost the same number of lambs (Von Below-Seleske).

Prevention. Radical prevention can be secured by the exclusion of lupins from the ration. Where this is undesirable the fields that produce poisonous lupins can be ascertained and devoted to the production of other crops. When a crop of lupins has already been produced on a dangerous field the poison may be extracted from the fodder or subjected to the action of an antidote. Fortunately the poison is concentrated on the surface of the lupin and is easily washed off.

Dammann advises to leave the cut forage exposed to the rain so that the poison may be washed off. A more prompt and effective plan would be to put the fodder under a stream of water from a hose, and it could be fed while still fresh and unaltered. Friedberger and Fröhner directs that the forage be steeped for forty-eight hours in a soda solution (1:100) to dissolve off the offensive matter, after which it may be washed and safely fed.

Glaser would put the lupins in a silo, in alternate layers with some material which rapidly undergoes acid fermentation (brewers grains, maize, pulped roots). The acid renders the poison insoluble and is directly antidotal. To develop this acid it is important to put the materials into the silo before they have become too far matured.

The destruction of the poison by steaming the fodder under a pressure of two atmospheres, as recommended by Kuhn and Roloff requires a too elaborate apparatus for ordinary use.

Therapeutic treatment. The first desideratum is to render insoluble any poison which has already entered the alimentary canal. Alkalies, as solvents and distributers of the poison must be carefully avoided and acids (acetic, nitric, hydrochloric, sulphuric) freely used. These may be mixed with the drinking water or given from a bottle. If appetite is still retained, they may be mixed with the food, or acid aliment (sour ensilage, old grains, or fermented swill) may be supplied.

The next resort is a purgative to eliminate the poison from the alimentary canal. But the cathartics usually given to the ruminants are dangerous. Sulphate of soda undergoing decomposition, furnishes an alkaline solvent for the poison. Castor oil is therefore to be preferred.

An abundance of water will favor the action of both bowels and kidneys and hasten the elimination of the poison which may have been already absorbed into the system.

European writers recommend the use of the flesh as human food, unless the animal had reached the last stage of the disease.

Symptoms of Lupinosis in the Horse. There is always the history of the presence of lupins in the oats, or of lupin straw as a food or litter. Though less fatal than in sheep the disease sets in with great severity, the symptoms referring especially to gastro-enteritis, and disorders of innervation. There is complete anorexia, impaired sensibility, dullness and stupor, the head resting on the manger or drooping with the nose near the ground. There is grinding of the teeth, colicy symptoms, and constipation, the fæces being passed as a few small, hard balls covered with mucus and fœtid. Urine is passed frequently in small amount and albuminous. There is more or less hyperthermia (rising at times to 102° to 103°), the respiration is hurried (36 to 40 per minute) and pulse is rapid (60 per minute). Jaundice is usually present but less prominent than in sheep. When moved the animal sways unsteadily or staggers. Butzert notices, in addition to the above, a thick orange colored discharge from the nose, and the formation of sores and scabs (mummification) of the lingual mucous membrane, of the lips, of the skin, of the face, and of the pastern, and swelling of the lower parts of the limbs.

Diagnosis. The development of disease with the above symptoms, in the inmates of a single stable, or in horses having a common ration, in which the lupines are found, will make diagnosis easy and reasonably certain.

Prognosis is hopeful or confident. The disease is not fatal in the horse.

Treatment should follow the same lines as in sheep.

Allied or identical diseases. Friedberger and Fröhner quote a number of outbreaks of hepatic inflammation or disorder with icterus in the absence of lupins, but on rations that were otherwise faulty. Haubner describes a “malignant icterus” in sheep fed on malted potatoes; Sander records a “hepatic typhus” in the horse when fed on inundated pastures; Reinemann and Jansen speak of a similar affection in animals fed on the straw of peas, beans and vetches.

CONGESTION OF THE LIVER.

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.

CONGESTION OF THE LIVER IN THE HORSE.

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.