Part 75

Bromide and iodide of potassium have been found to be effective in reducing hepatic enlargement and thus in conducing to a more healthy activity of the liver.

Ipecacuanha, Euonymus, etc. These agents are more or less hepatic stimulants and may be found beneficial as combined with the laxative or alkaline agents in securing a better functional activity in cases of torpor or deranged function.

Tonics, Bitters. Tonics are often useful when the health has been undermined by long continued hepatic disorder. The iron tonics are as a rule contraindicated as tending to check secretion of bile, unless they can be given with alkalies. Iron sulphate or chloride, combined with sodium or potassium carbonate so as to establish a mutual decomposition will obviate this objection. The vegetable bitters (gentian, cascarilla, calumba, salicin, serpentaria, aloes, nux vomica) combined with alkalies are often of great value. Quinia, like opium, checks secretion and is to be avoided or used with judgment and in combination with cholagogues.

HÆMOGLOBINÆMIA. AZOTÆMIA. AZOTURIA. HÆMOGLOBINURIA. TOXÆMIA FROM IMPERFECT HEPATIC FUNCTION.

Definition. Theories, of hysteria, uræmia, spinal myelitis, myelo-renal congestion, rheumatic lumbago, myosito-myelo-nephritis, rheumatic chill with destruction of muscle albuminoids. Yet it occurs in our semi-tropical midsummer with a temperature of 80 or 90, in spring and autumn, and rarely even in the cold, damp stable in midwinter in the absence of exercise. Constant conditions: One or more days absolute rest, preceding steady work, a strongly nitrogenous ration, continued during the rest, sudden active exertion accelerated breathing and unloading of peptones and proteids from portal vein and liver into the general circulation. Sanguineous albuminuria from excess of albuminous food, free ingestion of water, suppressed milk secretion, forced marches. Transfusion of blood. Excess of albumen dangerous, excess of red globules not dangerous. The blood concentration of diuresis or diaphoresis is not dangerous. Continuous muscle decomposition from work bars the disease. Stable miasm untenable. Poison may be drawn suddenly from the enormous mass of blood in the liver, spleen and portal system. The absence of icterus antagonizes the bile theory. Benzoic acid, unaltered peptones, and glycogen are examples of elements destructive to blood. Normal destruction of red globules in liver, spleen and bone marrow. Sudden access of resulting hæmoglobin to the blood. Other products of disintegrated globules. Poisons from food, and antitoxic action of liver in presence of glycogen. Carbon dioxide favors solution of red globules. Theories of hæmoglobinæmia in man. Lesions: Blood black, diffluent, iridescent, has no avidity for oxygen, with excess of urea and extractives, serum of clot red, globules, small, pale, distorted, not sticky, extravasations, liver, enlarged, congested, blood gorged, spleen congested, swollen: Lumbar or gluteal muscles pale, infiltrated, with loss of striation; bone marrow congested, hemorrhagic; kidneys congested infarcted; urine dark brown or red, with excess of urea and hæmoglobin. End of spinal cord has congestion or infiltration. Symptoms: History of high condition, constant work, high feeding, a day’s rest, then exercise and attack. To full life, follows flagging, droops, moves one or both hind limbs stiffly, knuckles, drags toes, crouches, trembles, perspires, breathes rapidly, is tender on back, loins, croup or thigh, muscles firm, paretic, and drops unable to rise. Urine retained, brown, red or black, sometimes glairy, later may have casts. Appetite may return. In mild cases, stiffness, lameness, with or without visible muscular lesions or tremors. Urine glairy, dense, with excess of urea and nitrogenous products. Recover under careful feeding and exercise, and relapse under original causes. Progress: May recover under rest. In bad cases accelerated breathing and recumbency forbid rest and recovery. Recovery in a few hours or after a week. Urinary casts with renal epithelium, imply nephritis and grave conditions. In persistent paresis, muscles waste. Modes of death. Mortality 20 per cent. Diagnosis, by history of onset, etc. Prevention: When highly fed and hard worked, give daily exercise, with comparative rest, reduce ration, and give laxative or diuretic. Plenty of water. Treatment: Rest, sling, diffusible stimulants, bleeding, bromides, water ad libitum, fomentations, unload liver and portal vein, purgative, eserine, barium chloride, enemata, diuretics, for remaining paresis, derivatives, strychnia, diet, laxative, non-stimulating, restore to work gradually.

Definition. An acute auto-poisoning occurring in plethoric horse on being subjected to active exertion after a period of idleness, and manifested by great nervous excitement and prostration, paresis commencing with the hind limbs and the passage of hæmoglobin in the urine.

Nature and Causes. The most varied conclusions as to the nature of this disease have been put forward by different authors. In England, Haycock called it hysteria, mistakenly supposing that it was confined to mares, and Williams attributed it to uræmic poisoning, conveniently ignoring the fact that the sudden manifestation of the most extreme symptoms in an animal which just before was in the highest apparent health and spirits contradicted the conclusion. In France (Trasbot) and Southern Europe (Csokor) it has been looked on as a spinal myelitis, a conclusion based on the disturbed innervation of the posterior extremities in the great majority of cases, but which is not always sustained by the pathological anatomy of the cord. In Germany veterinarians have viewed the disease from widely different standpoints. Haubner calls it myelo-renal-congestion (Nièren-Rückenmarks): Weinmann, a rheumatic lumbago; Dieckerhoff defines it as an acute general disease of horses, manifested by a severe parenchymatous inflammation of the skeleton muscles, with a bloody infiltration of the bone marrow, especially of the femur, and with acute nephritis and hæmoglobinuria. He attributes the attack to exposure to cold. If this were the real cause the attack would be far more common in very cold weather when the horse is suddenly exposed to cold drafts between open doors and windows, than when he is harnessed and driven so as to generate and diffuse animal heat. Yet attacks in the stable are virtually unknown, and in almost every instance the onset occurs during a short drive. Friedberger and Fröhner say that the epithet rheumatismal may be correctly applied to almost all cases that we meet in practice. They quote Goring as having produced the disease experimentally by exposure to cold, and go on to explain that rest in the stable before the attack causes the extreme sensitiveness to cold that is generated by a warm environment. The implication of the lumbar, pelvic and femoral muscles they explain by the stimulation of the nutritive metamorphosis by the action of cold on the sensitive nerves of the skin. The effect of this cutaneous irritation is exaggerated by the heat of the stable to which they have been previously subjected. The products of the destruction of the albuminoids of the muscles, pass into the blood as hæmoglobin, and produce the ulterior phenomena. The muscles of the hind quarters especially suffer because of their greater exposure and because they are subjected to the hardest work in propelling the animal machine. In this connection they quote the experiments of Lassar and Nassaroff in which sudden exposure to cold determines parenchymatous degeneration of muscles; also the cases of paroxysmal or winter hæmoglobinuria in certain susceptible men whenever they are exposed to an extremely low temperature.

There are serious objections to the acceptance of this as the essential cause, among which the following may be named:

1st. The disease is not confined to the cold season but occurs also at midsummer when the outdoor temperature is even higher than it is in the stable.

2d. In our Northern States it appears to be more common in spring and autumn or early winter, when the extreme colds have either already passed, or have not yet set in, but when the abrupt changes of weather (rain-storms, etc.) are liable to shut up the animal indoors for a day or more at a time.

3d. The popular names quoted with approval by these authors—Monday disease, Easter disease, Whitsuntide disease—indicate the prevalence in Europe also, of the malady in the milder, or more temperate seasons rather than during the prevalence of extreme cold.

4th. The fact that the disease rarely or never occurs in the stable, no matter how cold the season, how open the wooden walls or floor, nor how strong the draft between doors or windows, shows that the theory of cold as the sole or main cause must be discarded.

It is not necessary to ignore the action of cold as a concurrent factor in certain cases, or as a stimulant to reflex vaso-motor paresis, to muscular metamorphosis and the increase of hæmoglobin in the blood. It is only necessary that this should be held as subordinate and non-essential to the final result. Several other factors that are accorded a subordinate place by these writers, are so constant and so manifestly essential that they must be allotted a much more important position in the list of causes.

A =period of rest= is a constant precursor of an attack. The more extended the inquiry the more certain we become that a short rest is a prerequisite to equine hæmoglobinæmia. The horse that is kept at daily steady work may be said to be practically exempt. Even the non-professional observer recognizes the fact and names the disease after the weekly or yearly holiday or rest day which was the occasion of it. To him it is the Monday morning disease, the disease of the day following Thanksgiving, Christmas, New Year, or Fourth of July. It is the disease of wet weather, of heavy snowfalls, of the blizzard, or of the owner’s absence from home, of any time that entails one or two days of absolute inactivity in the stall.

But again the affection does not appear in the horse that is absolutely idle for a length of time. It is the =short period of rest in an interval of otherwise continuous work= that determines it. In short the subject must be in good muscular condition and with a hearty, vigorous appetite and good digestion. The short unwonted rest interrupts the disposal of the rich products of a vigorous digestion, and tends to overload the portal veins, the liver, the blood and tissues with an excess of proteids. The condition of the animal is so far one of plethora.

Another feature that bears this out is that the attack comes only in the animal that is =heavily fed on a strongly nitrogenous ration=. It is not the disease of the horse kept on straw, or hay, or which receives a limited amount only of grain. It does not occur in the animal which has its grain suspended or materially reduced during the one or two days of idleness. It does not select the horse that has had a laxative either in the form of food or medicine. This last may increase the sensitiveness to cold, but it certainly lessens the tendency to hæmoglobinæmia. The most rational explanation appears to be that it affords this protection by interfering with the thoroughness of digestion and absorption, by securing elimination from the portal veins and liver, and by reducing the amount of albuminoids in the blood.

A blood abnormally rich in albuminoids, as it is in the transient plethora induced by a short period of rest, in the well-conditioned working horse, without any restriction of his diet, may therefore be set down as one of the most important factors in producing hæmoglobinæmia. Nor is this without approximate examples in human pathology. Von Bamberger has shown that “hæmatogenous albuminuria” will occur in healthy individuals when there is an excess of albumen in the blood-plasma, as after a too free use of albuminous food, or after suppression of the milk secretion (Landois). A similar result comes from increase of blood pressure, as after drinking freely, or when, under emotion or violent exertion, the heart’s action is increased in force and the blood is thrown with greater impetus into the large renal arteries. Senator has found albuminous urine to attend and follow, for several days, upon forced marches made by young recruits. Here the muscular work is added to the increased blood tension superinduced by the more active contractions of the heart.

In this connection it is interesting to trace the changes in the blood after transfusion. The dilatability of the capillaries enables the system to accommodate itself to a very great increase in the volume of blood An increase of 83 per cent. may be borne without serious results, but above this limit there is increasing risk and an increase of 150 per cent. entails immediate danger to life. In the restoration of the blood to its normal condition, the secretion of water sets in promptly leaving an excess of albuminoids and blood globules. The next change is in the albuminoids which in two days are almost entirely transformed into urea. This leaves the blood abnormally rich in globules (Panum, Lesser, Worm-Müller), the red globules break up much more slowly and may still be in excess after the lapse of a month (Tscherjew).

In this light, temporary plethora cannot of itself be accepted as the main or essential cause of the disease. It must be admitted to be a more constant and important factor than the mere exposure to cold, but of itself it is inadequate to the production of hæmoglobinæmia. In the absence of exertion the general plethora fails to produce the specific disease; again, after transfusion a plethora of albumen lasts for one or two days, but hæmoglobinæmia sets in only in the first few minutes after the animal starts out from the stable, (never after an hour or two at work): once more, excess of globules may last for a month, but with steady work there is no danger of this disease, after the first mile or two has been traversed, on the first day of the resumption of labor.

A similar plethora of albuminoids and globules may be induced in a plethoric animal by a profuse diarrhœa, diuresis or perspiration, the blood having been robbed of its watery constituents, and concentrated especially as regards its globules and albuminoids, but hæmoglobinæmia never occurs as the result of such an artificial concentration. On the contrary a free secretion by the bowels or kidneys is of the greatest value in cutting short its progress after it has set in.

The doctrine of poisoning by hæmoglobin produced by excessive work and disintegration of the muscles is equally insufficient to account for an attack. Excess of muscular work and of muscle-decomposition-products, would not reach its maximum within the first few minutes after the animal has started from the stable, but, other things being equal, would increase with the continuance of work and the accumulation in the blood of a constantly increasing amount of these products. The sharp line of restriction by which the attack is limited to the initial period of work, while it is never seen after hard work continued for hours in succession, rules out this from the list of essential causes. It may be that the products of muscular decomposition aggravate the attack, but to set them down as the cause of the attack is to beg the whole question and to contradict the truth that continuous and severe muscular work with its consequent increase of waste products is a direct bar to the development of the disease. It should be noted in this connection that the increase in the waste of nitrogenous bodies, as shown by the increase of urea, is dependent far more on the amount of nitrogenous matters ingested than on the muscle work or decomposition. In eleven hours just before ascending the Faulhorn, Fick passed 21.686 grs. of urea per hour; in eight hours ascending the hill, 12.43 grs. per hour; and in six hours after the ascent he passed 13.39 grs. per hour.

A general survey of the field shows that it is not the simple increase of any normal waste product in the blood which determines hæmoglobinæmia, and on the other hand the suddenness and severity of the attack bears all the marks of a profound poisoning. The nature of the poison has not yet been definitely ascertained, yet one or two hypothesis may be hazarded, as furnishing a working theory, in anticipation of the actual demonstration which may be expected in the early future.

The action of a stable miasm as claimed by some writers is contradicted by the fact that the disease does not develop so long as the animal is left to inhale that miasm, and on leaving the stable, the life and vigor are usually remarkable.

The morbific agent must be sought in some source from which it can be supplied with great rapidity under the stimulus of a short but active exertion. The chylopoietic viscera furnish such a source. The healthy liver contains one-fourth of the entire mass of the blood. The torpid congested liver of the vigorous high conditioned horse, after a short period of idleness, on full, rich feeding, must hold much more than this normal ratio. The spleen, the natural store-house or safety valve of the portal veins, is also gorged with this liquid in the high fed, idle animal. This organ which is always turgescent after meals, is especially so in the over-fed horse, which for twenty-four hours has been denied the opportunity of working off by exercise, the superfluous products of an active digestion and absorption. Then the whole of the portal veins and the capillaries in which they originate are surcharged with rich blood which cannot make its way with the necessary dispatch through the inactive liver.

In this condition there is incomparably more than a quarter of the entire mass of blood, enriched to the highest degree in proteids, ready to be discharged through the liver and hepatic veins into the general circulation. Under the action of the hurried breathing and circulation, caused by the sudden and active exertion, this whole mass of rich blood is speedily unloaded on the right heart, the lungs and the systemic circulation. One can hardly conceive of a more effective method of inducing a sudden plethora, with an excess of both globules and albuminoids.

The presence of actual poisons in such blood is not so easily certified.

The absorption of bile elements and especially of taurocholic acid, which is a solvent of the red blood globules, and would set free their globulin might account for the characteristic condition of the blood. The powerful aspiratory action of the chest, would speedily empty the whole of the liver blood vessels, and lessening their tension below that of the biliary radicals would determine an active absorption of bile or of the more diffusible of the bile elements. A manifest objection to this view is the absence of an icteric tint in the mucous membranes of the affected animals. The visible mucosæ are of a brownish red hue, such as might come from hæmoglobin dissolved in the blood serum, rather than the yellow tint which might be expected from bile pigment. The theory of poisoning by bile acids therefore, would require an explanation of concurrent suppression or decomposition of the bile pigments.

Other sources, however, offer solvents for hæmoglobin, benzoic acid, which is derived from a cellulose in the fodders, and forms the source of hippuric acid, dissolves red globules (Landois). In the over-fed horse with active digestion, but inactive body and liver, this must accumulate in the liver, spleen and portal system, and when suddenly drawn into the blood without time for oxidation in the liver it will contribute to the condition of hæmoglobinæmia.