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.