Part 41

All this throws light on the immunity of horses on our western prairies and plains. Feeding on the indigenous grasses fresh or made into hay, they are saved from the noxious influence of those artificial products which are found in all countries to determine the development of broken wind. It needs not that we adopt the popular notion that any special plant growing in these pastures ensures the safety of the equine races. It is merely a repetition in the Western Hemisphere of the experience so long before obtained in the case of Spain. Parallel with the progress of cultivation in our western lands, we see this malady advancing. Fifty years ago it was virtually unknown in Michigan and adjacent states whereas now these states can almost emulate New York in the relative number of their victims. It must not however be supposed that this cultivated fodder is the sole cause of the westward march of this malady. With improved agriculture have come better roads, spring wagons and driving at a pace which was comparatively unknown to the early settlers.

In California the condition of Spain was for long pretty accurately repeated. With no winter worthy of the name, troops of horses were left at pasture throughout the whole year and those that were stabled subsisted chiefly on natural hay in which the indigenous grasses were commingled with white—but no red—clover. California long retained the reputation of having no broken winded horses.

In our Eastern states where the disease was thirty years ago so notoriously prevalent, the fields of luxuriant red clover might well have excited the envy of the English farmer. The hay made from this, full of seed and dust was given without stint to the farm horses, which during the rigor of the winter were often shut up in stable for a length of time continuously and dangerously gorged themselves with this provender. In the Eastern States with a steady falling off in the red clover, there is also a corresponding reduction in the number of cases of heaves. The grain allowed them, a mixture, supposed to consist of Indian corn, oats and buckwheat, given as a dry coarse flour, was little calculated to counteract the effects of the clover hay, and the entire absence of turnips and other succulent roots as a farm crop precluded their use as a preventive of the malady. We need not forget the prevalent ambition to possess a fast trotter, nor the effect of the climate on the air passages (See chronic bronchitis) in estimating the causes of this malady in the Eastern states.

The mere overloading of the stomach is a potent cause of the development of heaves. The horse is above all other animals compelled to undergo hard work on a full stomach. Coleman cites the experience of the coaching days when each horse had 20 lbs. of oats daily and not more than 5 lbs. of hay with no water before work. These horses were driven fast for long stages yet they never contracted broken wind under this treatment. Farmers’ and millers’ horses on the other hand were most subject to the disease because gorged continually with hay chaff and mealy food, and worked in this condition. “Nimrod” who confirms Coleman’s statement says “I have taken some pains to ascertain this fact by my own personal inquiries. One proprietor who has nearly fifty horses at work—many of which are in as fast coaches as any that travel on the road—assured me lately that he had not a broken winded horse in his yard; whereas before he stinted them in their hay he generally had one to five in that state.” Percivall testifies to its comparative infrequency in the English cavalry horses, which have their diet carefully regulated. Hay musty from bad harvesting or other cause and such as is rank from growing in low wet localities are caeteris paribus more injurious than good hay.

Every day observation shows that driving a horse upon a full stomach often causes broken wind and nothing will more surely aggravate it, when it does exist. The same remark may be made of the drinking of large quantities of water after feeding and just before going to work. Gross feeders are above all others the subjects of the complaint.

The question arises how a disturbing cause operating directly upon the digestive organs should affect the respiratory, in such a marked and permanent manner. It cannot be because of the gastric and abdominal distension since pregnant mares though in a state of much greater plentitude, are not thereby rendered liable to broken wind, and if they have previously suffered from this infirmity, the symptoms are usually less marked when breeding. The explanation first advanced by Dupuy appears to be the correct one. The lungs, the stomach, and certain other organs derive innervation from the vagus nerve, and certain disturbances of the stomach and intestines so impair the function of this nerve that the lungs are affected, at first functionally and afterwards structurally. In support of this view is the fact that broken wind is usually associated quite as much with digestive as respiratory derangement. The horse though a heavy feeder becomes unthrifty, hidebound and emaciated; his dung is passed in an undigested state like so much chopped straw, and flatus is continually passed from the bowels. Indeed the almost incessant passage of wind and fæces, during the first mile or two of a journey, is a disgusting evidence of the malady. The power of doses of shot, fat and other agents to temporarily allay the symptoms may be held to point in the same direction.

Beside causes operating on the side of the digestive organs others undoubtedly superinduce the disease, and among these severe exertions and chronic bronchitis ought to hold prominent positions.

Overexertion induces overdistension and rupture of the air cells by the forced retention of air within the lungs, by the closure of the glottis, while the chest is strongly compressed by the respiratory muscles. It is an essential condition to all severe exertion in man that the breath should be held, and though the horse appears equal to the same efforts of draught after the operation of tracheotomy has deprived him of the power of holding the breath, yet he would seem to be sooner exhausted (Goubaux, Colin, Bouley), from which it may be inferred that this power is frequently exercised, and it probably always is in any sudden severe effort as in starting a heavy load, or jumping a five-bar gate. This retention of air in the lungs during violent compression of the chest walls is precisely the condition met with during an access of coughing, and in both cases alike there is the tendency to overdistension of the minute tubes and air cells until they have lost their power of contraction, or they may even give way and allow the air to pass out and lodge in the lung tissue.

Another mode in which violent effort injures the lungs is by the rapid and continued inhalation of great quantities of air during rapid breathing, so as to dilate the lungs suddenly to their fullest extent. Sometimes from irregular distribution of the ærial current or from the want of tone in a particular part of the lung that gives way under the pressure and the air cells become overdistended or ruptured. This condition is especially met in the more rapid paces. It is well exemplified in the results of the deep breathing after cutting the vagi nerves.

In either case the result will be more certain if the effort is made upon a full stomach or with the functions of the vagus nerve impaired by a previous faulty diet.

That broken wind is a frequent concomitant or sequel of chronic bronchitis is undeniable, and theoretically nothing is more likely to cause dilatation and rupture of the air cells and consequent impairment of the innervation and contractility of the lung than violent fits of coughing, while the bronchial tubes have thickened and friable walls, or are partially plugged by tenacious mucus.

Broken wind is mainly a disease of old horses, though I have seen several cases in five-year-old animals, and Bouley records a case in a two-year-old colt out of a badly broken winded mare. This would seem to indicate an hereditary proclivity, and there is no doubt that the shallow, narrow, weak chest predisposing to this as to many other pulmonary complaints is transmitted from parent to offspring.

Nature of the Disease. Emphysema of the lungs is the most constant structural change met with in the bodies of animals which have suffered from broken wind. This condition of the horse’s lung appears to have been noticed by the early Greek writers. It was advanced as the cause of broken wind by Riding in 1704 (Pathologie Veterinaire), by Floyer in England in 1761 (Treatise on Asthma in Man), by Vitet in France in 1783 (Medicine Veterinaire, Lyon), by Freutzel in Germany, and Bracy Clark in England in 1795. It was only, however, after the admirable discoveries of Lænnec that the question was systematically investigated by Delafond, who has furnished the most comprehensive data on the subject. Out of fifty-four broken winded horses dissected by him no less than forty-five had the lungs extensively emphysematous. This emphysematous lung differs according to whether the emphysema is vesicular or interlobular.

In =vesicular emphysema= the smallest bronchial tubes and the air cells have become distended beyond the natural standard and remain permanently so, the lung tissue having lost its power of contraction. If such a lung is inflated and dried, and a thin slice taken from the surface of the emphysematous part the size of the minute orifices on the cut surface will show its condition. These fine openings are only the air cells cut across, and in their healthy state they will admit no larger object than the point of a needle or a fine bristle. They are slightly larger in adult and especially in old horses than they are in the young. If affected by emphysema they will often admit a hempseed or even a small pea. On opening a healthy chest the lung collapses, contracting on itself and expelling the contained air; if the lung is emphysematous the diseased portion does not collapse and if the entire lung is affected it continues to fill the chest and may even bulge outward after it has been opened. The color of the emphysematous lung is of a brighter red than are the healthy portions. If a diseased lung has been left exposed to the air for twenty-four to thirty-six hours and then cut across in all directions, the diseased lobules may be distinguished at a glance by this lighter shade, and such light portions if near the surface will be found to correspond to elevations above the general level of the lung. If the diseased lung is placed in water it floats on the surface like an inflated bladder scarcely at all sinking into the fluid. If the lung is blown full of air the emphysematous part is first filled causing the bulging on the surface to be still more marked than before. Vesicular emphysema rarely affects an entire lung; it is usually confined to the anterior lobes and to the thin lower and posterior borders of the organ.

=Interlobular emphysema= is the extravasation of air into the connection tissue between the lobules owing to rupture of the air cells, and smaller bronchial tubes. It may occur independently of the vesicular emphysema but more frequently, it is preceded by that form and results from it. It is manifested on the surface of the lung by irregularly formed transparent elevations movable from one place to another under the pressure of the finger contrary to what is the case in vesicular emphysema. These vary from the size of a pea to that of a hen’s egg. When the air exists in the cellular tissue between the lobules, it appears as intersecting lines circumscribing irregular spans, and seemingly dark colored to a superficial glance but seem to be transparent on a closer examination. Like the elevations on the surface these collapse on being pricked.

When a lung in this state has been inflated and dried it presents on the diseased parts the union of several air sacs into one by the rupture of their intervening walls so that a pea may be lodged in the cavity; it further shows wide and prolonged canals on the surface and in the intervals between the lobules—the dilated areolæ of the connective tissue. These abnormal conditions like the vesicular emphysema are chiefly met with in the anterior lobes of the lungs along their free borders and on their inner surface near the entrance of the bronchi.

One or both of these two forms of emphysema may be considered as essential conditions in all forms of broken wind. It does not follow that this is the primary disease; we have already seen that the cause of the malady is usually to be sought on the side of the digestive organs, and that impaired innervation, on the part of the vagus nerve or of the ganglia in the brain presiding over it, leads to these functional and structural changes in the lungs. If these changes are results and not causes, their extent will not necessarily bear a constant proportion to the intensity of the disease, though in reality they are generally found to do so.

From a series of injections of lungs from broken winded horses M. Demoussy arrived at the conclusion that the essential lesion of broken wind was an aneurismal dilatation of the capillary vessels of the lung. This is like the condition of the mucosa found in asthma in man and is explainable in both cases by the impaired innervation, as dilatation of these minute vessels is a natural consequence of the loss of vaso-motor nervous power, and contact with air saturated with carbonic acid.

Dilatation of the smaller bronchial tubes is frequently present and especially characterises such cases as supervene on chronic bronchitis. These dilated tubes contain a plastic, whitish, inodorous mucus.

Another frequent concomitant of the emphysematous lung is a dilatation of the right cavities of the heart, especially the auricle, and an attenuation of their walls. The same condition is noticed in pulmonary emphysema in man and like this is probably due to the slow and imperfect circulation in the diseased lung.

Collating these structural changes with the different causes of the disease we find that they harmonize with the theory of impaired function on the part of the vagus nerve or its presiding ganglia, whether this functional disturbance has its origin in disorder of the digestive organs, as in the great majority of cases, in severe muscular efforts, or in chronic bronchitis.

Section of the vagi nerves affords an exaggerated instance of their paralysis and its results. These are mainly emphysema, capillary dilatation, blood extravasation, inflammation and pulmonary collapse. Emphysema is the first result and due to the slow, deep respiration (Boddaert) and loss of contractibility (Longet); capillary dilatation results from the extreme distension of the air cells and the retention in them of air highly charged with carbonic acid (Donders); the other lesions occur later and own very different causes.

That this is the true nature of the disease would further appear from the occurrence of emphysema without broken wind, two cases of which are recorded by Percivall; and from the existence of broken wind without emphysema. Cases of this last variety have been recorded by Godine, Volpi, Rodet, D’Arboval, and Delafond in France; and by Sewall, Dick, Smith, Hallen and Gloag in Britain. In connection with this last class of cases it must be noted that dilatation of the right cavities of the heart sometimes gives rise to very similar symptoms, and that the signs of chronic bronchitis are often scarcely distinguishable from those of broken wind. In catarrhal bronchitis too, after the air tubes have been washed, it is sometimes impossible to decide whether the lining membrane has been the subject of inflammation or not.

Symptoms. The most prominent are the double lift of the flank with each expiratory act, in the absence of fever, the short, weak, dry and almost inaudible cough, the wheezing noise in breathing when that is accelerated by exertion, and the intestinal flatulence with the frequent passage of gas.

The =cough= usually heralds the advent of other symptoms. Often the character of the cough draws forth the remark that an animal is becoming broken winded and though no other symptom is seen at this time they thereafter rapidly develop themselves. At this early stage of the disease the cough is paroxysmal, coming on in fits during work or after a drink of cold water. Once the disease is established the horse rarely coughs more than once at a time. The cough is extremely short, weak and low and followed by a sort of wheeze. So specific is it that if once heard it can readily be recognized. The sudden effort made in coughing usually leads to the expulsion of gas from the flatulent bowels.

The =double lifting of the flank= in expiration is not peculiar to broken wind. It is seen as well in most diseases of the lungs and even of other organs (enteritis, peritonitis) which interfere with the freedom of the respiratory act. If however it is not attended by fever but associated with the broken winded cough, the wheezing respiration, the disordered and flatulent state of the bowels, the tumultuous beating of the heart against the left side after exertion, and the slight flow of clear, watery matter from the nose, it is pathognomonic. The act of inspiration is quick and free, that of expiration is not uniform and continuous as in health, but consists of two stages interrupted by a momentary arrest. In the first stage the posterior part of the abdomen is slightly raised and it falls in laterally; then comes an almost imperceptible period of inaction, followed at once by the further lifting of the flanks to complete the expulsion of air from the lungs. The first stage seems the natural collapse of the walls of the chest and forward movement of the diaphragm, the second a contraction of the abdominal muscles partly due to an exercise of will to overcome the obstacle to the expulsion of air.

In very bad or advanced cases these symptoms are more marked. The inspiration is sudden and manifested by a rapid expansion of the chest, and dropping of the belly previously supported by active contraction of the abdominal muscles. The two stages of the expiratory act are quite distinct. The first is manifested by a sudden falling in of the walls of the chest so that the ribs no longer stand out prominently beyond their interspaces; the abdomen equally rises inferiorly and falls in laterally so that a projecting ridge is formed from the lower end of the last rib to the point of the hip. This is specially marked during the period of inaction, and this is succeeded by the second effort quick and almost convulsive. These movements are so extensive that they are conveyed in a striking degree to any vehicle to which the animal is attached, especially if it has only two wheels, and a rider on horseback feels the movement still more disagreeably. When a horse is in this state the alternate rising and falling of the abdominal organs imparts a synchronous movement of protrusion and contraction to the anus and in thin subjects a rising and falling of the muscles on each side of the root of the tail. The nostrils too are kept constantly dilated.

There is a nasal discharge, but this is very inconsiderable in the early stages of the malady. It is a clear watery or slightly grayish albuminous material without any visible admixture of pus globules, and on drying it leaves a scarcely perceptible crust. At first it appears intermittently and in minute quantities, but in bad cases it becomes almost constant, and is especially profuse after exercise.