Text book of veterinary medicine, Volume 1 (of 5)

by James Law

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.