Diseases of the Horse's Foot

by H. Caulton Reeks

C. OSSIFICATION OF THE LATERAL CARTILAGES, OR SIDE-BONES.

Definition.—An abnormal condition of the lateral cartilages, in which the substance of the cartilage becomes gradually removed and bone formed in its place.

FIG. 143.—OSSIFIED LATERAL CARTILAGES (SIDE-BONES).

Symptoms and Diagnosis.—Side-bones are nearly always met with in heavy draught animals, and are rarely seen in the feet of nags. They are, moreover, nearly always confined to the fore-feet. In the ordinary way little need be said concerning their characteristics, and the way in which they may be detected. Neither need any concern be ordinarily manifested with regard to the effect they may have on the animal's gait and future usefulness. Seeing, however, that side-bone constitutes one of the recognised hereditary diseases, and that at the various agricultural and horse shows its existence or otherwise in a certain animal is a matter of great importance, some little attention must be given to these two points.

With a side-bone anywhere approaching full development, diagnosis is easy. The thumb is pressed into the coronet over the seat of the cartilage, when, in place of the elasticity we should normally meet with, we have the solid resistance offered by bone. In some instances diagnosis is even easier still. We refer to those cases in which the side-bone stands above the level of the coronet with such prominence as to be readily seen and recognised without manipulation, and where its growth has caused distinct enlargement and bulging of the wall of the affected quarter. It seems that in such cases the bone-forming process does not end with simply depositing bone in place of the removed cartilage, but that, after that is accomplished, the bone still continues to be produced, as in the case of an exostosis elsewhere.

Although diagnosis in cases such as these is easy, it becomes a very different matter when we are called upon to give an opinion in cases where ossification of the cartilage is only just commencing. Whether the result of our examination is to decide the sale or purchase of an animal, to determine his fitness or otherwise to enter the show-ring, or to merely advise a client as to whether or no a side-bone is in course of formation, our position is equally difficult, and in either case our examination must be searching.

Perhaps the best advice we can give is to say that the whole of the cartilage must be manipulated both with the foot on and off the ground. What the reason may be we do not pretend to say, but it is a well-known fact that in many instances the cartilage, with the foot bearing weight, is so rigid as to at once convey the impression that ossification has commenced or is even far advanced. And yet that same cartilage, with the foot removed from the ground, is as pleasantly yielding to pressure of the thumb as the most exacting of us could wish for. In any case, then, where doubt exists, the foot should be lifted to the knee, and the cartilage carefully examined with the foot in that position. If, then, at any spot above the normal contour of the os pedis we meet with hardness or rigidity, we are to look upon that foot with suspicion. Nevertheless, providing our conscience is sufficiently elastic, the animal may be passed sound so far as the existence of a side-bone is concerned. We know, however, that with commencing rigidity we may ere long expect one, and if our opinion is asked with regard to that particular, it must be admitted that with rigidity of the cartilage once commenced it is usually not long afterwards before a fully-developed side-bone makes its appearance.

As is only to be expected, the first noticeable hardening of the cartilage is to be found near the normal bone. We may thus look for it more particularly in the lower portions of the cartilage. We think we may say, too, that in the vast majority of cases the ossification of the cartilage commences in its anterior half. It is thus brought about that often we are called upon to examine and report on the condition when we have anteriorly a side-bone in course of formation, and posteriorly a perfectly normal cartilage. It is to the latter half of the cartilage that dealers and others mainly, if not wholly, devote their attention. A horse with the cartilage in this transition state will therefore pass muster, and a nice little point of ethics has again to be decided by the veterinary surgeon before giving his signature to a certificate of examination of an animal in this condition.

With regard to alteration in gait, we may say at once that side-bones in heavy animals are not often the cause of lameness. In fact, where the foot is well developed, when neither the foot as a whole nor the phalangeal bones give evidence of disease, and where the pasterns are fairly oblique and well formed, this alteration of the cartilages may be looked upon as of no serious import at all. Neither is the side-bone due to blows or other injuries likely to be productive of lameness—that is, always supposing, of course, that the foot in other respects is of good shape. If lameness is met with at all, then it is where we have a foot that is in other respects unsound, with badly contracted heels and upright 'stumpy' hoof, or where side-bones have occurred in a young animal, and have already reached a large size before the horse is put to labour. In this latter case, the added effects of concussion and the evil influences of shoeing are sufficient to turn the scale. Directly the animal, previously sound, is asked to work, lameness is the result.

It follows, therefore, that side-bone in the feet of young animals is of far more serious import than when occurring in older horses. In a nag animal they constitute a positive unsoundness, and lameness in this case is more often than not an accompanying symptom.

Causes.—To commence with, we may remark that, although met with sometimes in very early life, side-bones are seldom, if ever, congenital, and that more often than not they may be looked for in animals of three years old, or older, seldom earlier. They appear, in fact, only when the animal is shod and commences work.

This at once suggests two of the principal factors in their causation—namely, concussion and loss of normal function. Directly the horse is put to work he has for a great part of his time to travel upon roadways—either macadamized roads or town sets—where everything is calculated to bring concussion about. In addition to that he has the lateral cartilage itself thrown largely out of action by shoeing. We explained in Chapter III. (p. 66) that the chief function of the cartilage was to take concussion received by the plantar cushion and direct the greater part of it outwards and backwards. Now, with the animal shod, the plantar cushion does not itself, as normally it should, receive concussion. By the shoeing the frog is lifted from the ground, and the plantar cushion, together with the cartilage, taken largely out of active work. In other words, the normal outward and inward movements of the cartilage are enormously reduced.

It is fair, we think, to take it that the mere fact of the lateral cartilage persisting as cartilage is due in large measure to its constant movement. Directly, therefore, it is placed in a state of comparative idleness, then it commences to ossify, more particularly if there should at the same time be a tendency to a low type of inflammation of the parts.

Does this latter exist? We may safely say that it does. It is in this way: The secondary effect of loss of ground-pressure upon the frog and plantar cushion is to bring about contraction of the heels. With this we get compression of the parts within, with a certain amount of irritation and the exact low type of inflammatory phenomena calculated to assist in the bone-forming process.

The fact that concussion acts as a cause explains in great measure how it is that side-bones are more frequent in cart animals than in nags, and also why they should be more common in the fore-feet than in the hind. Taking, in both animals, a rough calculation as to the weight of body carried by feet of a certain size, we notice at once that the cart animal has proportionately more weight to carry than has the nag. Concussion to the foot is therefore greater. The greater part of the body-weight is borne by the fore-limbs. Concussion is therefore greater to the fore-feet than to the hind.

This, however, does not explain altogether the comparative immunity of the nag animal from this defect. He, too, must also be subject to the effects of concussion, especially when his higher and faster action is taken into account. To our minds there is only one explanation to be offered here. We point at once to the years of constant and judicious breeding of the nag. Compare that with the relatively few minutes that have been devoted to a more careful selection of the cart animal, and we at once see a possible explanation. That the explanation holds some amount of truth is borne out by the fact that, since a greater attention has been paid to the selection of our cart animals, side-bone has grown a great deal less common.

Is side-bone hereditary? We can best answer that by saying that, some several years ago, the Council of the Royal College of Veterinary Surgeons, at the request of the Royal Commission on Horse Breeding, drew up a list of those diseases 'which by heredity rendered stallions so affected unfit as breeding sires,' and that in that list was included side-bone.

Side-bones, therefore, are hereditary. We think, however, the statement needs qualifying. It is in this way: side-bones occur only at a certain, usually well-defined, time after birth, and we might say are never congenital. They occur only after the animal has been put to work, and are more or less plainly due to mechanical causes—namely, the ill effects of shoeing and concussion. The cause of their appearance, in short, is more plainly extrinsic than intrinsic, and side-bone in the horse is, as Professor McCall puts it, about as much due to heredity as is corn on the human foot.

Between these two opinions—that they are plainly hereditary, and that they just as plainly are not—it is well to strike a middle course. They are, we will say, hereditary in this way: So long as a cart animal is bred, to put it vulgarly, 'top-heavy' (that is, with a body out of reasonable proportion to the feet that have it to support), so long will the foot be subjected to a greater concussion, and so long will side-bones in such animals commence to make their appearance at about middle life.

In addition to the causes we have now mentioned, side-bones are often the result of other diseases of the foot. They thus occur as a sequel to sub-horny quittor, to suppurating corn, to complicated quarter sand-crack, or to the inflammation of the parts occasioned by a prick. They also arise in many instances from the effect of a prick or injury to the coronet. Among the latter we may mention treads from other animals, and treads inflicted by the animal himself with the calkin of an opposite shoe, or the repeated injury occasioned by the shafts being carelessly allowed to drop on to the foot. In severe cases of laminitis, too, the cartilages are nearly always affected. In this instance the inflammatory phenomena in the os pedis no doubt give rise to an abnormal activity of bone-forming cells. The cartilage is invaded, and the side-bone formed (see Fig. 118).

Treatment.—In the ordinary way the 'treatment' of side-bone is a thing but rarely mentioned. The explanation lies, of course, in the fact that side-bones are so rarely the cause of lameness. When lameness does occur with a side-bone, and we have reason to believe that the said side-bone is the cause of the lameness, it is well before talking of treatment to question ourselves thus: 'In what way does the side-bone cause lameness?' The now generally-accepted answer to that query is the explanation put forward several years ago by Colonel Fred Smith—namely, that the pain, and therefore the lameness, was due to the compression of the sensitive laminæ between the ossified and enlarged cartilage and the non-yielding and often contracted wall of the quarters. That, in fact, constitutes the basis upon which Smith's operation for side-bone (that of grooving the wall of the quarters) is founded.

Before describing the operation, however, we may say that we are now able to understand that older operators who claimed success for other methods of treatment, were to a very great extent justified in so doing.

For instance, take the combined treatments of firing and blistering, and the use of a bar shoe. Here the beneficial action of the cautery and the blister may be largely problematical. The bar shoe, however, would be almost certain to give good results. Frog-pressure with the ground would be again restored, and the contraction of the heels removed. Pinching of the sensitive structures would be diminished, and the lameness cured.

Take, again, the treatment of 'unsoling.' It was barbarous, we know barbarous, because unnecessary and easily avoidable. It was practised, however, certainly very little more than two decades ago, and practised by men of standing in the profession. Without dragging the case to light again by mentioning the names of those concerned, we may mention that not many years ago a highly respected member of the profession was, at the instigation of the Royal Society for the Prevention of Cruelty to Animals, prosecuted for practising unsoling for the relief of side-bone. Practically only one other member of the profession was able to come forward and defend the operation on the score of its utility. We see now, however, that—as does Smith's operation—unsoling does permit of the greater expansion of the heels. The contraction is done away with, the pressure on the sensitive laminæ again diminished, and the lameness relieved.

Not that we are attempting to defend the operation—far from it. We simply mention it as interesting, and quote this and the use of the bar shoe (with both of which methods older operators have claimed success) merely as evidence that the operation of Smith is based on a logical foundation.

When treatment is decided on, therefore, we may first advise blistering and the use of a bar shoe. After that, should the lameness continue, and should we still judge the side-bone to be the cause of it, the operation may be advised.

As we have said before, the operation consists in so grooving the wall as to allow of the quarters widening sufficiently to relieve pressure on the parts within. In one or two previous portions of this work we have considered operations involving this procedure. Before detailing the operation here, therefore, we will first describe the instruments necessary, and the most satisfactory methods of incising the horn.

To begin with, it must be remembered that all methods of hoof section have for their object the after-expansion of the horny box, and that this can only be brought about by making each groove complete from coronary margin to solar edge of the wall, and carrying it, throughout its length, deep enough to reach the commencement of the sensitive structures.

To this end, therefore, the operator must bear in mind the comparative thickness of the various parts of the wall, and must, in particular, remember the relative thinness of that portion of horn forming the outer boundary of the cutigeral groove, and accommodating the coronary cushion.

For the making of the incisions there is the special saw devised for this operation by Colonel F. Smith, A.V.D., and which we illustrate in Fig. 144. With this the wall is sawn through until the depth arrived at is equal to what is indicated by a previous examination of the thickness of the crust as viewed from the solar surface. Here Colonel Smith says: 'I strongly advise everyone to use a metal gauge (a thin piece of material) to introduce into the incision made by the saw, and run it up and down to ascertain whether the wall is properly divided throughout. The depth to which this should be done we know from the previous measurements of our gauge on the crust.'

FIG. 144.—SMITH'S SIDE-BONE SAW (EARLY PATTERN).

Should the saw be of a pattern in which the set of its teeth makes only a narrow incision,[A] it should, while operating, be kept well oiled, and should be withdrawn every few seconds in order that the horn-dust lying in its teeth may be examined. If this is getting slightly blood-stained, we know, of course, that the sensitive structures are reached, and the incision has been carried far enough. In so judging the depth of the incision, however, care must be taken to see that the top of the coronary cushion is not injured with the saw, for if this is done the blood trickling into the depth of the incision will tinge the horn-dust, and give the false impression that the incision is sufficiently deep.

[Footnote A: That is Smith's older pattern. The newer pattern (Fig. 145) has the teeth so set as to make an incision wide enough to be looked into. In this case the depth arrived at is to be judged by the appearance of the bottom of the incision.]

If the operator has had no previous experience of the use of the saw in this operation, he must also be careful to avoid placing too great a pressure on the teeth of its lower third. This is done by keeping the hand too greatly depressed. Again, this leads to wounding of the sensitive structures (this time at the lower end of the incision), and again the operator is confused by the blood thus allowed to run into the groove.

The only portion of horn difficult to operate on is that immediately under the coronet. This is best severed with a succession of downward movements, and is easier performed with Smith's later pattern of side-bone saw (Fig. 145) in which the set of the foremost teeth is reversed.

FIG. 145.—SMITH'S SIDE-BONE SAW (IMPROVED PATTERN).

In making these grooves we must say that we think the use of the special saw may be dispensed with, and the incisions just as easily, or, at any rate, just as successfully, made with the knife. Those who select to use this instrument should choose a narrow-topped and sharp searcher, or a modern shaped drawing-knife of suitable size, such as those depicted in Fig. 46, a and b, and they will find their work much easier if they will make the first steps in the incisions with an ordinary flat firing-iron. By the use of the latter instrument the grooves are made conveniently open along their tops, and room left for nicely finishing the more delicate manner of removing with the knife the softer horn near the sensitive structures.

Those whose leaning is towards the use of special instruments, but who, at the same time, do not care to use the saw, will find their wants supplied in the hoof plane (Smith's), Fig. 146, or the hoof chisel (Hodder's), Fig. 147. With the hoof plane the groove in the wall is made by a succession of downward scraping movements, while with the chisel the cut in the wall is made either from below upwards, or from above downwards, according as the foot is held forward or backward—whichever, in fact, comes most convenient.

FIG. 146.—HOOF PLANE (SMITH'S).

When using the knife or the hoof plane it is not often that the sensitive structures are injured. In all cases, however, no matter what the instrument used, the metal gauge should be employed when the sensitive structures have been touched, and the operation obscured by blood.

FIG. 147.—HOOF CHISEL (HODDER'S).

Our instruments at hand, the operation may be proceeded with. The first step is to ascertain the extent of the side-bone, and to determine the position of the incisions. To do this the coronet is felt with the thumb, and the anterior extremity of the side-bone noted. This is marked on the horn with a piece of chalk, and a vertical line dropped from this position to the inferior margin of the wall (Fig. 148,1). The line crosses the horn fibres obliquely, and is purposely made in that direction in order that its inferior end may be far enough back to avoid the last nail-hole. Should the side-bone reach very far forwards, it may be wise to cause this line to slant from before backwards (see dotted line a, Fig. 148). Unless this is done, it is found that in some feet so much of the wall is isolated at the bottom that insufficient is left to nail the shoe to.

The next line to be made is the rear one. Its correct position is ascertained by first noting the junction off the wall with the bar (see groove 2, Fig. 149); and its inferior end must be just anterior to the inflexion of the wall. This is done that we may avoid cutting the bar. The position of the lower end of the rear line thus ascertained, it is run upwards with the chalk in the direction of the horn fibres.

FIG. 148.—DIAGRAM ILLUSTRATING THE POSITION OF THE GROOVES IN THE WALL IN COLONEL SMITH'S OPERATION FOR SIDE-BONE. 1,2, and 3, mark the grooves in the order in which they are made; the dotted line a marks the position taken by the anterior line when the side-bone, is one reaching far forward, while the dotted lines b and c mark the position of the additional grooves to be made if thought necessary.

The third line is made in such a position as to divide into two equal portions the wall between lines 1 and 2. Here, however, some operators prefer to make two, or even three, lines, adding those as at b and c, Fig. 148; and Smith himself says that a multiplicity of lines is an advantage rather than not.

In any case, having once determined the position of the lines, they should be plainly marked out with chalk, and then viewed from a distance with the foot on the ground, in order to judge of their regularity. If we are satisfied with them, we then lightly mark them with the saw, with the hot iron, or with the knife, whichever instrument we may be intending to use.

Unless the details are methodically carried out as here described, it is probable that more of the foot will be isolated than is necessary, and that as a consequence very little is left to which to nail the shoe.

FIG. 149.—DIAGRAM ILLUSTRATING THE POSITION OF THE GROOVES MADE IN THE HOOF IN COLONEL SMITH'S OPERATION FOR SIDE-BONES. 1, 2, and 3, show the grooves in the wall in the order in which they are made; 4 shows the groove made at the junction of the sole with the wall.

The incisions are then made with the saw or the knife, with the foot held in a convenient position by an assistant. That usually found most comfortable for the first incision is with the foot held forwards and placed on an assistant's thigh in the position adopted for 'clenching up' when shoeing, while that for the rear incision is with the animal's knee flexed, and the foot held well up to the elbow. In this, however, each operator will suit himself.

Should the preliminary steps in making the incisions be performed with the iron, it will be easiest done with the foot on the ground.

When the incisions through the wall are complete, our attention must be given to the sole. A drawing-knife is here used, and a further incision made over the white line so as to destroy the union of the sole with the wall between incisions 1 and 2, and so completely isolate the portions of wall included within the four grooves (see groove 4, Fig. 149). When this is done it should be found that the portions of the isolated wall spring readily to pressure of the thumb.

The inferior or wearing margin of the isolated wall must now be so trimmed that it takes no bearing on the ground when the opposite limb is held up by an assistant and full weight placed upon the foot.

For a day or two after the operation lameness is intense. This is to be treated with hot poultices or hot baths, and and soon disappears. Three to four days later a bar shoe is nailed on (taking care that the bearing of the quarters is still eased), and the hot poultices still continued. Four days later still walking exercise may be commenced, to be followed shortly afterwards by trotting. At about the twelfth day some animals may conveniently be put to work, while in other cases a fortnight, or even a month, must elapse before this can be done. When put to work early, it is wise to fill in the fissures made in the wall with hard soap, with wax, or with a suitable hoof dressing, in order that irritation of the sensitive structures with outside matter may be prevented.

This operation is soon followed by remarkable changes in the shape of the foot. At about the third week the coronet shows signs of bulging, and the upper part of the wall operated on is often so protruding as to render the foot wider here than at the ground surface. This is a sign that the case is doing well.

Should no improvement be noticed at the end of three weeks or a month, or should the grooves become filled from the bottom (which they do remarkably fast), then the incisions must be deepened, the exercise reduced, and the fomentations or poulticing repeated. So treated, many cases of side-bone lameness will be relieved, if not entirely cured, and, should the worst happen, and no alteration in the lameness is noticeable, no harm will have been done to the foot. In this connection, the originator of the treatment says: 'I may assure those induced to doubt either their diagnosis or the value of hoof section that no harm is done to the foot, even should the operation be of no value. It may do much good; it cannot do harm. The operation will never succeed until the inherent timidity of sawing or cutting into the wall is overcome. The incisions must be deep, and of the same depth from the coronet to the ground.'[A]

[Footnote A: Journal of Comparative Pathology and Therapeutics, vol. iii., p. 313.]

It is well to remark here that the operation of hoof section cannot be expected to succeed in every case. The last man in the world to claim that for it would be its originator. Failure to relieve the lameness may be accounted for in a variety of ways. First, of course, will come errors in diagnosis. No one of us is infallible, and the lameness we have judged as resulting from side-bone may arise from another cause. There are, too, complications to be reckoned with, the existence or absence of which cannot always be definitely ascertained. Such are: Ringbone, especially that form of ringbone known as 'low'; bony deposits on the pedal bone, either on its laminal or plantar surface, or even changes in the navicular bursa.

CHAPTER XI

[DISEASES OF THE BONES]

A. PERIOSTITIS AND OSTITIS.

We head this section, Periostitis and Ostitis, for the reason that in actual practice it is rare for one of these affections to occur without the other. The periosteum and the bone are so intimately connected that it is difficult to conceive of disease of the one failing to communicate itself in some degree to the other. Pathologically, however, and for purposes of description, it is more convenient to describe separately the abnormal changes occurring in these two tissues.

With the main phenomena of inflammation occurring elsewhere we presume our readers are aware. Briefly we may put it, that under the action of an irritant, either actual injury, chemical action, or septic infection, the healthy tissues around react in order to effect repair of the parts destroyed. Also that this reaction involves the distribution of a greater blood-supply to the part, with an abundant migration of leucocytes, and the outpouring of an inflammatory exudate, together with symptoms of heat, pain, redness, and swelling of the affected area. And that in chronic inflammations, owing to persistence of the cause, the process of repair thus instituted does not stop at mere restoration of lost tissue, but continues to the extent of forming an abnormal quantity of such tissue as normally exists in the parts implicated.

The process of inflammation in bone is essentially the same. It takes place along the course of the bloodvessels, and is only modified in its attendant phenomena by the structure of the parts involved. Swelling, for instance, cannot take place in the centre of compact bone tissue. Otherwise, other changes occur exactly as in inflammations of other structures.

When the causal irritant has been excessively severe and the migration of leucocytes abundant, actual formation of pus may occur, the bony tissue being broken down and mingled with it, and an abscess cavity formed. In milder cases, affected and necrotic tissue is removed by a process of phagocytosis, and new tissue (this time osseous) formed in its place.

In the periosteum we may take it roughly that inflammation runs a course similar to that occurring in soft tissues elsewhere. There is but one exception, and that, as we shall mention shortly, is connected with its deeper layer.

As we know, the periosteum consists of two layers, an outer fibrous and an inner yellow elastic, and is extremely vascular. Numerous bloodvessels ramify in it, and, with their attendant nerves, break up to enter the numberless canals of the Haversian system. This extreme vascularity, of course, favours abundant exudation. The exudate, however, is, as it were, shut in by the dense fibrous layer of the membrane, and the result is that in periostitis it collects between the membrane and the bone, causing swelling and raising of the membrane, and giving rise to excruciating pain from pressure upon the nerves.

Should the periostitis be complicated by the formation of pus, then the vessels entering and supplying the bone are, in the suppurative area, destroyed. With their destruction it may happen that we get also death of a portion of the osseous tissue. This, however, when the suppuration is abundant, cannot commonly occur, as the bloodvessels within the bone—those of the medulla—commence to supply blood to the affected part. In cases of trouble with the bones of the foot, these last few remarks have a special significance. Here we have three bones whose medullary cavity is extremely small—almost nil, in fact—which explains in some measure how easy it is when suppuration exists to get necrosis and exfoliation of, say, portions of the os pedis. Necrosis and sloughing of the periosteum itself may also happen, but as the extreme vascularity of the membrane is a fairly strong safeguard against that it is of only rare occurrence.

In connection with the deep layer of the periosteum, and forming part of it, are found numerous bone-forming cells (osteoblasts). These, under ordinary conditions, are relatively quiescent. Under the slightest irritation or stimulation, however, their bone-forming functions are stirred into abnormal activity, thus explaining how easy it is (especially with bones so open to receive slight injuries as are those of the foot) to get ossific deposits, the starting-point of which we are quite unable to account for.

With this brief introduction we will now describe such pathological changes as occur in the separate structures, and which we are likely to encounter in the various diseases of the foot. While so doing, we shall draw attention to such diseases as we have previously described in which the pathological conditions we are considering may be met with.

1. PERIOSTITIS.

This we shall consider under (a) Simple Acute Periostitis, (b) Suppurative Periostitis, (c) Osteoplastic Periostitis.

(a) Simple Acute Periostitis.—This is the periostitis that follows on the infliction of a slight injury to the membrane—an injury without an actual wound and free from infective material. It is one, therefore, which we always judge as existing in those cases where we have distinct evidence or history of injury, but in which the injury has not been severe enough to lead to fracture or to the infliction of an actual wound.

Such cases may be those of lamenesses persisting after violent blows upon the foot—cases where the animal has been kicking against the stable fittings, or where the foot has been partially passed over by the wheel of a waggon. It may be, too, that in a case of 'nail-bound' a great deal of the pain and lameness is due to a simple periostitis caused by pressure of the bulged inner-layer of horn upon the sensitive structures.

Simple acute periostitis may also occur in cases where an actual wound is in existence, but where such wound, fortunately, remains aseptic. We may thus have this condition accompanying ordinary cases of pricked foot, of treads in the anterior region of the coronet, and of accidental injuries of other kinds.

In simple acute periostitis the membrane is thicker and redder than normal, and is easily stripped from the bone. As it is pulled off it is noticed that there are numerous fibril-like processes hanging to its inner surface, and which draw out from the substance of the bone. These are simply the vessels (bloodvessels and nerves) which, loosened by the inflammatory exudate, are readily detached and drawn from the Haversian canals into which they normally run. In addition to its increased redness, the membrane has a swollen and gelatinous appearance owing to its infiltration with the inflammatory discharges. Simple acute periostitis may and often does end in resolution. On the other hand, it may end in suppuration or may become chronic. If the latter, then the osteoblasts of the innermost layer become active, and abnormal deposits of bone are the result.

(b) Suppurative Periostitis.—This condition simply indicates that the inflammation is complicated by the presence of pus organisms. It is, therefore, a common termination of the simple acute form attending the infliction of a wound. The wound becomes contaminated, and the case of simple periostitis is soon changed into the suppurative form. Once having gained entrance to the wound, the pus increases in quantity, and slowly runs between the membrane and the bone. This, however, it does not do to any large extent, showing rather a tendency to penetrate the outer fibrous layer and gain the outside of the membrane.

Suppurative periostitis is met with in foot cases, commonly in connection with punctured foot. It occurs, too, as a complication in suppurating corn, in severe tread, in complicated sand-crack, as a result of the spread of suppurative matter in acute coronitis, and in sub-horny quittor.

In ordinary cases of suppurative periostitis the pus formed is yellow in colour, creamy thick, and free from pronounced odour—the so-called 'laudable' pus of the older writers. It so happens in many cases of foot trouble, however, that putrefactive organisms gain entrance side by side with those of pus. In this case the characters of the discharge are very different. It is distinctly more fluid, is of a pink or even light chocolate colour, and extremely offensive. In these instances the pus shows a marked tendency to spread, strips the periosteum from the bone, perforates the outer layer of the membrane, and finally infiltrates the surrounding tissues.

This forms a near approach to what is known in human surgery as an infective periostitis, and in our subjects is nearly always met with in cases of severe prick. Its rapidly spreading character makes it always a dangerous condition, and a punctured foot exuding a discharge of this nature should always be regarded as serious. The close contiguity of the joint (it can never be far distant in foot cases), the spreading character of the disease, and the rapidity with which the horse succumbs to arthritis, are all factors to be taken into consideration, and to lead to a warning-note being struck when attending a case of such kind.

A further instance of infective periostitis is that met with in acute laminitis. The discharge obtained from the sole in these cases very often bears the character we have just described, and when one considers the thinness of the keratogenous membrane, one is bound to admit that changes so grave occurring in it cannot fail to spread and infect the periosteum.

(c) Osteoplastic Periostitis.—This is more particularly a chronic process, and is, as the suffix 'plastic' indicates, associated with bone-forming changes in the membrane. It may occur as a consequence of slight but continued irritation, often without ascertainable origin (see Case 2, p. 392), or it may be the sequel of acute disease.

In this form of periostitis the membrane is again swollen and more vascular than in health, and is also easily separable from the bone. The exposed bone is generally rough, in some cases even spicular, and the inner layer of the removed membrane is rough and gritty to the touch—characters imparted to it by numerous minute fragments of bone that have been torn away with it from the more compact osseous tissue beneath.

The results of an osteoplastic periostitis are frequently met with in the bones of the foot, and are described by veterinary writers under such headings as 'Pedal Exostoses,' 'Ossifying Ostitis,' and 'Pedal Ossification' (see Figs. 152, 153, 154, and 155). In many of these cases the disease is purely chronic, and the original cause nearly always wanting. When the foot has been subjected to laminitis of some weeks' duration, the same condition is also met with, being at the same time associated with rarefactive osteoplastic ostitis, conditions which we shall shortly describe. Cases we have examined have undoubtedly shown this condition of osteoplastic periostitis, the rarefactive and osteoplastic changes in the bone itself, met with in older cases, occurring no doubt as a result of non-expansion of the horny box. So far as we are able to ascertain, there is every reason to believe that in chronic laminitis the accompanying periostitis leads to the formation of bone, and would, if it were possible, lead to increase in the size of the os pedis. If proof were wanted of this, it is only necessary to point out the increased growth at points where resistance is nil—namely, along the upper margin of the bone (see Fig. 118). However, increase in size elsewhere is prevented by the resistance of the hoof, so that, as the bone-forming process progresses, as it inevitably must under the inflammatory changes going on, it is, as it were, compensated for by rarefaction or bone-absorption changes occurring simultaneously with it.

2. OSTITIS.

We shall next deal with the inflammatory changes occurring in the bones themselves, and shall consider them under (a): Rarefying or Rarefactive Ostitis, (b): Osteoplastic Ostitis, and (c): Caries and Necrosis.

Inflammatory changes occurring in the medulla we may pass without consideration, for in the bones of the foot the medullary cavity is so small, and the changes taking place in it of such minor importance, that we may do this without in any way seriously prejudicing our work.

(a) Rarefying or Rarefactive Ostitis.—By this term is indicated an inflammation of the bone attended by its absorption, the absorption being due to the action of certain cells, termed osteoclasts. This condition may be due to the pressure of tumours, may occur as the result of injury when a piece of bone is stripped of periosteum, or may be the result of an inflammation occurring in the periosteum elsewhere.

A piece of bone undergoing rarefactive ostitis is redder than normal, and the openings of the Haversian canals are distinctly increased in size. As a result a greater number of them become visible. Their increase in size is due to the inflammatory absorption of the bony tissue forming them, and in the larger of them may be seen inflammatory granulation tissue surrounding the bloodvessels. This enlargement of the Haversian canals is well seen when the bone is macerated, the whole then giving the appearance of a piece of very rough pumice-stone.

This process of rarefaction or absorption of bone tissue may be confined to quite a small portion, or it may be spread over the whole of the bone, rendering it more porous than is normal, but stopping short of complete destruction of the bone tissue (a condition which is sometimes known as inflammatory osteoporosis (see Fig. 118)). In this latter case the condition is a chronic one, and the bone tissue remaining often appears to be strengthened by a compensatory process of condensation. For an example of rarefactive ostitis as met with in cases of disease of the feet, we refer the reader to laminitis (see Fig. 118). The osteoplastic or condensing process that appears to exist simultaneously with it explains, no doubt, how it is that bones so affected do not more commonly fracture.

A further example of this process is illustrated in Fig. 133. The pressure of a tumour (in this case a keraphyllocele) has led to rarefactive changes in the bone, forming a neat indentation in the normal contour of the bone which serves to accommodate the tumour.

(b) Osteoplastic Ostitis, Osteosclerosis, or Condensation of Bone.—This, too, is essentially a chronic process. It may occur as a result of, or, as we have just shown, exist simultaneously with the condition of, diffuse rarefactive ostitis. In this case there is a formation of new bone in the connective tissue surrounding the vessels in the Haversian canals. As a consequence the bone affected is greatly increased in density, and many of the Haversian canals by this means obliterated. The end result is an increase in size of the bones in such positions as the horny box admits of it, and a peculiar ivory-like change in their consistence.

For an example of this, we again refer the reader to the changes occurring in chronic laminitis.

(c) Caries and Necrosis.—Caries is a word which appears to be used with a considerable amount of looseness. In addition to the meaning implied by necrosis (namely, 'death' of the part), caries is generally used to indicate that there is also a condition of rottenness, decay, and stench. It is particularly applied, in fact, when the death of the bone is slowly progressive, and is due to the inroads made upon it by putrefactive or septic matter.

Necrosis of bone may be the result of any injury, such as severe blows, or pricks and stabs. In such cases it would appear that it is loss of a portion of periosteum that is the starting-point. With death of a portion of this membrane the vascular supply to a portion of the bone is cut off, and necrosis ensues. It may also result from the extension of inflammatory affections of the structures adjoining it, as, for instance, the spread of the infective material in severe tread, or the encroaches made by pus in cases of quittor, suppurating corn, or complicated sand-crack.

When the necrosed portion of bone is small, and is free from infective properties, it is quite possible that it may, as is the case with small spots of necrosis in softer tissues, be removed by a process of absorption. It must be remembered, however, that where the necrosis has occurred as a result of septic invasion this cannot be looked for, for in every case such reparative changes are worked solely by healthy tissue. If the tissues around the necrosis are engaged in dealing with organismal invasion and the poisonous products thus poured into their working area, their state of health is so weakened that they are unable to successfully combat with the two conditions simultaneously. As a consequence, the necrotic piece of bone persists, and acts as a permanent source of irritation.

It must be remembered, too, that if the dead portion of bone—even though it be free from septic matter—is very large, that it may itself act as a continual irritant, in which case it again persists, and cannot by natural means be removed.

In our cases necrosis of bone may be met with in punctured foot, in severe cases of tread, in cases of complicated crack, and in suppurating corn. It is met with, too, in navicular disease, in the extension of irritating discharges in cases of quittor, and in cases of chronic laminitis where the solar margin of the os pedis has penetrated the sole. In this latter case the protruding portion of bone is quickly denuded of its periosteum. Its blood-supply is destroyed, and necrosis follows.

Treatment.—In simple cases of periostitis, those caused by a blow but free from an actual wound, the most beneficial treatment is the continued application of cold by means of a hose-pipe or by swabs. If by these means we are successful in holding the inflammatory phenomena in check, any large formation of new bone is prevented, and the case does well.

When the case is complicated by a wound, then antiseptic measures, such as those described in the treatment of punctured foot, will at the same time have to be practised.

It must be admitted, however, that in all but the most simple cases ordinary treatment such as this is of very little use; for with only a slight exostosis in almost any position in the foot, excessive lameness presents itself and remains. In such cases nothing is left to us but the operation of neurectomy.

When the periostitis and ostitis is the result of a wound, and is complicated by caries or necrosis of the bone, the diseased portion of bone must in every case be laid bare and removed. It so happens that the majority of cases of this kind occur in positions where the diseased bone is easily got at. The lower margin of the os pedis or portions of the wings are commonly the seat of such changes. We meet with the former in cases of pricked foot, and with the latter in severe cases of tread, or as a complication in suppurating corn or in quittor. In such cases the animal must be cast and the foot secured. The wound is then followed up, the horn if necessary removed, and the bone curetted with a Volkmann's spoon; or, if showing itself as a sequestrum, removed with a scalpel and a strong pair of forceps. Care must be taken that every particle of the diseased bone is removed, and that no part of it is left to act as an after-source of irritation. With removal of the diseased portion and a strict attention to antisepsis healing soon takes place.

Reported Cases of Periostitis and Ostitis.—1. 'Figs. 150 and 151 represent the phalangeal bones of the off fore-leg of a thoroughbred horse named Osman, who was well known as a hunt steeplechaser of considerable merit in the Midland counties some twenty years ago. I may say that this horse was under my observation pretty regularly during the whole of his career, and up to the time of his death, from ruptured aorta, when eight years old. My attention was called to him as a yearling by his owner, who told me that he sometimes fancied the colt was lame. I went over to see him, and found that he was unmistakably lame on the off fore-leg. Careful examination showed no heat or enlargement anywhere. I advised rest and the colt became pretty sound, though not quite so—in fact, he never did become quite sound, and sometimes he was very lame indeed.

FIG. 150.—EFFECTS OF PERIOSTITIS ON THE PEDAL AND NAVICULAR BONES.

'Every imaginable sort of treatment was tried short of neurectomy, without avail. The curious part of the case was that there never was much heat or any apparent change of structure, nor was "pointing" a very noticeable feature. The foot always remained a good-looking one. As the horse won a good number of races he was of some value, and was seen by a good many members of the profession, who were by no means unanimous as to the cause of lameness. The favourite theory was that it was a sequence of "split pastern." A post-mortem examination showed that there was no fracture. There was no adherence of the tendon to the navicular bone nor any ulceration. The morbid changes consisted entirely of osseous deposit as shown in the photographs. The under surface of the navicular bone was much enlarged and roughened by this bony deposit, which extended on to the os pedis, causing complete anchylosis at each extremity of the navicular. The lateral cartilages were healthy. The interesting points in connection with the case are the insidious commencement of osseous disease, its extensive development, and the entire absence of any external manifestation, through its being confined entirely within the limits of the hoof.

FIG. 151.—EFFECTS OF PERIOSTITIS ON THE PEDAL AND NAVICULAR BONES.

'It should also be noted that the animal was able to undergo a severe course of training for some years, and to gallop successfully over some of the most trying courses in England. During the whole of this time he walked and galloped apparently sound, but trotted always lame, and generally dead lame.'[A]

[Footnote A: W. E Litt, M.R.C.V.S., Veterinary Record, vol. viii., p. 527.]

FIG. 152.—EFFECTS OF PERIOSTITIS ON THE OS PEDIS.

2. 'I herewith send you photographs of three cases of the above disease, occurring in the internal surfaces of the wings of the os pedis. The photos were kindly done for me by Dr. A. Lingard, Imperial Bacteriologist to Government of India. It is a cause of many cases of obscure foot lameness in India, and frequently accounts for the numerous entries on veterinary medical history sheets under the heading "Contused Foot."

'The course of the disease is as follows: The disease makes its appearance very soon after arrival in India, the animal being admitted to hospital suffering with undoubted foot lameness, generally slight. One is soon led to suspect this disease by negative symptoms of other disease being in existence. No coronary enlargement or flinching on pressure to the coronet, no shrinkage or wiring in of the heels, neither is the characteristic pointing of navicular present. In the early stages one has false hopes of recovery by finding gradual improvement for a time by fomentation and poultices, followed by irrigation and stimulants to the coronet, and perhaps the animal is discharged from hospital, to be returned after a few days worse than ever. The disease then becomes insidious and more pronounced, the nodding of the head, even at a walk, more exaggerated, and, in fact, the animal seems afraid to put his foot to the ground, and much resembles a horse with an abscess in his foot, either from prick or picked up nail. He absolutely nurses his foot. There is a certain amount of heat always present. The disease being now well developed, pressure is caused by the ends of the navicular bone, and they become involved at their points by bony deposits. The causes of this disease I attribute, firstly, to hereditary predisposition; and, secondly the exciting cause, standing confined on board ship, where no doubt pedal congestion takes place. And perhaps some subjects start it in their marches in mobs down country in Australia. Concussion may be the cause among older horses, but the specimens photographed were taken from remounts, that had either done no work or only very gentle work, in a deeply littered riding school.

FIG. 153.—EFFECTS OF PERIOSTITIS ON THE OS PEDIS.

'Treatment.—It is obvious from the position of this disease that treatment will be of no avail in producing a cure. As already stated, the disease is insidious and progressive, and it is hopeless to expect to arrest the growths once they are started. Unnerving would no doubt remove the symptom (lameness) of the disease, but an unnerved horse is not of much good for army purposes. I therefore consider that once the disease becomes firmly established it is an unfortunate and incurable one.

FIG. 154	FIG. 155

FIG. 154, 155—EFFECTS OF PERIOSTITIS ON THE OS PEDIS.

'Post-mortem reveals the small nodular growths on the inner surfaces of the wings of the pedal bone, and if long established the ends of the navicular bone are also involved. Exudation and gradual growth of false material around the nodules takes place, which also serves to increase pressure.'[A]

[Footnote A: Captain L.M.Smith, A.V.D., Veterinary Record, vol. xi., p. 229.]

3. 'This case was brought for my opinion. The horse was lame, and walked similar to one that had had laminitis, putting the heel down first upon the ground. I ordered the patient to be destroyed. You will note the ossification of the flexor pedis at its attachment to the pedal bone. I enclose photos of the ground, also of the articular, surfaces of the bone.'[A]

[Footnote A: F.B.Jones, M.R.C.V.S., Veterinary Record, vol. xi., p. 230.]