Chapter 24

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.

'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.

'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.]

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.

'_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.

'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.]

B. PYRAMIDAL DISEASE, BUTTRESS FOOT, OR LOW RINGBONE.

_Definition_.--A condition of periostitis and ostitis in the region of the pyramidal process of the os pedis, usually preceded, but sometimes followed, by fracture of the process, and characterized by deformity of the hoof and an alteration in the normal angle of the joint.

_Causes_.--In the majority of cases buttress foot is brought about by fracture of the pyramidal process. Thus, although distinct evidence of such is nearly always wanting, we may assume that the original cause is violent injury to the part in question. Properly, therefore, one would say that this condition should be described under Fractures of the Os Pedis. It appears, however, that other cases of the kind arise in which fracture is altogether absent, or in which it is plainly seen to be subsequent to the diseased processes in the bone. For that reason, and also for the reason that the condition has come to be known by the name we have given, we give it special mention.

_Symptoms and Diagnosis_.--Even when the condition arises as the result of fracture, the ordinary manifestations of such a lesion are absent. By reason of the situation of the parts within the hoof we are unable to detect crepitation, and the resulting lameness is perhaps--in fact, nearly always is--neglected until such time as any heat or swelling caused by the injury has disappeared, in which case we are denied what evidence we might have obtained from that. All that is presented is lameness, and lameness that is at times excessive. But with the lameness there is nothing distinctive. The foot is tender on percussion, and the gait suggestive of foot lameness, that is all. We are unable, therefore, to make an exact diagnosis, and the condition goes for some time undetected.

Later, however, changes in the form of the hoof and the coronet begin to appear. The skin of the coronet, especially in the region of the toe, becomes more or less thickened and indurated, and the same remark applies to the subcutaneous tissues. The most marked change, however, is the alteration in the shape of the hoof. The wall protrudes at the toe in a manner that has been termed 'buttress-like,' and has given to the condition one of its names. This, of course, entirely alters the contour of the horny box. From being more or less U-shaped, it approaches nearer the formation of the letter V, the point of the V being at the toe.

In the later stages the coronary enlargement is plainly seen to be due to an extensive formation of bone. It is, in fact, a reparative callus, and the reason it reaches so large a size is probably to be accounted for by the pull of the extensor pedis upon the detached pyramidal process. As might be expected, this displacement of the fractured portion, with its effect of giving greater length to the extensor pedis, leads to a backward displacement of the os coronæ upon the pedal bone. As a result there is a marked depression at the coronet, the depression being heightened in effect by the exostosis in front. Pyramidal disease is, as a rule, met with in the hind-feet, but occurs also in the fore.

_Pathological Anatomy_.--When occurring without fracture, the first observable change is a thinning of the articular cartilage of the pyramidal process, through which the bone beneath appears abnormally white. Later the thinning of the cartilage progresses until at last it becomes entirely obliterated. This destruction of the cartilage commences first at the highest point of the articular surface of the pyramid, and gradually reaches further backward into the joint. While this is taking place the new bone is being formed on the front of the os pedis, below and around the process, until, as we have already seen, an exostosis is formed, large enough to be noticeable at the coronet. This, of course, partly implicates the joint and the points of the insertion of the extensor tendon.

Finally, fracture may, or may not, take place. When it does, the exostosis is larger, and the general deformity of the hoof greater.

_Treatment_.--Ordinary treatment, such as point or line firing, repeated blisters, or hoof section, each of which we have tried, appears to be utterly useless. So far as we have been able to gather from the writings of other practitioners, however, neurectomy returns the animal for a time to usefulness. If the fore-limb is the seat of trouble, either plantar or median neurectomy may be practised; if the hind, then the best results are obtained by section of the posterior tibial.

_Reported Cases_.--1. This animal, a mare, had been rested for lameness behind for two or three weeks, and then sent out to work, going sound. This was repeated several times, and each time the coachman reported, "Goes very lame behind after she has been at work about fifteen to twenty minutes." She always pulled out sound when I saw her in a halter on the following day, so I had her ridden, and after about seven or eight minutes she began to go lame in a hind-limb. Her lameness got rapidly worse as she was being ridden, and within a quarter of mile of her first showing lameness, she dropped and carried the lame foot in a way that suggested a badly fractured pastern. There was no recognisable disease in the limb to account for this lameness.

'I divided the posterior tibial nerve, and she went back to work moving sound, and continued to work sound up to her death from one of the regularly fatal bowel lesions twist or rupture.

'She worked nearly two years after unnerving, and developed the usual thickening at the coronet.'[A]

[Footnote A: W. Willis, M.K.C.V.S., _Journal of Comparative Pathology and Therapeutics_, vol. xv., p. 366.]

2. 'The subject of this note was a chestnut mare, nine years old, and used for omnibus work.

'_History_.--For about two months the mare was lame on the off fore-leg, and in spite of treatment the condition became steadily worse. The off fore-foot was rather long and narrow, and the fetlock-joint was inclined to be bowed outwards, but the degree of lameness was out of proportion to these defects, and the diagnosis was obscure.

'Median neurectomy was performed on May 10, 1902, and reduced the lameness to about half of what it was before. On June 5 ulnar neurectomy was performed, with the result that the mare became sound, and went to work three weeks later. She continued to work soundly and well, being inspected from time to time.

'During February of 1903 the coronet began to enlarge in front and slightly to the outer side, and gradually a ridge of bone grew down from the coronet to the toe. The case, in fact, became a typical one of so-called "buttress foot," which my friend Mr. Willis has described as diagnostic of disease of the pyramidal process of the pedal bone. Meanwhile the swelling of the coronet, which appeared to be mainly composed of fibrous tissue, increased in size, until the whole of the front and sides became involved, assuming the appearance shown in Fig. 156.

'In spite of the coronary enlargement the mare worked well, and remained free from lameness till June 8, 1903, on which day the limb became swollen up to the site of the median operation. The appearance of the limb closely simulated an attack of lymphangitis. The mare was kept under observation till the 13th of the same month, during which time the swelling increased, as did also the lameness to a slight degree. During progression she brought the heel to the ground and "rocked the toe," as in a case of rupture of the perforans tendon. The mare was killed on June 13.

'_Post-mortem_.--In trying to pull away the hoof from the sensitive structures with a pair of farrier's pincers, the tendons and ligaments of the corono-pedal articulation gave way, leaving the pedal bone _in situ_. The flexor perforans tendon showed inflammatory softening, and was very nearly ruptured through at the level of the navicular bone. There was slight evidence of navicular disease. The articular cartilage of the corono-pedal joint had been almost completely removed, and there was sclerosis of the opposed bony surfaces, which by unequal wear had brought about deformity of the os coronæ and os pedis.

There was very old-standing fracture of the pyramidal process (see Fig. 157), with the formation of a false joint between the process and the pedal bone. There was also a recent fracture of the part of the pedal bone which carries the articulation for the navicular bone, and this and the tendon lesions probably accounted for the final symptoms of 'break-down.'

Neurectomy enabled us to get a year's useful work out of what would otherwise have been a hopeless cripple.[A]

[Footnote A: A.R. Routledge, M.R.C.V.S., _Journal of Comparative Pathology and Therapeutics_, vol. xvi., p. 371.]

C. FRACTURES OF THE BONES.

More or less by reason of the protection afforded them by the hoof fractures of the bones of the foot are rare. When occurring they are more often than not the result of direct injury, as, for example, violent blows, the trapping of the foot in railway points, the running over of the foot with a heavily-laden waggon, or violent kicking against a gate or a wall. They occur also as a result of an uneven step upon a loose stone when going at a fast pace, and as a result of sudden slips and turns, in which latter case they are met with when animals have been galloping unrestrained in a field, or when an animal, ridden or driven at a fast pace, is suddenly pulled up, or just as suddenly turned.

At other times fractures in this region take place without ascertainable cause, and cases are on record where animals turned overnight into a loose box in their usual sound condition have been found in the morning excessively lame, and fracture afterwards diagnosed.

1. FRACTURES OF THE OS CORONÆ.

Fractures of the os coronæ result from such causes as we have just enumerated, and are nearly always seen in conjunction with fractured os suffraginis. When this latter bone is also fractured diagnosis is comparatively easy, a certain amount of crepitus, even when the suffraginis is only split, being obtainable. When the os corona alone is fractured then diagnosis is extremely difficult, the smallness of the bone and the comparative rigidity of the parts rendering manipulation almost useless, and effectually preventing the obtaining of crepitus. It is, in fact, only when the bone is broken into many pieces that crepitus may be detected, and even then it is slight.

_Reported Cases_.--1. 'The subject was a four-year old hunter. While at exercise in the morning of August 10 he bolted, got rid of his rider, and ran about in a mad fashion, came into contact with a wheelbarrow in a narrow passage, and finally came into violent contact with a wall, which had the effect of throwing him down. The rider stated that the animal suddenly put down his head and managed to get off the bridle; he then bolted, and the only chance for the rider was to throw himself off.

'On examination I found the horse unable to place any weight on the off fore-leg, the pastern was swollen and painful, the hollow of the heel was also swollen, and there was marked constitutional disturbance.

'After a short time he would place the heel on the ground and elevate the toe to a slight degree. On manipulating the pastern slight crepitation could be discovered, and there was abnormal mobility in the corono-pedal articulation. On the near fore-leg there were extensive wounds in the region of the knee, and great laceration of the tissues. The animal was destroyed.

'On examining the leg I found the subcutaneous tissues infiltrated from below the knee to the foot, large masses of gelatinous blood-stained material being present along the flexor tendons and in the hollow of the heel. The inferior articular surface of the os suffraginis was denuded of cartilage anteriorly; the os coronæ was fractured into eight moderate sized, irregular fragments, and ten minute pieces. The surface of the perforans tendon as it glides over the smooth surface at the back of the os coronæ was lacerated, and minute portions of the bone were found embedded therein.'[A]

[Footnote A: E. Wallis Hoare, F.R.C.V.S., _Veterinary Record_, vol. xiv., p. 133.]

2. 'Here, again, fracture was the result of the animal bolting with his rider. Trying to avoid collision with a conveyance coming towards him, the animal slipped on a wooden pavement, sliding along until his near fore-leg came in contact with the wheel of a standing cab. There was considerable swelling from the knee downwards, great pain, and evidence of fracture in the region of the pastern.

'Post-mortem revealed the os suffraginis broken into about thirty pieces, and the os coronæ with a piece broken off the inside of its proximal end.[A]

[Footnote A: A.F. Appleton, M.R.C.V.S., _Veterinary Journal_, vol. xiii., p. 411.]

3. 'The patient was a brown mare used for heavy van work in London. About January 10 she was lame, and as she had a cracked heel, was treated by poulticing for a day, and then by antiseptic lotions. In a week she was sent to work, but the following day lameness returned, and continued till about February 15. No special symptom was detected which indicated the exact position of any cause of lameness. Then the lameness increased in severity, and some swelling around the coronet began to show itself.

'In consultation with another veterinary surgeon, two possible causes of this intense lameness were discussed: one, that we had septic infection of the coronet, and that probably the swelling of this part would soften, and sloughs occur; the other, that a fracture of the os pedis or os coronæ existed. The enlargement of the coronet was hard and firm, not particularly sensitive. It was decided to do nothing for a few days. In a week the pain abated, and the mare would put her foot on the ground, and ceased to "nurse" the limb as she had done. When moved over in the box she put a little weight on the foot, but limped very decidedly.

'Another week passed, and the pain and lameness further abated, but the swelling around the coronet continued. Perhaps it was a little less in front, but it had not decreased on the inside. It remained firm, and was not painful on pressure. It showed no soft places, and the upper part of the leg remained free from oedema.

'The diagnosis was now that a fracture existed, and it was proposed to send the mare to grass for a few months. The consulting veterinary surgeon suggested that before doing so a blister might be applied to the coronet. This was done. The mare was found next day again on three legs. She had apparently been down during the night. In a few days the coronet increased again in size, and within a week "broke out" in two places.

'The opinion now formed was that, with a fracture and this additional cause of inflammation around the joint, it would be most economical for the owner to have her killed. This was done, and a post-mortem examination was made by Mr. Hunting and Mr. Willis.

'_Post-mortem_.--The foot, cut off at the fetlock-joint, showed extensive swelling all round the coronet. There were two wounds on the skin--one on the front of the coronet, the other on the inner side. From both pus and blood had escaped. They both communicated under the skin with a large abscess cavity. The abscess did not communicate with the joint. The pastern bone was sound. On separating the pastern from the coronet bone the articular surfaces were of a healthy colour, but the soft tissues immediately surrounding them were inflamed. On the centre of the articular surface of the coronary bone a thin red ring was noticed, and the portion of cartilage within it seemed raised. With the point of a scalpel this portion was lifted, and was found to be not only cartilage, but a layer of bone completely detached from the os coronæ. On removing the bones from the hoof the rest of the bone was quite normal, as was the pedal bone.

'Fig. 158 shows the articular surface of the coronet with the fracture _in situ_; and Fig. 159 the surface from which the broken portion is removed and laid to the side of the foot.

'Some interesting questions arise. How was the fracture caused? When did it occur? Between the broken portion and the main bone there was a layer of granulation tissue, so that it is certain the injury existed before the blister was applied, and it may possibly have existed from the commencement of the lameness.'[A]

[Footnote A: R. Crawford, M.R.C.V.S., _Veterinary Record_, vol. viii., p. 478.]

2. FRACTURES OF THE OS PEDIS.

These also are a result of the causes we have before given. The os pedis is also liable to fractures from pricks, from treads in the region of the wings, and from the malnutrition and careless use of the foot sometimes following neurectomy.

It is interesting to note that, with fracture of this bone, lameness is nearly always excessive, but that at times it may be entirely absent. Crepitus is, of course, denied us, and in nearly every instance the case is only diagnosed when the lameness persists and pus commences to form, or when grave changes in the normal shape of the foot compel our attention to the parts. When it is the continued formation of pus that draws our notice to something more than ordinarily grave, it is in giving exit to the pus that the fracture is nearly always discovered.

_Reported Cases_.--Two interesting cases of fractured os pedis are reported by Mr. Gladstone Mayall, M.R.C.V.S., in the _Veterinary Record_, vol. xiv., p. 54:

1. 'The horse was brought in markedly lame on the off hind-foot, knuckling at the fetlock, and taking a long stride with the injured limb. There was a punctured wound at the toe. The horn was pared, and antiseptic poultices applied. Notwithstanding the antiseptic treatment pus continued to form. At the end of a week sufficient horn was removed to ascertain the cause of the constant suppuration. A movable object was found at the bottom of the wound, and a piece of bone as large as a sixpence finally removed. Recovery was uneventful.'

2. 'A filly was attended for a discharging fistula at the coronet. Externally it had all the appearances of a quittor. At first no history was given. The filly went scarcely lame at all, and had never been shod. Treatment with poultices and caustic injections was useless. Finally the filly was cast and the foot examined. A piece of bone, apparently part of the wing of the os pedis, was removed, and the case made a good recovery. Subsequent inquiries elicited the fact that the animal had kicked at and hit a gate-post, and it was judged that then the injury had occurred.'

3. 'The subject was a bay horse, nine years old, used for railway shunting. On August 7 he was found to be intensely lame of the near hind-limb, and, after inquiries, there was no evidence bearing on the cause, as is often the case, and at times this comes to light when least expected.

'I was called in consultation on September 2, and found him suffering acute pain, with great swelling around the coronet. The foot was examined thoroughly, and the diagnosis was fracture of the pedal bone, and immediate slaughter was recommended. However, that was not carried out, and he died on September 22.

'The post-mortem inspection revealed a complete fracture of nearly the whole of the articulating surface and the left wing of the pedal bone (as shown in Fig. 160).'[A]

[Footnote A: J. Freeman, M.R.C.V.S., _Veterinary Journal_, vol. xxxi., p. 324.]

4. A further interesting case is reported by Mr. William Hurrell.[A] Here the cause was presumably galloping in the field, for the subject, a cart mare running out at grass with her foal, was suddenly found to be lame.

[Footnote A: _Ibid_., vol. v., p. 408.]

As the lameness continued to increase in severity, Mr. Hurrell was called in on August 1, and diagnosed the case as one of foot lameness. On this date the foot was pared out, and a large accumulation of pus discovered, Poulticing and antiseptic dressings were continued until August 16, when a movable piece of the os pedis was found at the toe.

On August 25 this detached portion of the bone was removed, and turned out to be the whole of the anterior margin of the os pedis, measuring 3-1/2 inches long, and varying in width from 1/2 inch to 1-1/2 inches. On September 20 the mare was working without lameness.

3. FRACTURES OF THE NAVICULAR BONE.

Hidden within the wings of the os pedis, and protected as it is by its tendinous covering and the yielding substance of the plantar cushion, the navicular bone is even less liable to fracture than either of the other bones of the foot.

The most common cause of fracture of the navicular is that of stabs or deep pricks in the region of the point of the frog (see p. 216). Following that, the next most common cause is violent injury. We thus find the navicular bone fractured, together with one or both of the other bones of the foot, when the foot is run over by a heavy vehicle. One such case is reported by Mr. J.H. Carter, F.R.C.V.S., where the horse's foot was run over by a tram-engine, in which the os pedis and the navicular were fractured in several places.[A] A further case is on record where a sharp blow on the front of the hoof was the cause. In this case the os pedis and other structures were uninjured, but the navicular bone was fractured into three large, and about half a dozen small, pieces.[B]

[Footnote A: _Veterinary Journal_, vol. xxxi., p. 246.]

[Footnote B: _Veterinarian_ for 1857, p. 73.]

Fractures of the navicular may occur, however, in which history of a prick or of a violent injury is absent. See reported case below.

As with fractures of the os pedis and the os coronæ, so with this exact diagnosis is difficult--we may say almost impossible. With a history of violent injury, however, some little regard may be paid to a continued heat and tenderness of the foot, and a distinct inclination on the part of the animal to go on the toe. Even when the fracture is the result of a prick, and the bone is plainly felt with the probe, we still cannot be positive as to fracture.

_Reported Case_.--'The animal was a Hungarian, a troop-horse in the 3rd Hussars (G. 15). On November 22, 1881, on the march from Norwich to Aldershot, the horse suddenly made a violent stumble, very nearly coming on to his knees. The rider declared that he put his foot on a stone. The accident caused great lameness in the near fore-leg, and the horse had to be led the remainder of that day's march. On the following day he was also led; but, after going some sixteen or eighteen miles, he was so lame that he was left at the nearest billet (in Edmonton). He was here attended by Mr. Stanley, M.R.C.V.S., of Edmonton, who pronounced it a case of navicular disease. I first saw the animal on December 1, 1881, and quite agreed with Mr. Stanley that it was a case of foot lameness, though, from the horse's former history, I could not think it a case of ordinary navicular disease. I diagnosed it a case of fracture, without displacement, either of the os coronæ or the navicular bone, but was more inclined to the former than the latter. This was after a full hour's examination. I failed to find any heat in, or any flinching by manipulation of, any part of the limb; but, in walking, the horse was excessively lame, going on the toe, and, indeed, trying if possible to keep the foot entirely off the ground.

'On December 6 the horse was sent on to Aldershot by rail. He was then walking better, though still very lame. My only treatment for a short time was to apply cold water constantly to the coronet and foot. For two hours daily this was done by a hose, the remainder of the time by a cold swab. On December 14 I applied a strong blister over the coronet, reaching up to the fetlock. This was washed off about the end of December. The horse was then not nearly so lame. I then resumed the cold-water treatment, and he got gradually better, and was sent to light duty on February 18, 1882. He, however, only attended one field-day, and was taken into the Horse Infirmary again on March 8, very lame. Again, there was an entire absence of heat or pain on pressure, but the same action, viz., going on the toe. I forgot to remark that he always pointed the toe of the affected leg when standing in the stable, and this symptom continued. I put him under the cold-water treatment for a short time, and about the middle of March again applied a strong blister over the coronet up to the fetlock. This was washed off about the end of the month, and was succeeded by the cold water again. Towards the end of April there was no improvement at all, and I applied for permission to destroy the horse. This was carried out on April 27, at the recommendation of Mr. Gudgin, I.V.S., Aldershot, and a Board of veterinary surgeons.

'On making the post-mortem examination I first thought the bone was only partly fractured or cracked, but on manipulating it, after its being in hot water a short time, I saw the fracture was complete.'[A]

[Footnote A: S.W. Wilson, M.R.C.V.S., A.V.D., _Veterinary Journal_, vol. xv., p. 12.]

_Treatment of Fractures of the Bones of the Foot_.--It will be seen at once that in most cases anything in the way of bandaging is well-nigh useless. When the os coronæ is fractured, however, a little more may be added to the natural rigidity of the parts by enclosing the region of the pastern and the foot in a plaster-of-Paris bandage. The main treatment, however, in every case, will be a continual use of the slings for at least seven to eight weeks, by that means compelling the animal to give to the injured parts the necessary amount of rest.

With fracture of the os pedis, when such is caused by pricks and complicated by a flow of pus, then attention must be given to removal of the displaced piece of bone. The pus track is to be followed up with the searcher, sufficient horn removed with the knife, and the broken piece of bone removed with a scalpel and a pair of strong forceps, the operation to be afterwards followed up by antiseptic dressings to the opening. Until this is done the wound refuses to heal.

Fracture of the navicular bone, if in any way diagnosed with certainty, offers us an almost hopeless case, for it appears to be a commonly reported fact that attempts at reunion are rare. This, in all probability, is due to the pressure put upon it every now and again, when the animal's weight presses the bone between the os coronæ and the os pedis above and the perforans tendon below. Even should reunion take place, the resulting callus, interfering as it does with the movements of the perforans, leaves us a case of incurable lameness. When the fracture is complicated by the formation of pus, as in the case of prick, then the case, with the attendant purulent synovitis and arthritis, is even more hopeless still.

Diagnosis of fracture of either of the bones of the foot is, as we have said before, extremely difficult. It so happens, therefore, in those cases caused by violent blows, that anything approaching an accurate opinion cannot be given until some months after the injury. After some time we are met with unmistakable changes in the form of the foot, and are able to assume that the persisting lameness is due to pressure of a reparative callus within the hoof. In such cases the only treatment of any use is that of neurectomy.