Diseases of the Horse's Foot Part 40

_Treatment_.--In simple cases of periost.i.tis, 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 periost.i.tis and ost.i.tis 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 p.r.i.c.ked 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 Periost.i.tis and Ost.i.tis_.--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.

[Ill.u.s.tration: FIG. 150.--EFFECTS OF PERIOSt.i.tIS 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.

[Ill.u.s.tration: FIG. 151.--EFFECTS OF PERIOSt.i.tIS 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.]

[Ill.u.s.tration: FIG. 152.--EFFECTS OF PERIOSt.i.tIS 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 p.r.o.nounced, 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 p.r.i.c.k 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 s.h.i.+p, 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.

[Ill.u.s.tration: FIG. 153.--EFFECTS OF PERIOSt.i.tIS 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.

[Ill.u.s.tration: FIG. 154, 155--EFFECTS OF PERIOSt.i.tIS 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.]

B. PYRAMIDAL DISEASE, b.u.t.tRESS FOOT, OR LOW RINGBONE.

_Definition_.--A condition of periost.i.tis and ost.i.tis 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 b.u.t.tress foot is brought about by fracture of the pyramidal process. Thus, although distinct evidence of such is nearly always wanting, we may a.s.sume 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 'b.u.t.tress-like,' and has given to the condition one of its names. This, of course, entirely alters the contour of the h.o.r.n.y 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 coronae 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 pract.i.tioners, 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 "b.u.t.tress 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, a.s.suming 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.

[Ill.u.s.tration: FIG. 156.--A CASE OF b.u.t.tRESS FOOT.]

[Ill.u.s.tration: FIG. 157.--FRACTURE OF THE PYRAMIDAL PROCESS IN b.u.t.tRESS FOOT.]

'_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 coronae 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.