DIAGRAM ILLUSTRATING THE POSITION OF THE GROOVES IN THE WALL IN COLONEL SMITH'S OPERATION FOR SIDE-BONE.
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 lineamarks the position taken by the anterior line when the side-bone, is one reaching far forward, while the dotted linesbandcmark 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 atbandc, 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.
DIAGRAM ILLUSTRATING THE POSITION OF THE GROOVES MADE IN THE HOOF IN COLONEL SMITH'S OPERATION FOR SIDE-BONES.
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. Theincisions 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.
We head this section, PeriostitisandOstitis, 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 aninfectiveperiostitis, 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 befardistant 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 inevitablymustunder 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, termedosteoclasts. 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.—Cariesis 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.
Necrosisof 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.
EFFECTS OF PERIOSTITIS ON THE PEDAL AND NAVICULAR BONES
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.
EFFECTS OF PERIOSTITIS ON THE PEDAL AND NAVICULAR BONES
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.]
EFFECTS OF PERIOSTITIS ON THE OS PEDIS.
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.
EFFECTS OF PERIOSTITIS ON THE OS PEDIS.
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.
EFFECTS OF PERIOSTITIS ON THE OS PEDIS.
EFFECTS OF PERIOSTITIS ON THE OS PEDIS.
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.]
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.
A CASE OF BUTTRESS FOOT.
FIG. 156.—A CASE OF BUTTRESS FOOT.
FRACTURE OF THE PYRAMIDAL PROCESS IN BUTTRESS FOOT.
FIG. 157.—FRACTURE OF THE PYRAMIDAL PROCESS IN BUTTRESS 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 bonein 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.]
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.