 |
As we have said before, the operation consists in so grooving the wall as to allow of the quarters widening sufficiently to relieve pressure on the parts within. In one or two previous portions of this work we have considered operations involving this procedure. Before detailing the operation here, therefore, we will first describe the instruments necessary, and the most satisfactory methods of incising the horn.
To begin with, it must be remembered that all methods of hoof section have for their object the after-expansion of the horny box, and that this can only be brought about by making each groove complete from coronary margin to solar edge of the wall, and carrying it, throughout its length, deep enough to reach the commencement of the sensitive structures.
To this end, therefore, the operator must bear in mind the comparative thickness of the various parts of the wall, and must, in particular, remember the relative thinness of that portion of horn forming the outer boundary of the cutigeral groove, and accommodating the coronary cushion.
For the making of the incisions there is the special saw devised for this operation by Colonel F. Smith, A.V.D., and which we illustrate in Fig. 144. With this the wall is sawn through until the depth arrived at is equal to what is indicated by a previous examination of the thickness of the crust as viewed from the solar surface. Here Colonel Smith says: 'I strongly advise everyone to use a metal gauge (a thin piece of material) to introduce into the incision made by the saw, and run it up and down to ascertain whether the wall is properly divided throughout. The depth to which this should be done we know from the previous measurements of our gauge on the crust.'
Should the saw be of a pattern in which the set of its teeth makes only a narrow incision,[A] it should, while operating, be kept well oiled, and should be withdrawn every few seconds in order that the horn-dust lying in its teeth may be examined. If this is getting slightly blood-stained, we know, of course, that the sensitive structures are reached, and the incision has been carried far enough. In so judging the depth of the incision, however, care must be taken to see that the top of the coronary cushion is not injured with the saw, for if this is done the blood trickling into the depth of the incision will tinge the horn-dust, and give the false impression that the incision is sufficiently deep.
[Footnote A: That is Smith's older pattern. The newer pattern (Fig. 145) has the teeth so set as to make an incision wide enough to be looked into. In this case the depth arrived at is to be judged by the appearance of the bottom of the incision.]
If the operator has had no previous experience of the use of the saw in this operation, he must also be careful to avoid placing too great a pressure on the teeth of its lower third. This is done by keeping the hand too greatly depressed. Again, this leads to wounding of the sensitive structures (this time at the lower end of the incision), and again the operator is confused by the blood thus allowed to run into the groove.
The only portion of horn difficult to operate on is that immediately under the coronet. This is best severed with a succession of downward movements, and is easier performed with Smith's later pattern of side-bone saw (Fig. 145) in which the set of the foremost teeth is reversed.
In making these grooves we must say that we think the use of the special saw may be dispensed with, and the incisions just as easily, or, at any rate, just as successfully, made with the knife. Those who select to use this instrument should choose a narrow-topped and sharp searcher, or a modern shaped drawing-knife of suitable size, such as those depicted in Fig. 46, a and b, and they will find their work much easier if they will make the first steps in the incisions with an ordinary flat firing-iron. By the use of the latter instrument the grooves are made conveniently open along their tops, and room left for nicely finishing the more delicate manner of removing with the knife the softer horn near the sensitive structures.
Those whose leaning is towards the use of special instruments, but who, at the same time, do not care to use the saw, will find their wants supplied in the hoof plane (Smith's), Fig. 146, or the hoof chisel (Hodder's), Fig. 147. With the hoof plane the groove in the wall is made by a succession of downward scraping movements, while with the chisel the cut in the wall is made either from below upwards, or from above downwards, according as the foot is held forward or backward—whichever, in fact, comes most convenient.
When using the knife or the hoof plane it is not often that the sensitive structures are injured. In all cases, however, no matter what the instrument used, the metal gauge should be employed when the sensitive structures have been touched, and the operation obscured by blood.
Our instruments at hand, the operation may be proceeded with. The first step is to ascertain the extent of the side-bone, and to determine the position of the incisions. To do this the coronet is felt with the thumb, and the anterior extremity of the side-bone noted. This is marked on the horn with a piece of chalk, and a vertical line dropped from this position to the inferior margin of the wall (Fig. 148,1). The line crosses the horn fibres obliquely, and is purposely made in that direction in order that its inferior end may be far enough back to avoid the last nail-hole. Should the side-bone reach very far forwards, it may be wise to cause this line to slant from before backwards (see dotted line a, Fig. 148). Unless this is done, it is found that in some feet so much of the wall is isolated at the bottom that insufficient is left to nail the shoe to.
The next line to be made is the rear one. Its correct position is ascertained by first noting the junction off the wall with the bar (see groove 2, Fig. 149); and its inferior end must be just anterior to the inflexion of the wall. This is done that we may avoid cutting the bar. The position of the lower end of the rear line thus ascertained, it is run upwards with the chalk in the direction of the horn fibres.
The third line is made in such a position as to divide into two equal portions the wall between lines 1 and 2. Here, however, some operators prefer to make two, or even three, lines, adding those as at b and c, Fig. 148; and Smith himself says that a multiplicity of lines is an advantage rather than not.
In any case, having once determined the position of the lines, they should be plainly marked out with chalk, and then viewed from a distance with the foot on the ground, in order to judge of their regularity. If we are satisfied with them, we then lightly mark them with the saw, with the hot iron, or with the knife, whichever instrument we may be intending to use.
Unless the details are methodically carried out as here described, it is probable that more of the foot will be isolated than is necessary, and that as a consequence very little is left to which to nail the shoe.
The incisions are then made with the saw or the knife, with the foot held in a convenient position by an assistant. That usually found most comfortable for the first incision is with the foot held forwards and placed on an assistant's thigh in the position adopted for 'clenching up' when shoeing, while that for the rear incision is with the animal's knee flexed, and the foot held well up to the elbow. In this, however, each operator will suit himself.
Should the preliminary steps in making the incisions be performed with the iron, it will be easiest done with the foot on the ground.
When the incisions through the wall are complete, our attention must be given to the sole. A drawing-knife is here used, and a further incision made over the white line so as to destroy the union of the sole with the wall between incisions 1 and 2, and so completely isolate the portions of wall included within the four grooves (see groove 4, Fig. 149). When this is done it should be found that the portions of the isolated wall spring readily to pressure of the thumb.
The inferior or wearing margin of the isolated wall must now be so trimmed that it takes no bearing on the ground when the opposite limb is held up by an assistant and full weight placed upon the foot.
For a day or two after the operation lameness is intense. This is to be treated with hot poultices or hot baths, and and soon disappears. Three to four days later a bar shoe is nailed on (taking care that the bearing of the quarters is still eased), and the hot poultices still continued. Four days later still walking exercise may be commenced, to be followed shortly afterwards by trotting. At about the twelfth day some animals may conveniently be put to work, while in other cases a fortnight, or even a month, must elapse before this can be done. When put to work early, it is wise to fill in the fissures made in the wall with hard soap, with wax, or with a suitable hoof dressing, in order that irritation of the sensitive structures with outside matter may be prevented.
This operation is soon followed by remarkable changes in the shape of the foot. At about the third week the coronet shows signs of bulging, and the upper part of the wall operated on is often so protruding as to render the foot wider here than at the ground surface. This is a sign that the case is doing well.
Should no improvement be noticed at the end of three weeks or a month, or should the grooves become filled from the bottom (which they do remarkably fast), then the incisions must be deepened, the exercise reduced, and the fomentations or poulticing repeated. So treated, many cases of side-bone lameness will be relieved, if not entirely cured, and, should the worst happen, and no alteration in the lameness is noticeable, no harm will have been done to the foot. In this connection, the originator of the treatment says: 'I may assure those induced to doubt either their diagnosis or the value of hoof section that no harm is done to the foot, even should the operation be of no value. It may do much good; it cannot do harm. The operation will never succeed until the inherent timidity of sawing or cutting into the wall is overcome. The incisions must be deep, and of the same depth from the coronet to the ground.'[A]
[Footnote A: Journal of Comparative Pathology and Therapeutics, vol. iii., p. 313.]
It is well to remark here that the operation of hoof section cannot be expected to succeed in every case. The last man in the world to claim that for it would be its originator. Failure to relieve the lameness may be accounted for in a variety of ways. First, of course, will come errors in diagnosis. No one of us is infallible, and the lameness we have judged as resulting from side-bone may arise from another cause. There are, too, complications to be reckoned with, the existence or absence of which cannot always be definitely ascertained. Such are: Ringbone, especially that form of ringbone known as 'low'; bony deposits on the pedal bone, either on its laminal or plantar surface, or even changes in the navicular bursa.
CHAPTER XI
DISEASES OF THE BONES
A. PERIOSTITIS AND OSTITIS.
We head this section, Periostitis and Ostitis, for the reason that in actual practice it is rare for one of these affections to occur without the other. The periosteum and the bone are so intimately connected that it is difficult to conceive of disease of the one failing to communicate itself in some degree to the other. Pathologically, however, and for purposes of description, it is more convenient to describe separately the abnormal changes occurring in these two tissues.
With the main phenomena of inflammation occurring elsewhere we presume our readers are aware. Briefly we may put it, that under the action of an irritant, either actual injury, chemical action, or septic infection, the healthy tissues around react in order to effect repair of the parts destroyed. Also that this reaction involves the distribution of a greater blood-supply to the part, with an abundant migration of leucocytes, and the outpouring of an inflammatory exudate, together with symptoms of heat, pain, redness, and swelling of the affected area. And that in chronic inflammations, owing to persistence of the cause, the process of repair thus instituted does not stop at mere restoration of lost tissue, but continues to the extent of forming an abnormal quantity of such tissue as normally exists in the parts implicated.
The process of inflammation in bone is essentially the same. It takes place along the course of the bloodvessels, and is only modified in its attendant phenomena by the structure of the parts involved. Swelling, for instance, cannot take place in the centre of compact bone tissue. Otherwise, other changes occur exactly as in inflammations of other structures.
When the causal irritant has been excessively severe and the migration of leucocytes abundant, actual formation of pus may occur, the bony tissue being broken down and mingled with it, and an abscess cavity formed. In milder cases, affected and necrotic tissue is removed by a process of phagocytosis, and new tissue (this time osseous) formed in its place.
In the periosteum we may take it roughly that inflammation runs a course similar to that occurring in soft tissues elsewhere. There is but one exception, and that, as we shall mention shortly, is connected with its deeper layer.
As we know, the periosteum consists of two layers, an outer fibrous and an inner yellow elastic, and is extremely vascular. Numerous bloodvessels ramify in it, and, with their attendant nerves, break up to enter the numberless canals of the Haversian system. This extreme vascularity, of course, favours abundant exudation. The exudate, however, is, as it were, shut in by the dense fibrous layer of the membrane, and the result is that in periostitis it collects between the membrane and the bone, causing swelling and raising of the membrane, and giving rise to excruciating pain from pressure upon the nerves.
Should the periostitis be complicated by the formation of pus, then the vessels entering and supplying the bone are, in the suppurative area, destroyed. With their destruction it may happen that we get also death of a portion of the osseous tissue. This, however, when the suppuration is abundant, cannot commonly occur, as the bloodvessels within the bone—those of the medulla—commence to supply blood to the affected part. In cases of trouble with the bones of the foot, these last few remarks have a special significance. Here we have three bones whose medullary cavity is extremely small—almost nil, in fact—which explains in some measure how easy it is when suppuration exists to get necrosis and exfoliation of, say, portions of the os pedis. Necrosis and sloughing of the periosteum itself may also happen, but as the extreme vascularity of the membrane is a fairly strong safeguard against that it is of only rare occurrence.
In connection with the deep layer of the periosteum, and forming part of it, are found numerous bone-forming cells (osteoblasts). These, under ordinary conditions, are relatively quiescent. Under the slightest irritation or stimulation, however, their bone-forming functions are stirred into abnormal activity, thus explaining how easy it is (especially with bones so open to receive slight injuries as are those of the foot) to get ossific deposits, the starting-point of which we are quite unable to account for.
With this brief introduction we will now describe such pathological changes as occur in the separate structures, and which we are likely to encounter in the various diseases of the foot. While so doing, we shall draw attention to such diseases as we have previously described in which the pathological conditions we are considering may be met with.
1. PERIOSTITIS.
This we shall consider under (a) Simple Acute Periostitis, (b) Suppurative Periostitis, (c) Osteoplastic Periostitis.
(a) Simple Acute Periostitis.—This is the periostitis that follows on the infliction of a slight injury to the membrane—an injury without an actual wound and free from infective material. It is one, therefore, which we always judge as existing in those cases where we have distinct evidence or history of injury, but in which the injury has not been severe enough to lead to fracture or to the infliction of an actual wound.
Such cases may be those of lamenesses persisting after violent blows upon the foot—cases where the animal has been kicking against the stable fittings, or where the foot has been partially passed over by the wheel of a waggon. It may be, too, that in a case of 'nail-bound' a great deal of the pain and lameness is due to a simple periostitis caused by pressure of the bulged inner-layer of horn upon the sensitive structures.
Simple acute periostitis may also occur in cases where an actual wound is in existence, but where such wound, fortunately, remains aseptic. We may thus have this condition accompanying ordinary cases of pricked foot, of treads in the anterior region of the coronet, and of accidental injuries of other kinds.
In simple acute periostitis the membrane is thicker and redder than normal, and is easily stripped from the bone. As it is pulled off it is noticed that there are numerous fibril-like processes hanging to its inner surface, and which draw out from the substance of the bone. These are simply the vessels (bloodvessels and nerves) which, loosened by the inflammatory exudate, are readily detached and drawn from the Haversian canals into which they normally run. In addition to its increased redness, the membrane has a swollen and gelatinous appearance owing to its infiltration with the inflammatory discharges. Simple acute periostitis may and often does end in resolution. On the other hand, it may end in suppuration or may become chronic. If the latter, then the osteoblasts of the innermost layer become active, and abnormal deposits of bone are the result.
(b) Suppurative Periostitis.—This condition simply indicates that the inflammation is complicated by the presence of pus organisms. It is, therefore, a common termination of the simple acute form attending the infliction of a wound. The wound becomes contaminated, and the case of simple periostitis is soon changed into the suppurative form. Once having gained entrance to the wound, the pus increases in quantity, and slowly runs between the membrane and the bone. This, however, it does not do to any large extent, showing rather a tendency to penetrate the outer fibrous layer and gain the outside of the membrane.
Suppurative periostitis is met with in foot cases, commonly in connection with punctured foot. It occurs, too, as a complication in suppurating corn, in severe tread, in complicated sand-crack, as a result of the spread of suppurative matter in acute coronitis, and in sub-horny quittor.
In ordinary cases of suppurative periostitis the pus formed is yellow in colour, creamy thick, and free from pronounced odour—the so-called 'laudable' pus of the older writers. It so happens in many cases of foot trouble, however, that putrefactive organisms gain entrance side by side with those of pus. In this case the characters of the discharge are very different. It is distinctly more fluid, is of a pink or even light chocolate colour, and extremely offensive. In these instances the pus shows a marked tendency to spread, strips the periosteum from the bone, perforates the outer layer of the membrane, and finally infiltrates the surrounding tissues.
This forms a near approach to what is known in human surgery as an infective periostitis, and in our subjects is nearly always met with in cases of severe prick. Its rapidly spreading character makes it always a dangerous condition, and a punctured foot exuding a discharge of this nature should always be regarded as serious. The close contiguity of the joint (it can never be far distant in foot cases), the spreading character of the disease, and the rapidity with which the horse succumbs to arthritis, are all factors to be taken into consideration, and to lead to a warning-note being struck when attending a case of such kind.
A further instance of infective periostitis is that met with in acute laminitis. The discharge obtained from the sole in these cases very often bears the character we have just described, and when one considers the thinness of the keratogenous membrane, one is bound to admit that changes so grave occurring in it cannot fail to spread and infect the periosteum.
(c) Osteoplastic Periostitis.—This is more particularly a chronic process, and is, as the suffix 'plastic' indicates, associated with bone-forming changes in the membrane. It may occur as a consequence of slight but continued irritation, often without ascertainable origin (see Case 2, p. 392), or it may be the sequel of acute disease.
In this form of periostitis the membrane is again swollen and more vascular than in health, and is also easily separable from the bone. The exposed bone is generally rough, in some cases even spicular, and the inner layer of the removed membrane is rough and gritty to the touch—characters imparted to it by numerous minute fragments of bone that have been torn away with it from the more compact osseous tissue beneath.
The results of an osteoplastic periostitis are frequently met with in the bones of the foot, and are described by veterinary writers under such headings as 'Pedal Exostoses,' 'Ossifying Ostitis,' and 'Pedal Ossification' (see Figs. 152, 153, 154, and 155). In many of these cases the disease is purely chronic, and the original cause nearly always wanting. When the foot has been subjected to laminitis of some weeks' duration, the same condition is also met with, being at the same time associated with rarefactive osteoplastic ostitis, conditions which we shall shortly describe. Cases we have examined have undoubtedly shown this condition of osteoplastic periostitis, the rarefactive and osteoplastic changes in the bone itself, met with in older cases, occurring no doubt as a result of non-expansion of the horny box. So far as we are able to ascertain, there is every reason to believe that in chronic laminitis the accompanying periostitis leads to the formation of bone, and would, if it were possible, lead to increase in the size of the os pedis. If proof were wanted of this, it is only necessary to point out the increased growth at points where resistance is nil—namely, along the upper margin of the bone (see Fig. 118). However, increase in size elsewhere is prevented by the resistance of the hoof, so that, as the bone-forming process progresses, as it inevitably must under the inflammatory changes going on, it is, as it were, compensated for by rarefaction or bone-absorption changes occurring simultaneously with it.
2. OSTITIS.
We shall next deal with the inflammatory changes occurring in the bones themselves, and shall consider them under (a): Rarefying or Rarefactive Ostitis, (b): Osteoplastic Ostitis, and (c): Caries and Necrosis.
Inflammatory changes occurring in the medulla we may pass without consideration, for in the bones of the foot the medullary cavity is so small, and the changes taking place in it of such minor importance, that we may do this without in any way seriously prejudicing our work.
(a) Rarefying or Rarefactive Ostitis.—By this term is indicated an inflammation of the bone attended by its absorption, the absorption being due to the action of certain cells, termed osteoclasts. This condition may be due to the pressure of tumours, may occur as the result of injury when a piece of bone is stripped of periosteum, or may be the result of an inflammation occurring in the periosteum elsewhere.
A piece of bone undergoing rarefactive ostitis is redder than normal, and the openings of the Haversian canals are distinctly increased in size. As a result a greater number of them become visible. Their increase in size is due to the inflammatory absorption of the bony tissue forming them, and in the larger of them may be seen inflammatory granulation tissue surrounding the bloodvessels. This enlargement of the Haversian canals is well seen when the bone is macerated, the whole then giving the appearance of a piece of very rough pumice-stone.
This process of rarefaction or absorption of bone tissue may be confined to quite a small portion, or it may be spread over the whole of the bone, rendering it more porous than is normal, but stopping short of complete destruction of the bone tissue (a condition which is sometimes known as inflammatory osteoporosis (see Fig. 118)). In this latter case the condition is a chronic one, and the bone tissue remaining often appears to be strengthened by a compensatory process of condensation. For an example of rarefactive ostitis as met with in cases of disease of the feet, we refer the reader to laminitis (see Fig. 118). The osteoplastic or condensing process that appears to exist simultaneously with it explains, no doubt, how it is that bones so affected do not more commonly fracture.
A further example of this process is illustrated in Fig. 133. The pressure of a tumour (in this case a keraphyllocele) has led to rarefactive changes in the bone, forming a neat indentation in the normal contour of the bone which serves to accommodate the tumour.
(b) Osteoplastic Ostitis, Osteosclerosis, or Condensation of Bone.—This, too, is essentially a chronic process. It may occur as a result of, or, as we have just shown, exist simultaneously with the condition of, diffuse rarefactive ostitis. In this case there is a formation of new bone in the connective tissue surrounding the vessels in the Haversian canals. As a consequence the bone affected is greatly increased in density, and many of the Haversian canals by this means obliterated. The end result is an increase in size of the bones in such positions as the horny box admits of it, and a peculiar ivory-like change in their consistence.
For an example of this, we again refer the reader to the changes occurring in chronic laminitis.
(c) Caries and Necrosis.—Caries is a word which appears to be used with a considerable amount of looseness. In addition to the meaning implied by necrosis (namely, 'death' of the part), caries is generally used to indicate that there is also a condition of rottenness, decay, and stench. It is particularly applied, in fact, when the death of the bone is slowly progressive, and is due to the inroads made upon it by putrefactive or septic matter.
Necrosis of bone may be the result of any injury, such as severe blows, or pricks and stabs. In such cases it would appear that it is loss of a portion of periosteum that is the starting-point. With death of a portion of this membrane the vascular supply to a portion of the bone is cut off, and necrosis ensues. It may also result from the extension of inflammatory affections of the structures adjoining it, as, for instance, the spread of the infective material in severe tread, or the encroaches made by pus in cases of quittor, suppurating corn, or complicated sand-crack.
When the necrosed portion of bone is small, and is free from infective properties, it is quite possible that it may, as is the case with small spots of necrosis in softer tissues, be removed by a process of absorption. It must be remembered, however, that where the necrosis has occurred as a result of septic invasion this cannot be looked for, for in every case such reparative changes are worked solely by healthy tissue. If the tissues around the necrosis are engaged in dealing with organismal invasion and the poisonous products thus poured into their working area, their state of health is so weakened that they are unable to successfully combat with the two conditions simultaneously. As a consequence, the necrotic piece of bone persists, and acts as a permanent source of irritation.
It must be remembered, too, that if the dead portion of bone—even though it be free from septic matter—is very large, that it may itself act as a continual irritant, in which case it again persists, and cannot by natural means be removed.
In our cases necrosis of bone may be met with in punctured foot, in severe cases of tread, in cases of complicated crack, and in suppurating corn. It is met with, too, in navicular disease, in the extension of irritating discharges in cases of quittor, and in cases of chronic laminitis where the solar margin of the os pedis has penetrated the sole. In this latter case the protruding portion of bone is quickly denuded of its periosteum. Its blood-supply is destroyed, and necrosis follows.
Treatment.—In simple cases of periostitis, those caused by a blow but free from an actual wound, the most beneficial treatment is the continued application of cold by means of a hose-pipe or by swabs. If by these means we are successful in holding the inflammatory phenomena in check, any large formation of new bone is prevented, and the case does well.
When the case is complicated by a wound, then antiseptic measures, such as those described in the treatment of punctured foot, will at the same time have to be practised.
It must be admitted, however, that in all but the most simple cases ordinary treatment such as this is of very little use; for with only a slight exostosis in almost any position in the foot, excessive lameness presents itself and remains. In such cases nothing is left to us but the operation of neurectomy.
When the periostitis and ostitis is the result of a wound, and is complicated by caries or necrosis of the bone, the diseased portion of bone must in every case be laid bare and removed. It so happens that the majority of cases of this kind occur in positions where the diseased bone is easily got at. The lower margin of the os pedis or portions of the wings are commonly the seat of such changes. We meet with the former in cases of pricked foot, and with the latter in severe cases of tread, or as a complication in suppurating corn or in quittor. In such cases the animal must be cast and the foot secured. The wound is then followed up, the horn if necessary removed, and the bone curetted with a Volkmann's spoon; or, if showing itself as a sequestrum, removed with a scalpel and a strong pair of forceps. Care must be taken that every particle of the diseased bone is removed, and that no part of it is left to act as an after-source of irritation. With removal of the diseased portion and a strict attention to antisepsis healing soon takes place.
Reported Cases of Periostitis and Ostitis.—1. 'Figs. 150 and 151 represent the phalangeal bones of the off fore-leg of a thoroughbred horse named Osman, who was well known as a hunt steeplechaser of considerable merit in the Midland counties some twenty years ago. I may say that this horse was under my observation pretty regularly during the whole of his career, and up to the time of his death, from ruptured aorta, when eight years old. My attention was called to him as a yearling by his owner, who told me that he sometimes fancied the colt was lame. I went over to see him, and found that he was unmistakably lame on the off fore-leg. Careful examination showed no heat or enlargement anywhere. I advised rest and the colt became pretty sound, though not quite so—in fact, he never did become quite sound, and sometimes he was very lame indeed.
'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 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 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 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.
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 CORONAE.
Fractures of the os coronae 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 coronae 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 coronae 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 coronae 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 coronae 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 coronae. 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 coronae, 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 coronae 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 coronae 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 coronae 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.
CHAPTER XII
DISEASES OF THE JOINTS[A]
[Footnote A: Properly speaking, we have in the foot of the horse but one joint—namely, the corono-pedal articulation.
Although not a joint in the strict sense of the word, we, nevertheless, intend here to consider the navicular bursa as such. In this apparatus, although we have no articular cartilage proper, and no apposition of bone to bone, we still have a large synovial cavity, and in close proximity to it bone. We may, in fact, and do get in it exactly similar changes to those termed 'synovitis' and 'arthritis' elsewhere. Therefore, we include the changes occurring in it in this chapter, and hence the plural use of the word to which this note refers.]
A. SYNOVITIS.
Definition.—By the term 'synovitis' is indicated an inflammation of the synovial membrane. It may be either (a) Simple or Acute, or it may be (b) Purulent or Suppurative.
In the simple form there is little or no tendency for the affection to implicate the other structures of the joint, whereas in the suppurative form the joint capsule, the ligaments, and the bones soon come to participate in the diseased processes, giving us a condition which we shall afterwards describe as acute arthritis.
(a) SIMPLE SYNOVITIS.
1. Acute—(Causes).—Simple or acute synovitis is nearly always brought about by injury to the joint—by blows or bruises, or by sprains of the ligaments. At other times it occurs without ascertainable cause, and is then put down to the influence of cold, or to poisonous materials (as, for example, that of rheumatism) circulating in the blood-stream.
Pathology.—Uncomplicated acute synovitis never causes death. The pathological changes in connection with it have therefore been studied in cases purposely induced, and the animal afterwards slaughtered. It is then found that, as in inflammation elsewhere, the synovial membrane is showing the usual inflammatory phenomena—that it is thick and swollen as a result of the inflammatory hyperaemia and commencing exudation. Later, the synovial fluid becomes increased in quantity, is thin and serous, and after a time is seen to be mixed with the inflammatory exudation poured into it. We then find that it has lost its clear appearance, has become thick and muddy, and has floating in it flakes of fibrin.
If the case progresses favourably these materials are soon absorbed and resolution occurs. In rarer cases the thickening and congestion of the membrane increases, and the articular capsule becomes so distended with the increased synovia and accumulated inflammatory discharges that a kind of chemosis occurs. In other words, there oozes through, without actual rupture of the membrane, a thin, blood-stained, and purulent-looking discharge.
It is an important point to note that in cases of synovitis the fringes of the synovial membrane become swollen and blood-injected, forming noticeable red elevations at the margins of the cartilages. It is then that the diseased condition soon spreads and runs into arthritis.
Further, it is important, especially with regard to the question of the degree of pain and lameness likely to be caused, to note that often granulations are thrown out upon the looser folds of the membrane. As these increase in size they come to form fringed and villous membranous projections inserting themselves between the bones forming the articulation. In such cases there is no doubt that the intense pain sometimes observed in these cases is due to pinching of these prolongations of the synovial membrane by the opposing bones of the joint.
Symptoms and Diagnosis.—Acute synovitis of a joint leads to heat of the parts, pain, distension of the capsule, and, where the joint may be easily felt, fluctuation. In the articulation with which we are dealing, however, these last two symptoms are not easily detected, for the surrounding structures—namely, the lateral and other ligaments of the joint, the extensor pedis tendon in front, and the perforans behind, together with the dense and comparatively unyielding nature of the skin of the parts—are such as to prevent distension and fluctuation becoming marked to a visible extent. We are able to diagnose the case as one of foot lameness, and, with a history of a severe blow or other injury, are able to assume that this condition, perhaps attended with periostitis, is in existence.
When other symptoms present themselves diagnosis may be more certain. The animal becomes slightly fevered, throbbing pains in the joint manifest themselves by irregular pawing movements on the part of the patient. The animal comes out from the stable stiff, even dead-lame, and the limb is carried with the lower joints semiflexed. The breathing is hurried and the pulse firm and frequent, while in a bad case patchy perspiration breaks out at intervals on various parts of the body. If with this we get a puffy and tender swelling in the hollow of the heel, our diagnosis may be certain at any rate as to the existence of joint trouble, although, from reasons we have given, we may not be able to mark its exact nature.
2. Chronic.—Simple synovitis may in many instances become chronic. In this case we have simply a pouring into the synovial capsule of serous fluid, and with it an increased quantity of synovia—this time with an absence of the usual inflammatory phenomena. Beyond the swelling of the capsule there is little to be noticed. The joint becomes perhaps a little weaker, but pain or tenderness and heat are entirely absent. Such a condition, by reason of the natural rigidity of the parts, is not to be observed in the foot, although at times it must most certainly occur. Examples of such a condition are to be found in bog-spavin, in hygroma of the stifle, and sometimes in the fetlock. From a study of these, we know that they may be induced by frequent attacks of acute synovitis, from repeated slight injuries or bruises, or from strains to the ligaments of the joint; or that they may be chronic from the outset. We know, too, that in such cases the synovial membrane becomes thickened, and that in places it may have extended somewhat over the edges of the articular cartilages. It is only fair to suppose that such changes occur also in the pedal articulation. In that case we may take it for certain that the natural rigidity of the surrounding structures has the effect of pushing the thickened membrane further between the bones of the joint than occurs in a like condition elsewhere, leading, of course, to a lameness that is marked in degree but occult as to cause.
In our minds there is no doubt that many of the occult and chronic forms of foot-lameness we meet with in practice are in this way to be accounted for. We may, in fact, explain them by suggesting either a chronic synovitis alone, or a synovitis complicated with periostitis.
Treatment of Synovitis.—If a joint has been injured, as we have suggested, by slight blows or other causes—in other words, if the injury is subcutaneous, and no wound is in existence—then there is no treatment which offers better results than does the continued application of cold.
At the same time, the animal should be slung, or, if non-excitable and inclined to rest, allowed at intervals to lie on a thick and comfortable straw bed, the cold fomentations during such intervals being discontinued. When the case is a marked one and the animal valuable, benefit will be derived from the application of crushed ice.
The animal's condition must be watched, and the case helped as far as is possible by the administration of a mild dose of physic, by saline drinks, and, when necessary, by the giving of small but repeated doses of Fleming's tincture of Aconite in order to relieve the pain. In a chronic case the repeated application of a blister is indicated.
(b) PURULENT OR SUPPURATIVE SYNOVITIS.
In this condition we have synovitis complicated by the presence of pus. Unlike the simple form, it shows a marked disposition to spread, and quickly involves the surrounding structures. Very soon the ligaments of the joint, the periosteum, the articular cartilages, and the bones are implicated. This, of course, constitutes a condition of acute purulent arthritis. Under that heading, therefore, the condition will be later discussed.
B. ARTHRITIS.
(a) SIMPLE OR SEROUS ARTHRITIS.
With an attack of simple synovitis it may be always assumed that the changes commenced in the synovial membrane, communicate themselves more or less readily to the surrounding tissues, and are not confined to the synovial membrane alone. We may thus have the inflammatory phenomena asserting themselves in the surrounding ligaments, in the periosteum, in the bone, and in the articular cartilages. It depends, in fact, upon the severity of our case whether we call it synovitis or arthritis. The two conditions merge so the one into the other that no hard-and-fast rule may be laid down whereby they may with certainty be differentiated. Such symptoms, therefore, as we have given for synovitis may be also read as indicating a condition of simple arthritis. The course of the case will be very similar, and the treatment to be followed identical with that just given.
(b) ACUTE ARTHRITIS.
Causes.—An attack of acute arthritis may commence with the affection of the synovial membrane, and spread from that to the other structures. In other cases the disease of the synovial membrane, and after it the disease of the joint, may be secondary to diseases commencing in the structures around the joint. This affection may therefore follow on a case of acute coronitis, a case of suppurating corn, a case of quittor, a severe case of tread, or may attend a case of laminitis.
Symptoms.—In our cases we get very little beyond a magnification of such symptoms as we have described under acute synovitis. The heat and the pain is perhaps greater, and the lameness more marked. It is rather to the constitutional disturbance we must look, however, for a confirmation of our opinion that arthritis is in existence. This is always severe, and of an acute febrile nature. The pulse is fast, thin, and thready, the respirations enormously increased, and the temperature high. The appetite is in abeyance, the animal quickly becomes what is termed 'tucked-up,' or greyhound-like, in the body, and patchy perspirations break out about him. The limb is held with the joints all semiflexed, and severe and intense throbbing pains are indicated by the frequent pawing movements the animal makes in the air. Manipulation of the foot is resented, and the agonizing intensity of the pain so caused is shown by the drawn and haggard appearance of the eyes.
In a favourable case the symptoms from now onwards may gradually subside. The appetite returns, the breathing and other signs of disturbance show a return to the normal, weight is placed on the limb, and resolution slowly but surely takes place. In many of these, our favourable cases, however, resolution is incomplete, and recovery only takes place at the expense of anchylosis of the joint, a condition we shall refer to later.
In unfavourable cases, and these unfortunately are only too common, the condition terminates in suppuration.
(c) PURULENT OR SUPPURATIVE ARTHRITIS.
Definition.—By this term we indicate an arthritis complicated by the formation of pus within the joint.
Causes.—The organisms of pus may infect the joint by extension of a suppurating process from without. For example, in the case of a suppurating corn, in quittor, in tread, or in the case of a suppurating wound caused by a prick, the pus formed may in many instances be very near the capsular ligament of the articulation. Under such circumstances, unless there is a free and unhindered flow of the pus from an outside opening, inroads will be made by it upon the thin capsule. The latter is quickly penetrated, and pus is admitted to the interior of the joint.
In other cases infection of the joint may proceed from within, from a poisoned state of the blood-stream. The condition occurs, for instance, in bad attacks of laminitis. We ourselves, too, have seen two cases where suppuration of the pedal articulation occurred in the septic pyaemia of foals, a disease known commonly as 'joint-ill,' and characterized by an infected state of the circulation. Cases have also come under our notice where this condition has resulted from slight injuries in the region of the insertion of the extensor pedis inflicted by the animal himself when galloping away.
Perhaps, however, the most common cause of suppurative arthritis in the foot is direct penetration of the articulation in the case of pricks. The penetrating object is nearly always dirty—bacterially dirty, at any rate—and suppuration only too readily commences. Even should such a wound be inflicted by an aseptic body, infection would quickly ensue as a result of the wound gathering dirt from the ground, or even from admission to the joint of impure and bacilli-laden air.
Symptoms and Diagnosis.—This is one of the most serious conditions we are called upon to face when dealing with diseases of the foot, for in many cases it quickly ends in exhaustion and death of the patient, while in even the most favourable cases nothing better than a condition of complete and bony anchylosis is to be expected. The owner, therefore, should be warned accordingly.
As in the other joint affections, so here, we get all the symptoms of acute febrile constitutional disturbance. The pulse, the temperature, the respirations, and the general haggard, 'tucked-up,' and distressed appearances of the animal all tell too plain a tale. Our patient is in constant pain, and the seat of the trouble is clearly enough shown by the constant pawing movements of the affected foot. If he has room to get up and down in comfort the animal adopts for long periods at a stretch the recumbent position, and is not upon his legs long enough to take the necessary amount of food to keep him going. Even when down, it is plain to see that the animal is not at rest. The pawing movement is still maintained with the foot, and every now and again the eyes are opened and the headed lifted to give a troubled look round. The appetite, too, is capricious, and in many cases almost entirely lost.
In some slight degree the condition is less to be feared in a fore than in a hind foot—that is, so far as absolutely fatal results are concerned. With the condition confined to one fore-foot, the animal is able to get up and down with a moderate degree of comfort. At intervals, therefore, he rises to take nourishment, and as soon as his wants are satisfied again lies down.
With the disease in a hind-foot matters are not taken so comfortably. The patient finds that with each day's increasing weakness the difficulty that at first he had to raise himself with only one sound hind-foot becomes enormously increased. The consequence is that he fears to go down, and the standing position is maintained until sheer weakness overcomes him, and he goes down, not to rise again without assistance.
If judiciously attended he is, of course, put in slings before this stage is reached; but there are instances, as in the case of a cart-mare heavy with foal, where the use of slings is most decidedly contra-indicated.
If doubt before existed as to the nature of the case, it is at a later stage dispelled by the appearance, generally in the hollow of the heel, of a hot and painful swelling. This at first is hard, but later fluctuates. Finally it breaks at one or more spots, and there exudes from the opening or openings a purulent and oftentimes sanious discharge, which coagulates about each fistula after the manner of ordinary synovia.
With the discharge of the abscess contents there is some slight improvement in the symptoms. Here, with a suitable treatment, and with a patient of a particularly robust constitution, the case appears to turn, and slowly but surely progresses towards the only end we can hope for—namely, a more or less painless anchylosis of the articulation.
In less favourable cases the purulent discharge continues, and (always a bad sign) becomes more or less chocolate-like in colour, distinctly thin, and stinking. The diseased process spreads until the ligaments of the joint, both by reason of their infiltration with the inflammatory discharges, and also on account of the ravages made on them by the invading pus, either greatly stretch or altogether rupture.
The joint, after its ligaments have been destroyed in this manner, is loosened, and the bones are now freely movable. Their manipulation gives to the touch a sickening, grating sound—in other words, we have crepitus. This, of course, indicates that the articular cartilages have become greatly eroded by the inflammatory process, and so left what we may term 'raw' surfaces of bone to rub together. When the animal is put to the walk the toe of the foot is elevated, and the extreme mobility of the foot gives one the idea of fracture. With every step there is a peculiar sucking noise, comparable to that of a foot moving in a boot of water, and putrescent matter is squeezed from every opening each time the foot is put to the ground. Although we have seen cases even advanced thus far recover, it is questionable whether it is now wise to attempt to prolong life. Slaughter is far more humane, and, in our opinion, except with a valuable brood animal, more economical.
If the animal is allowed to linger, other symptoms will nearly always present themselves before death occurs. Whether in slings or not, a careful watch should be kept upon the sound limb. For some time the patient stands upon it incessantly, but sooner or later it happens that a farther visit show us the animal standing with full weight on the diseased foot, and making painful pawing movements with what before was the sound. We immediately jump to the conclusion 'laminitis.' And so it is, but it is a laminitis brought about by pyaemia. This is indicated by the swollen and oedematous nature of the lymphatics of the limb. Plainly enough they indicate the road by which the poison has travelled. It is in this way: Pus and putrefactive organisms have gained entrance to the lymphatics of the original diseased limb. From these they have rapidly gained the blood-stream and set up infection elsewhere. In this particular instance it is demonstrated by the laminitis and lymphangitis of the previously sound limb. With the poison thus circulating in the blood-stream, we often also get spots of infection commenced in one or other of the more vital organs—notably the lungs or the kidneys. The end of our case is then either a gangrenous pneumonia or complications induced by a condition of widespread pyaemia.
With the animal in slings there are one or two other symptoms that call for attention. In many cases, especially with animals of a lymphatic and indolent nature, the use made of them is inordinate. The patient rests so continually in them that alarming swellings commence to make their appearance about the rectum, or in the case of a mare about the vulva. The animal must then be let down at regular intervals and again raised when rest is obtained.
A more alarming symptom still is when the animal, instead of resting in the slings by his buttocks, casts his weight bodily into the belly-rest and hangs with a heavy head into the head-stall. This indicates complete exhaustion and a wish for death. Matters should therefore be explained to the owner, and his consent obtained for immediate destruction.
Pathology.—The pathological changes occurring in suppurative arthritis we shall pass over briefly. It is almost sufficient, in fact, to say that the whole of the joint becomes completely disorganized.
The synovial membrane becomes so tremendously thickened and injected as to be scarcely recognisable as such, the thickening in the later stages being due to large growths of granulation tissue which entirely alter the appearance of the membrane as we know it normally. In the early stages the contents of the joint are composed of thin pus and synovia. Later, as destruction of the synovial membrane proceeds, the flow of synovia is stopped, while the pus formation goes on until finally nothing but pus and dead tissue products fill the cavity. |
|
