Diseases of the Horse's Foot
by
Harry Caulton Reeks
Part 7 out of 8
Is side-bone hereditary? We can best answer that by saying that, some
several years ago, the Council of the Royal College of Veterinary Surgeons,
at the request of the Royal Commission on Horse Breeding, drew up a list of
those diseases 'which by heredity rendered stallions so affected unfit as
breeding sires,' and that in that list was included side-bone.
Side-bones, therefore, are hereditary. We think, however, the statement
needs qualifying. It is in this way: side-bones occur only at a certain,
usually well-defined, time after birth, and we might say are _never_
congenital. They occur only after the animal has been put to work, and are
more or less plainly due to mechanical causes--namely, the ill effects of
shoeing and concussion. The cause of their appearance, in short, is more
plainly extrinsic than intrinsic, and side-bone in the horse is, as
Professor McCall puts it, about as much due to heredity as is corn on the
human foot.
Between these two opinions--that they are plainly hereditary, and that they
just as plainly are not--it is well to strike a middle course. They are, we
will say, hereditary in this way: So long as a cart animal is bred, to put
it vulgarly, 'top-heavy' (that is, with a body out of reasonable proportion
to the feet that have it to support), so long will the foot be subjected to
a greater concussion, and so long will side-bones in such animals commence
to make their appearance at about middle life.
In addition to the causes we have now mentioned, side-bones are often
the result of other diseases of the foot. They thus occur as a sequel to
sub-horny quittor, to suppurating corn, to complicated quarter sand-crack,
or to the inflammation of the parts occasioned by a prick. They also arise
in many instances from the effect of a prick or injury to the coronet.
Among the latter we may mention treads from other animals, and treads
inflicted by the animal himself with the calkin of an opposite shoe, or the
repeated injury occasioned by the shafts being carelessly allowed to drop
on to the foot. In severe cases of laminitis, too, the cartilages are
nearly always affected. In this instance the inflammatory phenomena in the
os pedis no doubt give rise to an abnormal activity of bone-forming cells.
The cartilage is invaded, and the side-bone formed (see Fig. 118).
_Treatment_.--In the ordinary way the 'treatment' of side-bone is a thing
but rarely mentioned. The explanation lies, of course, in the fact that
side-bones are so rarely the cause of lameness. When lameness does occur
with a side-bone, and we have reason to believe that the said side-bone
is the cause of the lameness, it is well before talking of treatment to
question ourselves thus: 'In what way does the side-bone cause lameness?'
The now generally-accepted answer to that query is the explanation put
forward several years ago by Colonel Fred Smith--namely, that the pain, and
therefore the lameness, was due to the compression of the sensitive laminae
between the ossified and enlarged cartilage and the non-yielding and often
contracted wall of the quarters. That, in fact, constitutes the basis upon
which Smith's operation for side-bone (that of grooving the wall of the
quarters) is founded.
Before describing the operation, however, we may say that we are now able
to understand that older operators who claimed success for other methods of
treatment, were to a very great extent justified in so doing.
For instance, take the combined treatments of firing and blistering, and
the use of a bar shoe. Here the beneficial action of the cautery and the
blister may be largely problematical. The bar shoe, however, would be
almost certain to give good results. Frog-pressure with the ground would be
again restored, and the contraction of the heels removed. Pinching of the
sensitive structures would be diminished, and the lameness cured.
Take, again, the treatment of 'unsoling.' It was barbarous, we know
barbarous, because unnecessary and easily avoidable. It was practised,
however, certainly very little more than two decades ago, and practised by
men of standing in the profession. Without dragging the case to light again
by mentioning the names of those concerned, we may mention that not
many years ago a highly respected member of the profession was, at the
instigation of the Royal Society for the Prevention of Cruelty to Animals,
prosecuted for practising unsoling for the relief of side-bone. Practically
only one other member of the profession was able to come forward and defend
the operation on the score of its utility. We see now, however, that--as
does Smith's operation--unsoling does permit of the greater expansion of
the heels. The contraction is done away with, the pressure on the sensitive
laminae again diminished, and the lameness relieved.
Not that we are attempting to defend the operation--far from it. We simply
mention it as interesting, and quote this and the use of the bar shoe (with
both of which methods older operators have claimed success) merely as
evidence that the operation of Smith is based on a logical foundation.
When treatment is decided on, therefore, we may first advise blistering and
the use of a bar shoe. After that, should the lameness continue, and should
we still judge the side-bone to be the cause of it, the operation may be
advised.
As we have said before, the operation consists in so grooving the wall as
to allow of the quarters widening sufficiently to relieve pressure on
the parts within. In one or two previous portions of this work we have
considered operations involving this procedure. Before detailing the
operation here, therefore, we will first describe the instruments
necessary, and the most satisfactory methods of incising the horn.
To begin with, it must be remembered that all methods of hoof section have
for their object the after-expansion of the horny box, and that this can
only be brought about by making each groove complete from coronary margin
to solar edge of the wall, and carrying it, throughout its length, _deep
enough to reach the commencement of the sensitive structures_.
To this end, therefore, the operator must bear in mind the comparative
thickness of the various parts of the wall, and must, in particular,
remember the relative thinness of that portion of horn forming the outer
boundary of the cutigeral groove, and accommodating the coronary cushion.
For the making of the incisions there is the special saw devised for this
operation by Colonel F. Smith, A.V.D., and which we illustrate in Fig. 144.
With this the wall is sawn through _until the depth arrived at is equal to
what is indicated by a previous examination of the thickness of the crust
as viewed from the solar surface_. Here Colonel Smith says: 'I strongly
advise everyone to use a metal gauge (a thin piece of material) to
introduce into the incision made by the saw, and run it up and down to
ascertain whether the wall is properly divided throughout. The depth to
which this should be done we know from the previous measurements of our
gauge on the crust.'
[Illustration: FIG. 144.--SMITH'S SIDE-BONE SAW (EARLY PATTERN).]
Should the saw be of a pattern in which the set of its teeth makes only a
narrow incision,[A] it should, while operating, be kept well oiled, and
should be withdrawn every few seconds in order that the horn-dust lying in
its teeth may be examined. If this is getting slightly blood-stained,
we know, of course, that the sensitive structures are reached, and the
incision has been carried far enough. In so judging the depth of the
incision, however, care must be taken to see that the top of the coronary
cushion is not injured with the saw, for if this is done the blood
trickling into the depth of the incision will tinge the horn-dust, and give
the false impression that the incision is sufficiently deep.
[Footnote A: That is Smith's older pattern. The newer pattern (Fig. 145)
has the teeth so set as to make an incision wide enough to be looked into.
In this case the depth arrived at is to be judged by the appearance of the
bottom of the incision.]
If the operator has had no previous experience of the use of the saw in
this operation, he must also be careful to avoid placing too great a
pressure on the teeth of its lower third. This is done by keeping the hand
too greatly depressed. Again, this leads to wounding of the sensitive
structures (this time at the lower end of the incision), and again the
operator is confused by the blood thus allowed to run into the groove.
The only portion of horn difficult to operate on is that immediately under
the coronet. This is best severed with a succession of downward movements,
and is easier performed with Smith's later pattern of side-bone saw (Fig.
145) in which the set of the foremost teeth is reversed.
[Illustration: FIG. 145.--SMITH'S SIDE-BONE SAW (IMPROVED PATTERN).]
In making these grooves we must say that we think the use of the special
saw may be dispensed with, and the incisions just as easily, or, at any
rate, just as successfully, made with the knife. Those who select to use
this instrument should choose a narrow-topped and sharp searcher, or a
modern shaped drawing-knife of suitable size, such as those depicted in
Fig. 46, _a_ and _b_, and they will find their work much easier if
they will make the first steps in the incisions with an ordinary flat
firing-iron. By the use of the latter instrument the grooves are made
conveniently open along their tops, and room left for nicely finishing the
more delicate manner of removing with the knife the softer horn near the
sensitive structures.
Those whose leaning is towards the use of special instruments, but who, at
the same time, do not care to use the saw, will find their wants supplied
in the hoof plane (Smith's), Fig. 146, or the hoof chisel (Hodder's), Fig.
147. With the hoof plane the groove in the wall is made by a succession of
downward scraping movements, while with the chisel the cut in the wall is
made either from below upwards, or from above downwards, according as
the foot is held forward or backward--whichever, in fact, comes most
convenient.
[Illustration: FIG. 146.--HOOF PLANE (SMITH'S).]
When using the knife or the hoof plane it is not often that the sensitive
structures are injured. In all cases, however, no matter what the
instrument used, the metal gauge should be employed when the sensitive
structures have been touched, and the operation obscured by blood.
[Illustration: FIG. 147.--HOOF CHISEL (HODDER'S).]
Our instruments at hand, the operation may be proceeded with. The first
step is to ascertain the extent of the side-bone, and to determine the
position of the incisions. To do this the coronet is felt with the thumb,
and the anterior extremity of the side-bone noted. This is marked on the
horn with a piece of chalk, and a vertical line dropped from this position
to the inferior margin of the wall (Fig. 148,1). The line crosses the horn
fibres obliquely, and is purposely made in that direction in order that its
inferior end may be far enough back to avoid the last nail-hole. Should the
side-bone reach very far forwards, it may be wise to cause this line to
slant from before backwards (see dotted line _a_, Fig. 148). Unless this is
done, it is found that in some feet so much of the wall is isolated at the
bottom that insufficient is left to nail the shoe to.
The next line to be made is the rear one. Its correct position is
ascertained by first noting the junction off the wall with the bar (see
groove 2, Fig. 149); and its inferior end must be just anterior to the
inflexion of the wall. This is done that we may avoid cutting the bar. The
position of the lower end of the rear line thus ascertained, it is run
upwards with the chalk in the direction of the horn fibres.
[Illustration: FIG. 148.--DIAGRAM ILLUSTRATING THE POSITION OF THE GROOVES
IN THE WALL IN COLONEL SMITH'S OPERATION FOR SIDE-BONE. 1,2, and 3, mark
the grooves in the order in which they are made; the dotted line _a_ marks
the position taken by the anterior line when the side-bone, is one reaching
far forward, while the dotted lines _b_ and _c_ mark the position of the
additional grooves to be made if thought necessary.]
The third line is made in such a position as to divide into two equal
portions the wall between lines 1 and 2. Here, however, some operators
prefer to make two, or even three, lines, adding those as at _b_ and
_c_, Fig. 148; and Smith himself says that a multiplicity of lines is an
advantage rather than not.
In any case, having once determined the position of the lines, they should
be plainly marked out with chalk, and then viewed from a distance with
the foot on the ground, in order to judge of their regularity. If we are
satisfied with them, we then lightly mark them with the saw, with the hot
iron, or with the knife, whichever instrument we may be intending to use.
Unless the details are methodically carried out as here described, it is
probable that more of the foot will be isolated than is necessary, and that
as a consequence very little is left to which to nail the shoe.
[Illustration: FIG. 149.--DIAGRAM ILLUSTRATING THE POSITION OF THE GROOVES
MADE IN THE HOOF IN COLONEL SMITH'S OPERATION FOR SIDE-BONES. 1, 2, and 3,
show the grooves in the wall in the order in which they are made; 4 shows
the groove made at the junction of the sole with the wall.]
The incisions are then made with the saw or the knife, with the foot
held in a convenient position by an assistant. That usually found most
comfortable for the first incision is with the foot held forwards and
placed on an assistant's thigh in the position adopted for 'clenching up'
when shoeing, while that for the rear incision is with the animal's knee
flexed, and the foot held well up to the elbow. In this, however, each
operator will suit himself.
Should the preliminary steps in making the incisions be performed with the
iron, it will be easiest done with the foot on the ground.
When the incisions through the wall are complete, our attention must be
given to the sole. A drawing-knife is here used, and a further incision
made over the white line so as to destroy the union of the sole with the
wall between incisions 1 and 2, and so completely isolate the portions of
wall included within the four grooves (see groove 4, Fig. 149). When this
is done it should be found that the portions of the isolated wall spring
readily to pressure of the thumb.
The inferior or wearing margin of the isolated wall must now be so trimmed
that it takes no bearing on the ground when the opposite limb is held up by
an assistant and full weight placed upon the foot.
For a day or two after the operation lameness is intense. This is to be
treated with hot poultices or hot baths, and and soon disappears. Three to
four days later a bar shoe is nailed on (taking care that the bearing of
the quarters is still eased), and the hot poultices still continued. Four
days later still walking exercise may be commenced, to be followed
shortly afterwards by trotting. At about the twelfth day some animals may
conveniently be put to work, while in other cases a fortnight, or even a
month, must elapse before this can be done. When put to work early, it is
wise to fill in the fissures made in the wall with hard soap, with wax, or
with a suitable hoof dressing, in order that irritation of the sensitive
structures with outside matter may be prevented.
This operation is soon followed by remarkable changes in the shape of the
foot. At about the third week the coronet shows signs of bulging, and the
upper part of the wall operated on is often so protruding as to render the
foot wider here than at the ground surface. This is a sign that the case is
doing well.
Should no improvement be noticed at the end of three weeks or a month, or
should the grooves become filled from the bottom (which they do remarkably
fast), then the incisions must be deepened, the exercise reduced, and the
fomentations or poulticing repeated. So treated, many cases of side-bone
lameness will be relieved, if not entirely cured, and, should the worst
happen, and no alteration in the lameness is noticeable, no harm will have
been done to the foot. In this connection, the originator of the treatment
says: 'I may assure those induced to doubt either their diagnosis or the
value of hoof section that no harm is done to the foot, even should the
operation be of no value. It may do much good; it cannot do harm. The
operation will never succeed until the inherent timidity of sawing or
cutting into the wall is overcome. The _incisions must be deep, and of the
same depth from the coronet to the ground_.'[A]
[Footnote A: _Journal of Comparative Pathology and Therapeutics_, vol.
iii., p. 313.]
It is well to remark here that the operation of hoof section cannot be
expected to succeed in every case. The last man in the world to claim that
for it would be its originator. Failure to relieve the lameness may be
accounted for in a variety of ways. First, of course, will come errors in
diagnosis. No one of us is infallible, and the lameness we have judged as
resulting from side-bone may arise from another cause. There are, too,
complications to be reckoned with, the existence or absence of which cannot
always be definitely ascertained. Such are: Ringbone, especially that form
of ringbone known as 'low'; bony deposits on the pedal bone, either on its
laminal or plantar surface, or even changes in the navicular bursa.
CHAPTER XI
DISEASES OF THE BONES
A. PERIOSTITIS AND OSTITIS.
We head this section, Periostitis _and_ Ostitis, for the reason that in
actual practice it is rare for one of these affections to occur without the
other. The periosteum and the bone are so intimately connected that it is
difficult to conceive of disease of the one failing to communicate itself
in some degree to the other. Pathologically, however, and for purposes of
description, it is more convenient to describe separately the abnormal
changes occurring in these two tissues.
With the main phenomena of inflammation occurring elsewhere we presume
our readers are aware. Briefly we may put it, that under the action of an
irritant, either actual injury, chemical action, or septic infection,
the healthy tissues around react in order to effect repair of the parts
destroyed. Also that this reaction involves the distribution of a greater
blood-supply to the part, with an abundant migration of leucocytes, and
the outpouring of an inflammatory exudate, together with symptoms of heat,
pain, redness, and swelling of the affected area. And that in chronic
inflammations, owing to persistence of the cause, the process of repair
thus instituted does not stop at mere restoration of lost tissue, but
continues to the extent of forming an abnormal quantity of such tissue as
normally exists in the parts implicated.
The process of inflammation in bone is essentially the same. It takes place
along the course of the bloodvessels, and is only modified in its attendant
phenomena by the structure of the parts involved. Swelling, for instance,
cannot take place in the centre of compact bone tissue. Otherwise, other
changes occur exactly as in inflammations of other structures.
When the causal irritant has been excessively severe and the migration of
leucocytes abundant, actual formation of pus may occur, the bony tissue
being broken down and mingled with it, and an abscess cavity formed. In
milder cases, affected and necrotic tissue is removed by a process of
phagocytosis, and new tissue (this time osseous) formed in its place.
In the periosteum we may take it roughly that inflammation runs a course
similar to that occurring in soft tissues elsewhere. There is but one
exception, and that, as we shall mention shortly, is connected with its
deeper layer.
As we know, the periosteum consists of two layers, an outer fibrous and
an inner yellow elastic, and is extremely vascular. Numerous bloodvessels
ramify in it, and, with their attendant nerves, break up to enter the
numberless canals of the Haversian system. This extreme vascularity, of
course, favours abundant exudation. The exudate, however, is, as it were,
shut in by the dense fibrous layer of the membrane, and the result is that
in periostitis it collects between the membrane and the bone, causing
swelling and raising of the membrane, and giving rise to excruciating pain
from pressure upon the nerves.
Should the periostitis be complicated by the formation of pus, then the
vessels entering and supplying the bone are, in the suppurative area,
destroyed. With their destruction it may happen that we get also death of
a portion of the osseous tissue. This, however, when the suppuration is
abundant, cannot commonly occur, as the bloodvessels within the bone--those
of the medulla--commence to supply blood to the affected part. In cases of
trouble with the bones of the foot, these last few remarks have a special
significance. Here we have three bones whose medullary cavity is extremely
small--almost nil, in fact--which explains in some measure how easy it is
when suppuration exists to get necrosis and exfoliation of, say, portions
of the os pedis. Necrosis and sloughing of the periosteum itself may also
happen, but as the extreme vascularity of the membrane is a fairly strong
safeguard against that it is of only rare occurrence.
In connection with the deep layer of the periosteum, and forming part of
it, are found numerous bone-forming cells (_osteoblasts_). These, under
ordinary conditions, are relatively quiescent. Under the slightest
irritation or stimulation, however, their bone-forming functions are
stirred into abnormal activity, thus explaining how easy it is (especially
with bones so open to receive slight injuries as are those of the foot) to
get ossific deposits, the starting-point of which we are quite unable to
account for.
With this brief introduction we will now describe such pathological changes
as occur in the separate structures, and which we are likely to encounter
in the various diseases of the foot. While so doing, we shall draw
attention to such diseases as we have previously described in which the
pathological conditions we are considering may be met with.
1. PERIOSTITIS.
This we shall consider under _(a)_ Simple Acute Periostitis, _(b)_
Suppurative Periostitis, _(c)_ Osteoplastic Periostitis.
_(a) Simple Acute Periostitis_.--This is the periostitis that follows on
the infliction of a slight injury to the membrane--an injury without an
actual wound and free from infective material. It is one, therefore, which
we always judge as existing in those cases where we have distinct evidence
or history of injury, but in which the injury has not been severe enough to
lead to fracture or to the infliction of an actual wound.
Such cases may be those of lamenesses persisting after violent blows upon
the foot--cases where the animal has been kicking against the stable
fittings, or where the foot has been partially passed over by the wheel of
a waggon. It may be, too, that in a case of 'nail-bound' a great deal of
the pain and lameness is due to a simple periostitis caused by pressure of
the bulged inner-layer of horn upon the sensitive structures.
Simple acute periostitis may also occur in cases where an actual wound is
in existence, but where such wound, fortunately, remains aseptic. We may
thus have this condition accompanying ordinary cases of pricked foot, of
treads in the anterior region of the coronet, and of accidental injuries of
other kinds.
In simple acute periostitis the membrane is thicker and redder than normal,
and is easily stripped from the bone. As it is pulled off it is noticed
that there are numerous fibril-like processes hanging to its inner surface,
and which draw out from the substance of the bone. These are simply the
vessels (bloodvessels and nerves) which, loosened by the inflammatory
exudate, are readily detached and drawn from the Haversian canals into
which they normally run. In addition to its increased redness, the membrane
has a swollen and gelatinous appearance owing to its infiltration with the
inflammatory discharges. Simple acute periostitis may and often does end
in resolution. On the other hand, it may end in suppuration or may become
chronic. If the latter, then the osteoblasts of the innermost layer become
active, and abnormal deposits of bone are the result.
_(b) Suppurative Periostitis_.--This condition simply indicates that
the inflammation is complicated by the presence of pus organisms. It is,
therefore, a common termination of the simple acute form attending the
infliction of a wound. The wound becomes contaminated, and the case of
simple periostitis is soon changed into the suppurative form. Once having
gained entrance to the wound, the pus increases in quantity, and slowly
runs between the membrane and the bone. This, however, it does not do to
any large extent, showing rather a tendency to penetrate the outer fibrous
layer and gain the outside of the membrane.
Suppurative periostitis is met with in foot cases, commonly in connection
with punctured foot. It occurs, too, as a complication in suppurating corn,
in severe tread, in complicated sand-crack, as a result of the spread of
suppurative matter in acute coronitis, and in sub-horny quittor.
In ordinary cases of suppurative periostitis the pus formed is yellow
in colour, creamy thick, and free from pronounced odour--the so-called
'laudable' pus of the older writers. It so happens in many cases of foot
trouble, however, that putrefactive organisms gain entrance side by side
with those of pus. In this case the characters of the discharge are
very different. It is distinctly more fluid, is of a pink or even light
chocolate colour, and extremely offensive. In these instances the pus
shows a marked tendency to spread, strips the periosteum from the bone,
perforates the outer layer of the membrane, and finally infiltrates the
surrounding tissues.
This forms a near approach to what is known in human surgery as an
_infective_ periostitis, and in our subjects is nearly always met with in
cases of severe prick. Its rapidly spreading character makes it always
a dangerous condition, and a punctured foot exuding a discharge of this
nature should always be regarded as serious. The close contiguity of
the joint (it can never be _far_ distant in foot cases), the spreading
character of the disease, and the rapidity with which the horse succumbs to
arthritis, are all factors to be taken into consideration, and to lead to a
warning-note being struck when attending a case of such kind.
A further instance of infective periostitis is that met with in acute
laminitis. The discharge obtained from the sole in these cases very often
bears the character we have just described, and when one considers the
thinness of the keratogenous membrane, one is bound to admit that changes
so grave occurring in it cannot fail to spread and infect the periosteum.
_(c) Osteoplastic Periostitis_.--This is more particularly a chronic
process, and is, as the suffix '_plastic_' indicates, associated with
bone-forming changes in the membrane. It may occur as a consequence of
slight but continued irritation, often without ascertainable origin (see
Case 2, p. 392), or it may be the sequel of acute disease.
In this form of periostitis the membrane is again swollen and more vascular
than in health, and is also easily separable from the bone. The exposed
bone is generally rough, in some cases even spicular, and the inner layer
of the removed membrane is rough and gritty to the touch--characters
imparted to it by numerous minute fragments of bone that have been torn
away with it from the more compact osseous tissue beneath.
The results of an osteoplastic periostitis are frequently met with in the
bones of the foot, and are described by veterinary writers under
such headings as 'Pedal Exostoses,' 'Ossifying Ostitis,' and 'Pedal
Ossification' (see Figs. 152, 153, 154, and 155). In many of these cases
the disease is purely chronic, and the original cause nearly always
wanting. When the foot has been subjected to laminitis of some weeks'
duration, the same condition is also met with, being at the same time
associated with rarefactive osteoplastic ostitis, conditions which we
shall shortly describe. Cases we have examined have undoubtedly shown this
condition of osteoplastic periostitis, the rarefactive and osteoplastic
changes in the bone itself, met with in older cases, occurring no doubt
as a result of non-expansion of the horny box. So far as we are able to
ascertain, there is every reason to believe that in chronic laminitis the
accompanying periostitis leads to the formation of bone, and would, if it
were possible, lead to increase in the size of the os pedis. If proof were
wanted of this, it is only necessary to point out the increased growth at
points where resistance is nil--namely, along the upper margin of the bone
(see Fig. 118). However, increase in size elsewhere is prevented by the
resistance of the hoof, so that, as the bone-forming process progresses, as
it inevitably _must_ under the inflammatory changes going on, it is, as it
were, compensated for by rarefaction or bone-absorption changes occurring
simultaneously with it.
2. OSTITIS.
We shall next deal with the inflammatory changes occurring in the bones
themselves, and shall consider them under (_a_): Rarefying or Rarefactive
Ostitis, (_b_): Osteoplastic Ostitis, and (_c_): Caries and Necrosis.
Inflammatory changes occurring in the medulla we may pass without
consideration, for in the bones of the foot the medullary cavity is so
small, and the changes taking place in it of such minor importance, that we
may do this without in any way seriously prejudicing our work.
_(a) Rarefying or Rarefactive Ostitis_.--By this term is indicated an
inflammation of the bone attended by its absorption, the absorption being
due to the action of certain cells, termed _osteoclasts_. This condition
may be due to the pressure of tumours, may occur as the result of injury
when a piece of bone is stripped of periosteum, or may be the result of an
inflammation occurring in the periosteum elsewhere.
A piece of bone undergoing rarefactive ostitis is redder than normal, and
the openings of the Haversian canals are distinctly increased in size. As a
result a greater number of them become visible. Their increase in size is
due to the inflammatory absorption of the bony tissue forming them, and in
the larger of them may be seen inflammatory granulation tissue surrounding
the bloodvessels. This enlargement of the Haversian canals is well seen
when the bone is macerated, the whole then giving the appearance of a piece
of very rough pumice-stone.
This process of rarefaction or absorption of bone tissue may be confined
to quite a small portion, or it may be spread over the whole of the bone,
rendering it more porous than is normal, but stopping short of complete
destruction of the bone tissue (a condition which is sometimes known
as inflammatory osteoporosis (see Fig. 118)). In this latter case the
condition is a chronic one, and the bone tissue remaining often appears to
be strengthened by a compensatory process of condensation. For an example
of rarefactive ostitis as met with in cases of disease of the feet,
we refer the reader to laminitis (see Fig. 118). The osteoplastic or
condensing process that appears to exist simultaneously with it explains,
no doubt, how it is that bones so affected do not more commonly fracture.
A further example of this process is illustrated in Fig. 133. The pressure
of a tumour (in this case a keraphyllocele) has led to rarefactive changes
in the bone, forming a neat indentation in the normal contour of the bone
which serves to accommodate the tumour.
_(b) Osteoplastic Ostitis, Osteosclerosis, or Condensation of Bone_.--This,
too, is essentially a chronic process. It may occur as a result of, or, as
we have just shown, exist simultaneously with the condition of, diffuse
rarefactive ostitis. In this case there is a formation of new bone in the
connective tissue surrounding the vessels in the Haversian canals. As a
consequence the bone affected is greatly increased in density, and many
of the Haversian canals by this means obliterated. The end result is an
increase in size of the bones in such positions as the horny box admits of
it, and a peculiar ivory-like change in their consistence.
For an example of this, we again refer the reader to the changes occurring
in chronic laminitis.
_(c) Caries and Necrosis_.--_Caries_ is a word which appears to be used
with a considerable amount of looseness. In addition to the meaning implied
by necrosis (namely, 'death' of the part), caries is generally used to
indicate that there is also a condition of rottenness, decay, and stench.
It is particularly applied, in fact, when the death of the bone is slowly
progressive, and is due to the inroads made upon it by putrefactive or
septic matter.
_Necrosis_ of bone may be the result of any injury, such as severe blows,
or pricks and stabs. In such cases it would appear that it is loss of a
portion of periosteum that is the starting-point. With death of a portion
of this membrane the vascular supply to a portion of the bone is cut off,
and necrosis ensues. It may also result from the extension of inflammatory
affections of the structures adjoining it, as, for instance, the spread of
the infective material in severe tread, or the encroaches made by pus in
cases of quittor, suppurating corn, or complicated sand-crack.
When the necrosed portion of bone is small, and is free from infective
properties, it is quite possible that it may, as is the case with small
spots of necrosis in softer tissues, be removed by a process of absorption.
It must be remembered, however, that where the necrosis has occurred as a
result of septic invasion this cannot be looked for, for in every case such
reparative changes are worked solely by healthy tissue. If the tissues
around the necrosis are engaged in dealing with organismal invasion and
the poisonous products thus poured into their working area, their state of
health is so weakened that they are unable to successfully combat with the
two conditions simultaneously. As a consequence, the necrotic piece of bone
persists, and acts as a permanent source of irritation.
It must be remembered, too, that if the dead portion of bone--even though
it be free from septic matter--is very large, that it may itself act as a
continual irritant, in which case it again persists, and cannot by natural
means be removed.
In our cases necrosis of bone may be met with in punctured foot, in severe
cases of tread, in cases of complicated crack, and in suppurating corn.
It is met with, too, in navicular disease, in the extension of irritating
discharges in cases of quittor, and in cases of chronic laminitis where the
solar margin of the os pedis has penetrated the sole. In this latter case
the protruding portion of bone is quickly denuded of its periosteum. Its
blood-supply is destroyed, and necrosis follows.
_Treatment_.--In simple cases of periostitis, those caused by a blow but
free from an actual wound, the most beneficial treatment is the continued
application of cold by means of a hose-pipe or by swabs. If by these means
we are successful in holding the inflammatory phenomena in check, any large
formation of new bone is prevented, and the case does well.
When the case is complicated by a wound, then antiseptic measures, such as
those described in the treatment of punctured foot, will at the same time
have to be practised.
It must be admitted, however, that in all but the most simple cases
ordinary treatment such as this is of very little use; for with only a
slight exostosis in almost any position in the foot, excessive lameness
presents itself and remains. In such cases nothing is left to us but the
operation of neurectomy.
When the periostitis and ostitis is the result of a wound, and is
complicated by caries or necrosis of the bone, the diseased portion of
bone must in every case be laid bare and removed. It so happens that the
majority of cases of this kind occur in positions where the diseased bone
is easily got at. The lower margin of the os pedis or portions of the wings
are commonly the seat of such changes. We meet with the former in cases
of pricked foot, and with the latter in severe cases of tread, or as a
complication in suppurating corn or in quittor. In such cases the animal
must be cast and the foot secured. The wound is then followed up, the horn
if necessary removed, and the bone curetted with a Volkmann's spoon; or, if
showing itself as a sequestrum, removed with a scalpel and a strong pair
of forceps. Care must be taken that every particle of the diseased bone
is removed, and that no part of it is left to act as an after-source of
irritation. With removal of the diseased portion and a strict attention to
antisepsis healing soon takes place.
_Reported Cases of Periostitis and Ostitis_.--1. 'Figs. 150 and 151
represent the phalangeal bones of the off fore-leg of a thoroughbred horse
named Osman, who was well known as a hunt steeplechaser of considerable
merit in the Midland counties some twenty years ago. I may say that this
horse was under my observation pretty regularly during the whole of his
career, and up to the time of his death, from ruptured aorta, when eight
years old. My attention was called to him as a yearling by his owner, who
told me that he sometimes fancied the colt was lame. I went over to see
him, and found that he was unmistakably lame on the off fore-leg. Careful
examination showed no heat or enlargement anywhere. I advised rest and the
colt became pretty sound, though not quite so--in fact, he never did become
quite sound, and sometimes he was very lame indeed.
[Illustration: 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.
[Illustration: 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.]
[Illustration: 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.
[Illustration: 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.
[Illustration: 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.]
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.
[Illustration: FIG. 156.--A CASE OF BUTTRESS FOOT.]
[Illustration: 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 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.
[Illustration: FIG. 158.--FRACTURE IN SITU (OS CORONAE).]
'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.
[Illustration: FIG. 159.--WITH BROKEN PORTION REMOVED.]
'_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.'
[Illustration: FIG. 160.--FRACTURED OS PEDIS.]
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.
If the suppurative process has commenced from within, the pus that is
formed is, as a rule, thick and creamy, comparatively unstained, and free
from marked odour. If, on the other hand, air has gained access to the
joint, or the suppurative process has started from the materials introduced
by a foreign body, the joint contents are thin, blood-stained, and
stinking.
The inflammatory changes in the joint soon spread to the ligaments, and to
the soft structures in contact with them. This means that the ligaments
become infiltrated with inflammatory exudate, that the fibrous bundles
composing them become separated, and that the ligaments are weakened and
easily stretched. As a consequence, a certain amount of displacement or
dislocation of the bones is allowed.
In like manner the inflammatory changes keep spreading until we have the
periosteum next the ends of the bones affected. The periostitis thus set
up invariably takes the osteoplastic form, and as a result of this we have
growths of new bone in the near neighbourhood of the joint. It is in the
later stages of the disease--that is, when the pus has been evacuated and
reparative changes commenced--that this osteoplastic periostitis is most
marked, and it plays a large part in bringing about the condition of
anchylosis, which we shall afterwards describe.
Grave changes also occur in the articular cartilages. They quickly lose
their peculiar glistening polish, their semitransparency is lost, and the
natural tint of a pearl-like blue gives way to a dirty yellow. Later this
is followed by erosion of the cartilages at such points as they happen to
be in greatest contact. The ends of the bones are thus exposed, and their
medullary cavities exposed to infection. As a result we get in them the
changes we have already described under Ostitis.
_Treatment_--_(a) Preventive_.--Seeing that many of these cases have their
starting-point in stabs or penetrating wounds of the sole, we shall be
concerned first with a consideration of the correct treatment to be adopted
when we know the wound to have reached the articulation.
Only too frequently the treatment practised is that of poulticing. In other
portions of this work we have pointed out the advantages that a continued
antiseptic bathing has over the application of a poultice, the greater
readiness with which the solution comes into contact with the deeper parts
of the wound, and the far greater chance there is of maintaining water in
an antiseptic condition than there is of keeping a poultice in the same
state. There is no doubt, that in this case also, the cold or warm
antiseptic bath is to be preferred to the poultice. It is questionable,
however, whether even the bath is sufficient for our purpose here. We have
in this case a deep punctured wound, and a wound that in every probability
is infected with the organisms of pus or of putrefaction. It is a wound,
moreover, which is likely to impede the thorough access to it of the
solution in which the foot is fomented, on account of the flakes of
coagulated fibrin which fill it.
The most rational treatment, therefore, if we get to the case early enough,
is to irrigate the wound freely with a solution of carbolic acid in water
(1 in 20), or with a solution of perchloride of mercury (1 in 1,000),
injected by means of a glass syringe, or the pattern of syringe devised for
quittor. This injecting should be done thoroughly, and by that we mean that
several syringefuls of the solution should be injected, the joint after
each injection being manipulated so as to distribute the solution as far as
possible over it. When this is done the opening in the sole may be plugged
with a little perchloride of mercury, or, better still, with a little piece
of tow saturated with a concentrated solution of perchloride of mercury
or a solution of iodoform in alcohol and an antiseptic pad of tow or lint
placed over all. The foot should then be bandaged and encased in a boot or
sacking protective. The bandage should be removed daily and the antiseptic
pad changed. At each visit the animal's condition must be carefully
noted. So long as constitutional disturbance is slight, the foot appears
comfortable, is free from marked heat and tenderness, and pawing movements
are absent, and so long as the discharge on the pad appears non-purulent,
free from marked odour, and small in quantity, then this dressing may be
persisted in.
This treatment of open joint, preventive as it is of arthritis, is also
indicated in the case of open navicular bursa. In several instances we have
practised this treatment for the dressing of wounds implicating the bursae
of tendons and the capsules of joints. It is also spoken of favourably by
Mr. C.H. Flynn in the _American Veterinary Review_ for June, 1888, whose
treatment is as follows: 'Place the patient in a clean, well-ventilated,
and drained stable. Have all the litter removed, and insist on the stall
being kept clean. Either place the animal in slings, or tie the head so as
to prevent lying down. Clip the hair and cleanse the parts well. He prefers
the corrosive sublimate solution (1 in 1,000). Should the wound be of two
or more days' standing, inject the joint with the corrosive sublimate
solution. Now dry the parts with a clean towel and sprinkle the wound with
iodoform. Over this place a thick layer of absorbent cotton-wool, filled
with iodoform, bandage securely, and keep the patient on a moderate diet,
preserving the utmost quietude possible. Should the bandage remain in
position and the animal free from pain, leave the bandage and dressing in
place from five days to a week. Then change it, and should the discharge
be little, do not disturb it, but renew the iodoform and cotton dressing,
leaving it on for another week.'
Other treatments for the same condition are practised, in which the wound
is dusted with powdered iodoform, with potassium permanganate, or with
corrosive sublimate, or where the wound, instead of being dusted, has
the corrosive sublimate applied in the form of a plug. In each case the
preliminary irrigation with the corrosive sublimate solution is dispensed
with. This, however, should on no account be omitted. In our opinion it
constitutes the very essence of the rationality of the treatment.
_(b) Curative_.--It may happen, however, and often does, that this first
injection of an antiseptic is unsuccessful in preventing organismal
infection of the wound. In this case grave constitutional disturbance and
other untoward symptoms such as we have already described quickly make
their appearance.
The animal should now be placed in slings and preparations made for
actively treating the wound with antiseptics. Whether we fail or not, we
have the satisfaction of knowing that we have given to the patient the best
and the only chance of recovery.
It should be remembered, however, and should be pointed out to the owner,
that with purulent arthritis fully developed, with the grave constitutional
changes it occasions, and with the ever-present danger of a general
septic invasion of the blood-stream, that the human surgeon under such
circumstances offers to his patient the alternatives of amputation or
probable death. With us no such alternative is possible. It is either
return the joint to some semblance of its former usefulness, or destroy the
patient.
In this case we advise the injection of the original wound, and also such
fistulous openings as may have formed, with the 1 in 1,000 sublimate
solution. Also, in order to avoid the sometimes abortive attempts of the
antiseptic pad, to maintain a condition of asepsis around the wound, we
advise the continual soaking of the whole foot in a cold antiseptic bath.
This may be either carbolic acid 1 in 20, or--what is less volatile,
perhaps more effectual, and certainly more economical--perchloride of
mercury 1 in 1,000.
It has been our good fortune, even when we have seen the foot almost
detached from the limb by the devastating inroads of the pus, to see
the suppurative process by this means gradually overcome, a reparative
anchylosis set in, and the animal restored to good health and usefulness,
if not to soundness.
Once the suppurative process is checked and anchylosis commences, it is
good treatment to smartly blister the whole of the region of the coronet,
the pastern, and the wound itself with a mixed blister of cantharides and
biniodide of mercury, repeated at intervals of a fortnight. This prevents
to some extent further infection of the wound, and assists also in
promoting the changes that tend to anchylosis.
_(d)_ ANCHYLOSIS.
The word anchylosis signifies the stiffening of a joint. When one has read
the serious changes occurring within the joint in the more serious forms
of arthritis, it is easy to understand how it comes about. In suppurative
arthritis, for instance, we have the synovial membrane destroyed, the
articular cartilages partly or wholly obliterated, and the former
boundaries of the joint entirely lost. If the animal lives, nature is
bound to make repair of a sort. The synovial membrane and the articular
cartilages utterly destroyed, as we have described, cannot again be
replaced. Nature can only build again from such materials as are left to
her. In this case the material is bone.
It must be remembered, however, that often the bone has been so diseased
that spots of necrosis or caries within it are bound to remain unless moved
by operative interference. Such diseased portions, when dealing with the
foot, are beyond reach of the surgeon's knife, and we have no alternative
but to allow them to remain. We get, therefore, in many cases, a condition
of rarefactive ostitis occurring side by side with a slowly progressive
caries within the bone, while outside is occurring an osteoplastic
periostitis. The concurrence of these conditions leads in time to great
increase in size of the parts, together with increasing anchylosis and
deformity.
C. NAVICULAR DISEASE.
_Definition_.--Chronic inflammatory changes occurring in connection with
the navicular bursa, affecting variously the bursa itself, the perforans
tendon, or the navicular bone, and characterized by changes in the form
of the hoof and persisting lameness. The disease is commonly noticed
in thoroughbreds or in horses of the lighter breeds, and is but seldom
observed in heavy cart animals. Usually it is met with in one or both
fore-feet. Although of extremely rare occurrence, it has been noticed in
the hind.
_History_.--To English veterinarians appears to belong the credit of
discovering navicular disease. As early as 1752 we find one, Jeremiah
Bridges, in 'No Foot, No Horse,' drawing attention to 'coffin-joint
lameness,' and advocating for its treatment setoning of the frog. It
appears, too, that Moorcroft, prior to his departure for India in 1808, was
acquainted with what was then known as coffin-joint[A] lameness, having
drawn attention to it in 1804 in a letter to Sir Edward Codrington.[B] In
1819 Moorcroft made it even plainer still that he was fully acquainted with
what we now know as navicular disease. This we learn from a letter written
by him to Sewell, in which he laid claim to being the originator of
neurectomy. In this letter he says:
[Footnote A: The coffin-joint at this time included the navicular bursa.]
[Footnote B: Percival's 'Hippopathology,' vol. iv., p. 132.]
'On dissecting feet affected with these lamenesses, the flexor tendon was
now and then observed to have been broken, partially or entirely, but
more commonly to have been bruised and inflamed in its course under the
navicular or shuttle bone, or at its insertion into the bone of the foot.
Sometimes, although seldom, the navicular bone itself has been found to
have been fractured; at others its surface has been deprived of its usual
coating, and studded with projecting points or ridges of new growth, or
exhibiting superficial excavations more or less extensive.'[A]
[Footnote A: _Ibid_.]
_Pathology and Point of Commencement of the Disease_.--The exact position
in which the diseased process starts has for a long time been a subject
of discussion, and even now it is doubtful whether the point has been
definitely settled. To mention but a few among many: We find Mr. Broad, of
Bath, strenuously insisting on the fact that the disease commences in the
interior of the navicular bone. Just as strenuously we find the editor of
the journal in which the matter is being discussed, the late Mr. Fleming,
asserting that the disease commences in the bursa.[A] Others, too, hold
that the disease commences primarily in the tendon. Wedded to this view was
the discoverer, Mr. Turner, of Croydon; while Percival commits himself to
the statement that it is either the central ridge or the postero-inferior
surface of the navicular bone, or the opposed concavity in the perforans
tendon, that shows the earliest signs of the disease. The observations made
by Dr. Brauell, the first Continental writer to fully describe the disease,
led him to the statement that neither the bone nor the bursa was the
_invariable_ starting-point of the trouble, but that usually it commenced
in inflammation of the bursa itself.
[Footnote A: Percival's 'Hippopathology,' vol. iv., p. 132.]
Without, therefore, committing ourselves to an expression of opinion as
to the precise starting-point of the affection, we shall describe the
pathological changes occurring in navicular disease as noted in (1) the
bursa, (2) the cartilage, (3) the tendon, and (4) the bone.
1. _Changes in the Bursa_.--Upon the internal surface of the bursal
membrane is first noticed a slight inflammatory hyperaemia, accompanied
by more or less swelling and tumefaction, owing to its infiltration with
inflammatory exudate. The portion covering the hyaline cartilage of the
navicular bone has lost its peculiar pearl-blue shimmer, and become a dirty
yellow.
Remembering that the bursal membrane is a synovia-secreting one, and
bearing in mind what happens in ordinary synovitis and arthritis (with
which, of course, this may be very closely compared), we shall first expect
changes in the bursal contents. It is highly probable, though difficult of
proof, that in the very early stages the chronic inflammatory stimulus has
the effect of increasing the flow of synovia. In every case, however, where
it can with any certainty be said that navicular disease exists, it is too
late to meet with this condition. The disease has then progressed until
destruction of the secreting layer of the bursal membrane has been
seriously interfered with, and in this case we find a distinct deficiency
in the quantity of synovia in the bursa. In advanced cases it is even found
that the bursa is _absolutely dry_.
2. _Changes in the Cartilage_.--Directly that portion of the bursal
membrane covering the cartilage is the subject of inflammatory change, the
cartilage itself, by reason of its low vitality, soon suffers.
Under a process, which we may term 'dry ulcerative,' the cartilage covering
the ridge on the lower surface of the bone commences to become eroded, and
in appearance has been likened, both by English and Continental writers, to
a piece of wood that has been worm-eaten (see Fig. 161).
[Illustration: FIG. 161.--NAVICULAR BONE (POSTERO-INFERIOR SURFACE) SHOWING
THE 'WORM-EATEN' APPEARANCE CAUSED BY EROSION OF THE HYALINE CARTILAGE, AND
COMMENCING RAREFACTIVE ARTHRITIS.]
'At this stage, or much earlier'--we are quoting Colonel Smith,
A.V.D.--'may be found calcareous deposits in the fibro-cartilage and the
bone. They are scattered like fine sand here and there, generally across
the inferior half of the face of the bone; they are sometimes numerous,
frequently scanty, occasionally entirely absent. The amount of calcareous
degeneration depends upon the lesions present. If much destruction of bone
exists, there will be but few calcareous deposits; whilst if there are many
calcareous deposits, there may be but slight ulceration of bone tissue, and
perhaps none at all. In fact, I have held the opinion, and see no reason to
modify it, that calcareous deposits are safeguards against caries.'[A]
[Footnote A: _Journal of Comparative Pathology and Therapeutics_, vol. vi.,
p. 195.]
3. _Changes in the Tendon_.--The effect of these calcareous deposits on
the under surface of the bone is to produce a certain amount of roughness.
Seeing that with every movement of the foot the perforans tendon is called
upon to glide over this surface, it is clear that a secondary effect must
be that of inducing erosion and destruction of the tendon. The point at
which this usually commences is at the bottom of the depression that
accommodates the ridge on the bone. With erosion of the cartilage and of
the tendon at points exactly opposite each other, we have two surfaces come
together that are prone to readily unite, and fibrous tissue adhesions
often take place between the bone and the tendon. In some measure this
accounts for the torn and ragged appearance of the tendon. Adhesions take
place, and, under some small strain, are broken down. This may happen more
than once or twice, and with each breaking of the adhesion between the bone
and tendon, fibres from the latter are lacerated and torn from their place
(see Fig. 162).
4. _Changes in the Bone_.--The changes occurring in the bone are
essentially those of a rarefactive ostitis. These changes are described by
many writers, and, whether originating primarily in the bone or not, it
seems certain that extensive changes may have occurred within the bone,
with but little or nothing to be noted on its outer surface. It would seem
that the first change is one of congestion of the vessels of the bone's
cancellous tissue. With the cause, whatever it may be, in constant
operation, the congestion persists until a low type of inflammation is set
up, interfering, not only with the flow of synovia in the adjoining bursa,
but with the nutrition of the bone itself. As the disease progresses, there
is softening and enlarging of the cancellated tissue towards the centre
of the bone. The cells break up, and absorption takes place. This goes on
until a large portion of the interior of the bone is in a state of dry
necrosis, with, in many cases, but slight signs of mischief on the exterior
of the bone.
In other cases, however, the changes in the interior of the bone are
accompanied by well-marked lesions on its gliding or postero-inferior
surface, and by evidences of an osteoplastic periostitis along its edges.
That an osteoplastic periostitis has been in existence is witnessed by the
appearance along the edges of the bone of numerous outgrowths of bone,
termed osteophytes (see Fig. 163).
[Illustration: FIG. 162.--A FOOT WITH THE SEAT OF NAVICULAR DISEASE
EXPOSED. On the anterior surface of the perforans fibres of the tendon are
seen to be torn away from their abnormal adhesion with the navicular bone,
while others are seen to be still attached thereto. The surface of the
navicular bone itself exhibits small defects in the bony substance, which
have been brought about by a rarefactive ostitis. _a_, The perforans tendon
cut through and reflected; _b_, the sole.]
The interosseous and postero-lateral ligaments of the articulation
often participate in the inflammatory changes, and in many cases become
completely ossified. The true articulatory surface of the bone, that
articulating with the os pedis and with the os coronae, is never affected.
_Causes_.--In enumerating the causes of navicular disease, we shall
follow the example of Colonel Smith and classify them under certain
headings--namely, (1) _Hereditary Predisposition_; (2) _Compression_; (3)
_Concussion_; (4) _A Weak Navicular Bone_; (5) _A Defective or Irregular
Blood-supply to the Bone_; and (6) _Senile Decay_.
[Illustration: FIG. 163.--THE NAVICULAR BONE FROM A CASE OF LONG-STANDING
NAVICULAR DISEASE. The erosion of the cartilage on its central ridge is
most marked, and the porous appearance of the bone thus uncovered points
to the existence within it of a rarefactive ostitis. Along its edges
large osteophytic outgrowths speak of the effects of an osteoplastic
periostitis.]
1. _Hereditary Predisposition_.--That navicular disease is hereditary is
a fact that has for a long time been insisted on, and has come to be so
generally admitted that we do not intend to dwell on it here. As we have
said before, it is found in the lighter breeds of horses (and, according
to Zundel, especially in the English breeds), and is there seen to be
frequently transmitted from parent to offspring.
2. _Compression_.--By this is meant the compression of the navicular bone
between the os pedis and the os coronae in front, and the perforans tendon
behind.
In order to appreciate this explanation of the causation of navicular
disease at its true value, it will be well to consider briefly the
physiology of the parts in question.
The navicular bone is what we may term a complement of the os pedis. It
exists, in fact, simply in order that the os coronae may have a sufficiently
large articulatory surface to play upon. One wonders at first that Nature
did not arrive at this by originally placing a larger bone below. Colonel
Smith explains this by suggesting that this would in all probability have
meant its fracture. In progression the hind part of the foot comes to the
ground first, and upon the hinder portion of the articulation would fall
the first effects of concussion, together with the greater part of the
body-weight. A yielding joint was in this position necessary, and that
formed by the navicular bone fills all requirements.
In this connection one next considers the part played by the front limbs
during progression. As Zundel expresses it, they are columns of support
rather than of impulsion, and, as the body-weight is thrown forward by the
hind-limbs, it is the duty of the fore-limbs to receive it. The shock or
concussion of the body-weight thus thrown forwards is first received by
the muscles uniting the limb to the trunk, and a great part of it there
minimized by their sling-like attachment. It is further absorbed by the
shoulder-joint, and from there passed on to the almost vertical bony column
represented by the radius and ulna, the knee, and the metacarpus. On
reaching the first phalanx, a portion of the remaining force is passed on
to the front of the phalanges and loses itself in front of the hoof, while
the other portion is transmitted to the flexor tendons, finally to the
perforans, and to the posterior parts of the foot. During progression,
therefore, the navicular bone is constantly pushed downwards and backwards
by the bony column, and is just as constantly pushed forwards and upwards
by the resistance of the perforans tendon. This means, of course, that
the navicular bone is more or less constantly subject to compression,
and constant pressure, as we know full well, is a pretty sure factor
in bringing about malnutrition of the parts, with atrophy or chronic
inflammatory changes as an end result.
Even with the limb at rest the pressure on both sides of the navicular bone
is still constant. The only circumstances under which we can conceive of
it being entirely absent, in fact, are when the tension on the tendon is
relaxed, and the body-weight altogether removed by the animal adopting the
recumbent position.
The compression theory as to the causation of navicular disease was, we
believe, first originated by Colonel Smith. He, at any rate, has laid much
stress on it in his writings. If we accept it, and we see every reason
that we should, then we must, with the author, admit the possibility of
navicular disease arising from long standing in one position.
3. _Concussion_.--This we are bound to admit as a cause, and in so doing
partly explain the comparative, almost total, immunity of the hind-feet
from the disease. The fore-limbs, as we have already pointed out, are
little more than props of support, and the force of the propelled
body-weight is transmitted largely down their almost vertical lines, to
end largely in concussion in the foot. With the hind-limbs matters are
different. 'These,' as Percival explains it, 'have their bones obliquely
placed, so as to constitute, one with the other, so many obtuse angles, to
the end, that by forming powerful levers, and affording every advantage for
action to the muscles attached to them, they may be fitted for the purpose
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