little with serum, and a few fibrous exsudations are also to be seen; the cartilaginous covering of the femur is of a dull white, here and there spotted dark. In the third stage, the inner and upper part of the sac is more particularly involved, pus has broken into the joint and produced much destruction; partly in the ligaments, partly in the cartilaginous covering of the condyles. In places this is destroyed, the bared condyle looks grey, is soft and spongy. Commonly each condyle is separated from its fellow, so that not only does the synovial membrane form, with the abscess, one common cavity, but the two condyles separated from each other and the shaft are found lying free in the bag. If the whole length of the femur be taken out, it will be found to be in the second stage, necrotic only as far as the abscess in the soft parts had reached. In the third stage, on the contrary, it is necrotic almost throughout to the trochanter. Its surface is greyish black, its external table (tabula vitrea) eaten away and rough; the parts still smooth are covered with thready remains of the periosteum, and in some places with little osteophytes which give the surface an uneven appearance. If the bone be sawn through in a fresh state, it presents inside the medullary cavity a dark red appearance, its interstitial tissue is soaked in a brown red, grey or grey-brown-red (graubraun röthlichen), exsudation according to the stage of the inflammation. If the cavity be however still full of medulla, this material will be studded with a quantity of dark red spots (apoplectic clots), which will be found, according to their age, in a more or less complete state of putrescent suppuration. Indeed, the whole internal parts of the bone present the appearance of a widely diffused phlebitis, with transitions into exsudation and suppuration.'

The paper from which the above abridgments and extracts are taken has not excited in England as much attention as it deserves. In France, an abstract of the thesis was published in the Archives Générales de Médecine' for August 1858, and in the November number of the same journal, M. Gosselin points out that the disease thus described is identical with Chassaignac's Osteo-myelitis, but occurs in younger persons, and is situated in the epiphysis; he then divides the bony inflammations in a way *Op. cit. p. 114 et seq.

that appears to be unscientific, and terms the disease which Klose has described, Ostéite épiphysaire aigue suppurée. Three cases, two of which only appear to belong strictly to the class of cases described by Klose, show that a similar malady is known in the West of Europe.

It has not been my fortune to see any disease at all similar, nor can I find any account in English medical journals which would lead me to believe that such has occurred in this country. Therefore it is apparently better to give these observations of a most destructive and happily rare form of joint disease without further comment.

CHAPTER XI.

STRUMOUS ARTICULAR OSTEITIS.

PATHOLOGY.

OSTEITIS may be produced by other constitutional taints besides scrofula-syphilis, for instance, and rheumatism. It is, however, rare for syphilis to attack the spongy end of a long bone; it affects in preference the harder portions, commencing on the surface. Of the rheumatic disease, as it appears in the joint ends of bones, we shall speak in another chapter.

Strumous inflammation of bone has a great tendency to affect the cancellous structure; it is apt to attack the irregular bones of the carpus and tarsus, also the ends of long bones; in this latter situation, it is almost exclusively a disease of childhood, or of the age before puberty: affecting a bone throughout cancellous, as those of the carpus or tarsus, it is, I believe, nearly as prevalent in adult life. The inflammation generally commences in the interior of the spongy structure, but may also begin in the cortex and periosteum. These latter modes of beginning are more characteristic of the syphilitic and rheumatic form, and are very rare in primary strumous osteitis. Another mode of commencement, approaching a slower form of the disease described in the last chapter, is that the whole epiphysis may become involved. Occasionally in those long bones, as the metacarpal and metatarsal, which have an epiphysis only at one extremity, the shaft and the non-epiphysal end are simultaneously attacked. In early life, the entire separation, vascular, nervous and indeed histological, between the diaphysis and epiphysis, sunders the diseases of either from those of the other as much as though they occurred in different parts. It may also be observed, that the joint ends of the bones are in this stage of life undergoing ossification, and it is the increased nutrient excite

ment attending that act which makes osteitis so prevalent in early life.

The first appearance of the disease (speaking of makroscopic anatomy) is hyperæmia: this is much more marked in a spongy bone than it can ever become in inflammation of dense osseous tissue; it may at first affect only one, or perhaps two or three spots, in the bone; or it may be more widely spread, and attack the whole spongy texture. It is, however, to be remembered, that hyperæmia is neither inflammation, nor an infallible sign of that condition, and we must not, in making pathological observations on the epiphyses of young children, imagine that every congested joint-end is inflamed, or will necessarily become inflamed. It has once or twice happened to me, to find in the same subject nearly all the larger epiphyses hyperæmic, and I believe that we could look into the bones of very few children between the ages of two and ten, without finding some such congestive state; yet how comparatively rare is inflammation of a joint-end! The truth is, that the nutritive activity brought about by the ossifying action in the epiphysis, is very apt indeed to produce a congested condition of the part; and the large bone-ends which are found in strumous children are the accompaniment of such tendency to congestion. As the child gets older and stronger, this hyperæmia disappears, and in the great majority of instances is followed by no evil results whatever. It is, however, certain, that in a given number of cases, the congestion predisposes to inflammation, and the merely passive is followed by an active condition. Thus inflammation may be set up in an epiphysal end, which was previously in an abnormal state, and such, in the greater number of cases, is the mode in which the disease now under consideration commences. All such attacks are in the beginning very slow, and hang for months, perhaps even years, between a state merely of sluggish functional performance and of active disease. It happens however sometimes, that inflammation of a joint-end commences at a later age, when the ossific process has entirely ceased, and when all congestion owing to that cause shall have terminated; such cases are more rapid in their progress, produce a somewhat different set of symptoms, end more frequently than the other form in necrosis of some of the cancellous part of the bone, and the joint itself does not

necessarily become involved. The seat of the hyperæmia, whether merely congestive or inflammatory, is not the bony structure itself, but the membranous lining of the cancelli, which, in health, is pink and vascular. The bony lamella which surround the cancellous cavities are very slightly supplied with Haversian canals (see Chapter I., p. 6), hence hyperemia of the osseous plates themselves can hardly reach such a point as to produce increased redness. The congestion is to be seen by sawing through the bone, when it will be found to impart, to the surface of the section, a hue varying from a mere flush to a purple colour. This hue extends in some instances (the most cachectic) equably over the whole section; in others it is chiefly marked in certain spots; each such spot being surrounded partly or entirely by lighter coloured portions. Such arrangement gives to the section-surface a marbled or mottled look, not easily forgotten when once seen. The appearances may be merely signs of that congestion so prevalent in young children; but actual inflammation is marked by some other signs-either by thickening of the osseous tissue, or by effusion of a pinkish serum. The former stands on the boundary line between increased nutrition and inflammation, the latter is the result of a stasis whose occurrence plainly marks the transition from the one process to the other. Thus, if on sawing through a spongy bone taken from the dead subject we find only redness, we may set down the abnormal vascularity as merely passive congestion; but if there be thickening, that is, if the plates of the cancelli are increased in thickness and their cavities diminished, still more if the reddened portions be soaked in a pinkish blood-stained serum, we may assert that the bone is inflamed.

This thickening of the bony lamellæ is an action analogous to, or rather identical with the increase in any structure subject to irritation; it is like the thickening of the cellular tissue under slight and remittent pressure; like the thickening of tendinous sheathes, or of fascia under many circumstances of extraordinary use, and therefore of nutrient irritation. It is also the mildest, and generally the incipient, stage of inflammation; hence in soft parts, when an areolar tissue is attacked by inflammation, it first hardens; then, in the centre of the hardened mass, suppurates; this latter action spreads, and perhaps soon involves the whole

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