Chapter XXIII: CLINICAL DIAGNOSIS (continued)

SKIAGRAPHY

As an aid to the differentiation of _gouty_ from _non-gouty_ forms of _arthritis_ skiagraphy has scarcely fulfilled the somewhat optimistic claims at one time made on its behalf. As to _acute_ gout, radiography reveals nothing abnormal in the bones, though Tousey holds that this of itself at once enables us to exclude _osteomyelitis_, which, he says, “these cases sometimes resemble.”

Turning now to _chronic articular gout_, Huber in 1896 drew attention to certain _focal areas of rarefaction_, or diminished density, in the distal extremities of the phalanges. These localised transparent areas in the bone-ends are discrete, circular, or oval in shape. When located near the edges of the bones, they are of segmental contour, and, viewed in profile, give the appearance of small punched-out holes, simulating syphilitic dactylitis. Despite their proximity to the diseased joints, they apparently do not communicate with the articular cavities.

These bony changes Huber held distinctive of gout, and Koehler, Drinberg, and Jacobsohn and other subsequent writers confirmed Huber’s findings, and, like him, held these areas of rarefaction to be the result of _uratic deposits_ at their sites. Strangeways has dissected bones in which these transparent areas were demonstrated by X-rays. The examination revealed that the bone was definitely excavated, filled with a gelatinous-looking substance, and in advanced cases of gout, moreover, a characteristic deposit of urates clung, as it were, to the margins of the cavities.

Similar focal areas of decreased density were noted by Strangeways in certain cases of _rheumatoid arthritis_, and both he and Burt found it impossible on the X-ray findings to differentiate between these and gout, _i.e._, without invoking the aid of clinical data.

Apart from these transparent areas, Wynne many years ago pointed out that small _nodes_ or _bony deposits_ are sometimes met with flanking the sides of the phalanges. More recently Ironside Bruce by _radiography_ has again drawn attention to these bony outgrowths near the extremities of the phalanges (Bruce’s nodes). At first these were thought by Bruce to be composed of _urates_, but Strangeways from a study of macerated specimens has demonstrated their true _bony_ nature, and also that _uratic deposits are not opaque to X-rays_, as was formerly thought.

In skiagrams of chronic gout all stages of _ankylosis_ may be seen in the interphalangeal joints. In some it is merely fibrous, in others merging therefrom into bony, and not infrequently true synostosis is observed. Deflections or subluxations are frequent features, due either to the thrust of tophi or small bony outgrowths or to peri-articular contractures.

So much for the skiagraphic findings in chronic gout, and now to discuss their valency as aids to diagnosis of this arthritic disorder. The chief controversy centres around the significance of the _focal areas of rarefaction_ which have been found in the bones of the wrists, hands, ankles, and feet of gouty subjects. Here we may comment on one grave handicap, viz., the lack of certainty as to whether the cases radiographed by different observers were true instances of _gouty_ arthritis.

To justify our expression of doubt we may take, for example, the series reported by Drinberg and Jacobsohn. The said “transparent areas” were present in all the eighteen cases, but the presence of _tophi_ was only established in three. Now, as McClure and McCarty rightly contend, “since the tophus is the only universally accepted pathognomonic sign of gout, for studies of that disease only those patients should be chosen in whom tophi are found, and sodium urate crystals from them microscopically demonstrated.” No one can, I think, gainsay the legitimacy of this stipulation.

In accordance with their contention, McClure and McCarty record their radiographic findings in a series of cases all of which exhibited _tophi_, and from which sodium urate crystals were isolated. Now, in all these cases the _focal areas of diminished density_, generally held to be peculiar to gout, were present; but they add that “similar changes were present in two other cases which were clinically gout, but in which no tophi were demonstrated.” Also “in another case without tophi, but which was clinically gout, the focal areas of decreased bony density were not found.”

In addition, they examined the skiagrams of 100 cases of _chronic arthritis_ which “had not been diagnosed clinically as _gout_.” In thirteen of the examples “the focal areas of decreased density, the so-called gouty bony changes, were found, and were fully as well defined as in the cases of true gout.”

Judging from the skiagraphic appearances, there seemed no reason to suppose that the factors responsible for the production of these rarefied areas were in any way different from those at work in true gout. Now, most authorities have claimed that the bony changes were due to _uratic deposits_ in the bones; but it is at least possible that their origin may be otherwise explained.

Thus Nichols and Richardson have shown that, given _focal absorption of lime salts_, changes apparently identical with those currently attributed to the presence of _tophi_ may result. These same, though they may not be demonstrable either macroscopically or microscopically, are detectable by X-rays.

Such foci of absorption, viz., areas of decreased density, frequently are located in regions subjected to _pressure_. Thus they may occur at the inner surfaces of the heads of the first metatarsal bones, or they may form underneath large tophaceous deposits in the soft tissues.

Now, Strangeways has shown that it is impossible by radiography to detect _tophi in bones_. Accordingly we have at present no means of deciding in any given case whether the localised _transparent areas_ in the bones are due to _tophi_ or to _focal absorption_ of lime salts. If we are to cling to the conception that they are due to _tophi_, then it is clear that _tophi in the bones_ are more common than is currently suspected, and that, _ergo_, the frequency of gouty arthritis is underestimated. For these transparent foci in bones, according to McClure and McCarty, occur in from 10 to 12 per cent. of cases of chronic arthritis “which clinically are not gout.”

Yet these authorities hold that, despite the fact that they occur in cases of _non-gouty_ arthritides, they have some diagnostic significance. For, taking the work of other observers in conjunction with their own observations, they come to the following conclusions:—

(1) The focal areas of decreased density, heretofore considered
as peculiar to gout, are rarely absent in that disease.

(2) Their absence would be some evidence against the existence
of gout in a given case.

(3) On the other hand, their presence is no more than
suggestive of gout, since they are found in from 10 to 12 per
cent. of cases which clinically are not gout.

(4) The focal areas of decreased density, usually held due to
tophi, are probably very often merely focal areas of absorption
of lime salts.

In continuation these authorities have endeavoured to identify the nature of the _arthritis_ that occurs in _gout_. Like other workers in this sphere, the study of the radiographs obtained of gouty joints reveals that a variety of changes occur in the bones and joints of the hands and feet in gouty subjects. These, they consider, may be classified conveniently as follows:—

(1) Cases marked by _focal areas of rarefaction_, without any
other perceptible change;

(2) Cases presenting, in addition to these translucent areas,
minor degrees of lipping at the articular margins;

(3) Cases in which the changes in (1) and (2) are conjoined
with either localised atrophy of the bones entering into an
affected joint, or with generalised atrophy of all the bones in
the affected limb;

(4) In addition to all the above changes, narrowing of certain
joint spaces with marked proliferative and atrophic changes
occurs.

In reviewing these findings of McCarty and McClure, it is important to recollect that they were found in a series of cases all of which exhibited _tophi_. Moreover, it will be seen that the radiographic changes in some are reminiscent of _atrophic_ or rheumatoid arthritis, in others of _hypertrophic_ arthritis or osteoarthritis, while, lastly, the appearances typical of _infective_ arthritis are also represented. In addition, if we recall that _focal areas of rarefaction_, indistinguishable from those met with in _gout_, also occur in all types of _non-gouty_ arthritis, we at once see how impossible it is to detect anything in the _radiographic_ findings distinctive of _gouty_ as opposed to _non-gouty_ arthritides.

McClure and McCarty, comparing the radiographic changes in gouty as opposed to _non-gouty_ arthritis, observe that, though _rarefactive foci_ occur in all varieties of _non-gouty_ arthritis, they are conjoined with _other bony or joint changes_. On the other hand, _translucent_ areas _unassociated with any bone or joint alterations_ have been found only in _gout_. But whether this can be claimed as distinctive of _gouty arthritis_ is, they think, uncertain, since relatively few opportunities for X-ray examination of _non-gouty_ arthritis in its _early_ stages have been forthcoming.

Continuing, of their four radiographic types of gouty arthritis the second resembles osteoarthritis; but the third and especially the fourth group, they consider, “fall into a peculiar class,” this inasmuch as their characters resemble the _infective_ type of _non-gouty_ arthritis. They claim, however, that a differentiation, radiographically speaking, can be effected, this because of the “sharply localised” extreme degree of bony atrophy which occurs in the infective type of non-gouty arthritis. However, as they admit that radiographs of the latter (infective non-gouty arthritis) have been noted which “closely resemble” the “atrophic and proliferative changes occurring in gout,” their final conclusion is that in the skiagrams even of typical gouty arthritis there is nothing in the bony or arthritic changes that is _diagnostic_ of gout.

For myself, I must admit that I have come to the same conclusion as McClure and McCarty, viz., that the skiagraphic findings in _gouty_ and _non-gouty_ arthritis trench so much the one upon the characters of the other that I should be loth indeed to base a diagnosis of gout simply on the revelations of _skiagraphy_. The chief interest to my mind, as I have previously observed, centres round those examples in which _peri-articular tophi_ are associated with underlying bony and arthritic changes (as revealed by X-rays) indistinguishable from those typical of _infective_ arthritis of _non-gouty_ type.

We have seen also that _local foci of rarefaction_ may be met with in _infective_ arthritis of _non-gouty_ type. Moreover, the _proliferative_ and marked _atrophic_ bony changes found in some instances of gouty arthritis are quite compatible with their _infective_ origin. Witness how impossible it is to differentiate skiagraphically between _atrophic_ arthritis and _gouty_ arthritis, and at the same time let it not be forgotten, on the other hand, that the dividing line between the _infective_ arthritides and the more acute forms of _atrophic_ or rheumatoid arthritis is by no means sharply defined. Review this also in light of the fact of the close resemblance that obtains between _acute articular gout_, especially the polyarthritic variety, and types of arthritis of avowedly _infective_ origin, and we see at once how close is the clinical similitude. We turn to _radiography_, and here again we are met with the same family resemblance, suggestive of a probable community of origin. How clear then the inference that it is on _tophi_, and tophi alone, that we must base an absolute diagnosis of _gouty_ arthritis. Moreover, since tophi are not detectable by _skiagraphy_, our mainstay must be physical examination directed to their detection. As for those cases of so-called “clinical gout,” viz., unattested by tophi, it is probable that their absolute identification, as such, will never be attainable on purely clinical, but on _bacteriological_, data, which, it is to be hoped, will before long be forthcoming.

DIFFERENTIAL DIAGNOSIS

_Infective Arthritis._—According to Goldthwait, of Boston, no changes can be detected by skiagraphy in bone or cartilage in infective arthritis. The density of the former is in no way diminished, while the cartilage retains its normal thickness. If, however, the infective arthritis is of destructive character, new bone may be thrown out in the process of repair. If then in such cases sole reliance be placed on the X-ray appearances without any reference to the clinical history and course of the disorder, then, as Goldthwait says, this irregular formation of bone is likely to be confused with the X-ray findings in osteoarthritis. It is, however, possible, according to him, to distinguish the nature of the case by careful scrutiny of the skiagraphs.

The new formation of bone in these destructive forms of arthritis conforms in every way to that seen as a result of _septic osteitis_ or periostitis. In other words, the osteophytic outgrowths take origin at the _focus of infection_, wherever that may be, and not, as in _gout_ and _osteoarthritis_, at the _margin of the cartilage_. Still one must recollect that in gout _exostoses_ (Bruce’s nodes) develop sometimes at the _sides_ of the phalanges. These outgrowths are not peculiar to gout, but may be met with in _infective_ forms of arthritis. I am inclined therefore to refer their origin to a local osteitis or periostitis of infective source. That Bruce’s nodes, though not diagnostic of gout, are frequently met with therein, is, I submit, but further evidence of the intrusion of an _infective_ element in the genesis of _gouty arthritis_.

_Hypertrophic or Osteo-arthritis._—This is marked by proliferative changes at the margins of the articular ends of the bones. With the advance of the disease the shafts of the related bones become increasingly dense. In _chronic gout_, too, the margins of the cartilages may be studded with little nodules. Radiographically speaking, they cannot be distinguished from those met with in osteoarthritis, save only that they never attain the massive size met with in the latter disorder. The diagnosis in doubtful cases will practically always rest on the clinical history, and more pertinently on the presence of _tophi_.

_Rheumatoid or Atrophic Arthritis._—If the changes in the cartilage and bone in osteoarthritis are active and proliferative, these same in rheumatoid arthritis are retrograde and passive in character. In short, hypertrophy of these structures in the former, atrophy in the latter, constitute the distinguishing features.

The morbid process in the articular ends in rheumatoid arthritis is one of rarefaction and softening. The cartilage may undergo total or partial absorption, a change to be detected in the very early stages. The bones participate in the pathological change, the first evidence of which is an abnormal translucency to the rays, usually, but not always, confined to that portion of the shaft entering into the joint. Eventually the articular ends of the phalangeal and metacarpal bones may undergo erosion, in some cases to a very marked degree, the bones more or less telescoping into each other.

Now, owing to the fact that in _gout_ also considerable disintegration of the bone may result, the appearances in some instances may resemble those found in the skiagraphs of _rheumatoid_ joints. Stress has been laid on this similarity by Strangeways, and it was also previously remarked by Goldthwait. The latter, however, claims that while in _atrophic_ or _rheumatoid_ arthritis the bone, though thin, maintains its outline, on the other hand in _gout_ the outline of the bone is not distinguishable owing to its more complete destruction by the morbid process. Goldthwait holds that the resemblance of chronic articular gout to rheumatoid arthritis is most noticeable when the _articular ends_ of the bone in both instances are the seat of the disease. In other examples, however, the _shafts_ of the bones being affected by the gouty disorder, they may show punched-out areas. These latter, however, are but _focal areas of rarefaction_ seen in profile, and inasmuch as they may be met with in infective arthritides of non-gouty type, too much reliance cannot be placed on their presence as distinctive of gout, much less as a criterion of differentiation from other arthritides.

We have to remember, too, that marginal proliferative changes may occur in rheumatoid arthritis. They are, like those met with in gout, miniature replicas of the bony outgrowths of osteoarthritis.

In conclusion, the resemblance between the skiagrams of chronic gout and rheumatoid arthritis is so close as absolutely to forbid our sole reliance on skiagraphy to effect a differential diagnosis. In short, skiagraphy, though of great and probably increasing value, cannot for one moment be allowed to usurp the place of careful clinical observation, to which it must be held always subsidiary. Last, but not least, pending fresh radiographic revelations, our diagnosis of chronic articular gout and alike its differentiation from rheumatoid arthritis and other arthritides must rest on the one unimpugnable criterion, the presence of _tophi_.