Gout, with a section on ocular disease in the gouty

by Llewellyn J. Llewellyn

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.