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.
CHAPTER XXIV
IRREGULAR GOUT
“It is not a sacred disease. There will therefore be no profaneness in handling it freely,” affirmed Benjamin Rush of gout some hundred years since.
Nevertheless one approaches with diffidence this debatable ground, so hedged in by high sanction and tradition. Albeit reverence for authority must, in the interests of progress, be tempered by that spirit of inquiring scepticism which would sift the chaff from the grain, this the more emphatically in that of all morbid conditions “irregular” gout, by the very vagueness of its clinical content, lends itself the more easily to unbridled inference, hazardous conjecture, and fanciful surmise.
As for the unlicensed freedom too often exercised in relegating disorders to this category, Rush would appear to have out-heroded Herod, pace the following rhetorical reflections, for they could scarcely rank as clinical observations. “The great toe and the joints of the hands and feet are no more its exclusive seats,” said Rush, “than the stomach is the throne of yellow fever. In short, gout may be compared to a monarch whose empire is unlimited. The whole body crouches before it.... The gout affects the glands and lymphatics. It produced a salivation of a profuse nature in Major Pearce Buller, which continued for two days. It produced a bubo in the groin in a citizen of Philadelphia. He had never been infected with the venereal disease. Of course no suspicion was entertained by me of its being derived from that cause.... Scrofula and all the forms of dropsy are the effects in many cases of a disposition of the gout to attack the lymphatic system.... A distressing collection of air in the rectum, which renders frequent retirement from company necessary to discharge it, is likewise a symptom of gout.”
It is difficult to conceive that any such pronouncement could have emanated from a physician of Rush’s standing and repute, a contemporary, be it noted, of Heberden, to whose masterly commentaries on the history and cure of gout all posterity is indebted. Nevertheless as recently as 1854 Sir Spencer Wells claimed that “any attempt to describe the nervous diseases of females caused by gout would lead to an enumeration of almost all forms of their diseases, especially those usually considered as hysteric. The intestinal derangements with tympanitis, neuralgia, or colic, the hysteric pain in the right epigastrium, the cardialgia and gastrodynia, the hysteric vomiting and epigastric spasms, the morbid sensibility of the pharynx and fauces, hysterical palpitation, asthma or bronchitis, loss or alteration of the voice, some forms of hysteric paraplegia or hemiplegia more or less complete, chorea or tetanus, some of the curious paroxysmal affections observed in hysteria, and all the varieties of neuralgia and simulated inflammation, commonly called hysteric, frequently arise from the presence in the blood of the impurities which are the true characteristics of gout.”[43]
Truly, in light of this heavy indictment, one scarcely wonders that Rush classed the domain of gout as limitless. But one must recollect that, nosologically speaking, our forefathers were sadly hampered. Anomalous symptoms and disorders had to be referred to one or other of the available titles of disease, and what term more elastic than the timeworn “gout,” so easy to saddle with vicarious responsibilities?
But pari passu with advancing knowledge of the pathology of the nervous system and the rise of hysteria to the status of a clinical entity gout was shorn of the excrescences heaped on it by Laycock, Wells, and others.
But nevertheless the emancipation of gout from nervous and other alien disorders was slow of achievement, and largely, I think, through the wide acceptation of Murchison’s theory of a pathological state allied to gout and termed by him “lithæmia,” or the “uric acid diathesis.”
According to this authority, the deposit of lithates in the urine is a “manifestation of a morbid condition of the blood and of the entire system,” the outcome of a functional derangement of the liver. Such hepatic disturbance might endure for years without manifesting any other symptom than a frequent deposition of urates and occasionally uric acid in the urine. But, added Murchison, the same if neglected “may ultimately be the means of developing gout.”
Clinically it manifested itself by a variety of symptoms—depression of spirits, irritability, lethargy, headache, pains and aches in the limbs, vertigo, insomnia, dyspepsia, palpitation, raised blood pressure. Such were the motley group of disorders affiliated by Murchison to lithæmia. But his disciples, more ardent, set no limit to the manifestations of uric-acidæmia.
Not only gout, but rheumatism and allied disorders, were amongst its progeny, and Osler tells us that one writer enumerates not fewer than thirty-nine separate morbid conditions associated with lithæmia. But leaving aside the extravagant claims of Haig and his followers, the impression even now is but too prevalent that gout and lithæmia are convertible terms. There is little or nothing to justify the assumption that an increased output of uric acid in the urine or deposition of urates therein is diagnostic of gout. Such, moreover, presupposes the further assumption that uric acid is the cause of gout.
We may affirm that certain symptoms betoken malassimilation of food or defective tissue metabolism. But it is by no means certain, as Murchison held, that a functional disorder of the liver is the fons et origo mali, much less that uric acid is the sole noxious substance. Yet in a masterly discussion of the subject Pratt, of Boston, tells us that as recently as 1895 a “leading clinical teacher” affirmed that “headache, migraine, depression of spirits, shooting pains, cramps, palpitation, vertigo, are a part of the symptomatology of lithæmia.”
Surely, if we are to make any pretence of reducing the phenomena of lithæmia or irregular gout to a scientific precision worthy of the present status of medicine, we should fight shy of such sweeping assertions. The caveat, we fear, is not superfluous. For as that judicial physician, Austin Flint, once satirically observed, “the designation ‘uric acid diathesis’ is used by some physicians in a rather indefinite way to describe various morbid states which may not at any time be accompanied by deposits of urates, and in which there is no proof of an excess of uric acid in the blood.”
Caustic as was this stricture, it was no less prophetic than apposite. For recent blood analyses have, as Pratt states, demonstrated that there is no increase of uric acid in the blood in that medley of disorders attributed by Murchison and his followers to “lithæmia,” or “the uric acid diathesis.” Here we would inveigh strongly against the too prevalent habit of stigmatising as “gouty” such symptoms as headache, vertigo, palpitation, etc., not only without any evidence of their being of this nature, but frequently when no attempt has been made to eliminate “errors of refraction,” aural disorder, etc. Moreover, granted that such possible sources have been excluded, we have no justification in invoking “gout.” For, as noted, all modern observations fail to demonstrate the presence of uricæmia. Under such circumstances, given that the anomalous symptoms are inexplicable, would it not be wiser to content ourselves with the assumption that their presence postulates, not lithæmia, but a toxic condition of the blood plasma? This at least carries with it the inference that a search should be made for the focus of toxic absorption, whereas for but too many the term lithæmia, even when undemonstrated, is held to be self-explanatory and final.
Turning to another aspect of this subject, we are reminded by Duckworth that Hutchinson “directed attention to various maladies affiliated with what he terms rheumatic gout and gout, but differing somewhat from both, and these include various eye troubles, such as iritis, hæmorrhagic retinitis, and some forms of glaucoma, lumbago, sciatica, chronic rheumatoid arthritis, Heberden’s nodes, and possibly hæmophilia.”
As to the so-called “gouty” origin of the various eye troubles, these will be dealt with separately by Mr. Beaumont in his section. For the rest, hæmophilia may, we think, be safely discarded, Heberden’s nodes relegated to osteoarthritis, while rheumatoid arthritis has long since vindicated its claim to clinical individuality.
But as to lumbago and sciatica, these cannot be so easily disposed of, as a reflection of Heberden’s brings home to us. “It must be owned,” says he, “that there are cases in which the criteria of both are so blended together that it is not easy to determine whether the pain be gout or rheumatism.” Our own attitude towards this vexed point was precisely defined in a previous chapter in which we dealt with the affinities between gout and other diseases.
Having dealt with the broader and more extravagant claims made on behalf of the clinical content of irregular gout, we now restrict our purview to those disorders, chiefly visceral in site, which even to-day are referred by some to this category. We shall in the first instance deal with that variety known as retrocedent gout, and shall subsequently proceed to discuss other so-called irregular manifestations of the disorder.