If the diagnosis of acute types of articular gout often presents difficulties, these same are, if anything, accentuated when we approach its chronic manifestations. For, apart from uratic deposits, the anatomical lesions that ensue in joints the seat of long-continued gout have no specific character. In short, there is nothing pathognomonic of gout in the changes produced, and which, as a matter of fact, we know to be capable of production, by many different morbid agencies. Surely this lack of specificity in its structural lesions should make us very chary of admitting to the category of chronic articular gout any examples of arthritis destitute of uratic deposits.
In our chapter on classification we emphasised the desirability of restricting the usage of the term chronic articular gout to that type long since known as tophaceous gout, this because there is little, if any, doubt that that variety known as chronic deforming gout (syn. arthritis deformans uratica) is largely made up of examples of rheumatoid or atrophic arthritis and hypertrophic arthritis or osteoarthritis.[41]
As to osteoarthritis, I do not for a moment deny that uratic deposits may be met with in its victims. One frequently meets with patients, the subjects of osteoarthritis of the hip, who at the same time exhibit tophi in the ears.
But such to our mind are to be regarded as merely instances of osteoarthritis occurring in subjects of “gouty diathesis.” This apparent blending of the two disorders must not be allowed to impair the clarity of our conception as to the essential distinctness of gouty arthritis and osteoarthritis.
Sir W. Hale White has some pregnant observations on this point. Many patients, he says, “with chronic arthritis are quite wrongly said to have gout; usually they have osteoarthritis. The presence of bony outgrowths is strongly against gout, though it is not conclusive, for such may occur in true gout either more or less all round the joint or in the form of little nodules, but they never attain the considerable size common in arthritis,” and he adds: “If no urate of soda is visible anywhere the diagnosis may be very difficult.”
To proceed, the general and local phenomena of chronic articular gout are such as scarcely lend themselves to succinct definition, and for their description we would refer the reader to the chapter dealing with its clinical aspects. As that careful observer Sir Alfred Garrod states: “Chronic gout is at times confined to one or two joints, but sometimes numerous articulations are involved.” In other words, chronic articular gout may be mono-, oligo-, or poly-articular in distribution; and naturally the process of differentiation is modified accordingly.
This being so, I purpose dealing in the first instance with chronic monarticular gout, and in succession with the types of oligo- and poly-articular location.
Occasionally gout in its recurrences clings obstinately to the great toe and tarsal joints. But since the advent of radiography there should be little or no difficulty in differentiating a chronic gouty arthritis of the great toe from the only other arthritic lesion with which it is likely at this stage to be confounded, viz., osteoarthritis. But at the same time we would refer the reader back to the chapter dealing with the differential diagnosis of the localised variety of acute gout, as therein we dealt fully with other possible sources of fallacy, i.e., static deformities, etc. We shall therefore now proceed to discuss those exceptional cases in which chronic gout is located not in one of the small, but in one of the larger, articulations.
Given a chronic arthritis of one of the larger joints, say the ankle, knee, or elbow, we should be careful not to jump too readily to the conclusion that it is of “gouty” nature. The more obscure it appears the more need for caution. Needless to say, if the objective changes be but minimal and the condition be, so to speak, practically a mere arthralgia, there rests upon us the paramount necessity of careful discrimination before labelling it as “gouty” in kind.
Thus, if it be the knee, it may be a referred pain due to hip disorder, e.g., osteoarthritis or tuberculous disease, or it may be symptomatic of an inflammatory process, or, having regard to the usually mature or advanced age of the subject, it may be a neoplasm in the bones.
On the other hand, suppose the subject come complaining not much of pain in his joint, but more troubled because of its enlargements. If now on examination we find also that there is little or no tenderness, but simply a condition of peri-articular thickening or intra-articular effusion, what shall be our method of procedure? Certainly not to leap forthwith to the conclusion that it is gouty. No, not even if he exhibit tophi in his ears.
Now, as to pain and tenderness, it is a blessed feature of gouty arthritis that, generally speaking, in the chronic forms pain becomes much attenuated. But let us at the same time recollect that syphilitic arthritis, both secondary and tertiary, is relatively painless. But it is the much rarer tertiary form, be it remembered, which is usually monarticular. By the bye, too, we should never forget that a Charcot’s joint is also painless.
Coming now to the objective phenomena, is the case predominantly one of peri-articular infiltration or intra-articular effusion? As to the former, while you never know, still tuberculous joint disease is exceptionally rare at the age at which we usually meet gout. On the other hand, gummatous synovitis, with or without osteoperiostitis, is occasionally met with. It is just such a case as this that may be confounded with gout, the irregular lumpy thickening of the sub-synovial tissues with effusion being wrongly attributed to a gouty process with uratic deposits. Do not be misled if a history of injury be forthcoming in such cases, for it is not uncommon and may be given in good faith.
Now what if synovial effusion of chronic or recurring form be the striking objective feature of the case under review? In this event always recollect that of all the causes of monarticular disorder injury is far and away the most frequent. Not a few cases of monarticular joint disease come annually to the Royal Mineral Water Hospital, Bath, under the diagnosis of “gout” and “rheumatism.” But in all too many the symptoms are referable in truth to ligamentary strain, displaced cartilage, or foreign bodies, lesions always to be sought for and excluded in monarticular joint affection. Duckworth has it that hydrarthrosis is met with in chronic articular gout, in his deforming variety. He states that “hydrarthrosis is less commonly due to gout than to rheumatism,” but, we would remark, apart from traumatic lesions, more commonly due to gonorrhœa or syphilis than to either of them.
But the reader may say, this dissertation notwithstanding, Where does gout come in? Precisely so, and if his experience tallies with mine, he will find that chronic articular gout localised in one of the larger joints, and one only, is exceptionally rare. Personally, I should never feel justified in making the diagnosis unless I had elicited a history of (1) recurring classic outbreaks in the great toe with (2) an absence of traumatic infective and nerve arthropathies and, on the other hand, (3) demonstrable existence of uratic deposits in situ in the peri-articular tissues, the cartilage or bones as revealed by skiagraphy, or in the related bursæ.
In conclusion, if all these various pitfalls have been avoided, it will almost without exception be found that the final differentiation in doubtful cases will rest between gout and osteoarthritis; and in the vast majority, I had almost said all, it is the latter morbid process that will be found responsible.
This all too lengthy disquisition will not have been in vain if it instil caution. For it is in the monarticular types of joint affection that errors of catastrophic proportion occur more commonly than in any other form of joint disorder.
The course of chronic articular gout, as has been observed, may be chequered by acute outbreaks involving three, four, or more of the larger joints. But, apart from this, there are those so-called asthenic and afebrile types of gout in which two or more joints may be the seat of a chronic gouty arthritis. In my experience it is the knees that are most frequently attacked. The joints are enlarged, the seat of more or less effusion, but the distinctive feature is the presence of deformity due to the irregularly rounded or ovoid swellings produced by uratic deposits. Enlargement of the patellæ is also present, and they lose their sharp edges, and sometimes they as well as the neighbouring articular ends are studded with small bony outgrowths, but of minimal size compared with those met with in osteoarthritis. The related bursæ, too, are often the seat of deposits, a valuable clue to diagnosis. Needless to say, such marked cases are nearly always the outcome of oft-repeated attacks, the ultimate deformity being the result of successive accretions of urate of soda laid down in the trail of the exacerbations.
The frequency with which this misconception occurs is very noticeable. If a middle-aged woman of florid complexion and corpulent habit begins to complain of pain and stiffness in her knees with more or less swelling thereof, there is a very prevalent tendency to attribute not only her joint disorder to gout, but any gastric or nervous symptoms that she may simultaneously complain of are translated as being confirmatory of the assumption. It gathers weight too from the traditional and widespread belief that “the change of life” is the period par excellence at which women develop the morbid vagaries associated with “irregular gout.”
Now, as Bassett Jones and I have pointed out in a previous work, this condition, symmetrical villous synovitis of the knees, is a very common joint disorder in women at or near the menopause. Frequently they give a history of numerous pregnancies, or of rapidly increasing obesity, while with or without this latter they display a faulty postural attitude, indicative of lowered muscular and ligamentary tone. Following in the wake of these, the subject develops a symmetrical flatfoot, which, according to the stage at which it is seen, may be of flexible or rigid type.
Now, such is the mutual static interdependence of the component parts of the lower limb that this condition of flatfoot promotes or favours the incidence of villous overgrowths in the proximal joints, the knees. As to the modus operandi we have put forward the following explanation: “The everted foot, with its sunken arch, as before stated, determines an alteration in the normal coaptation of the articular surfaces in the knee, and this incongruence is revealed in skiagraphs by the marked prominence laterally of the external tibial tuberosity beneath the external femoral condyle. Coincidently, and for the same reason, additional strain is thrown upon the internal lateral ligament. This in turn favours a state of passive congestion or hyperæmia of the synovial membrane, which becomes relaxed and thrown into folds, especially at its reflexions near the edges of the cartilages. If, as often happens, the individual is the subject of varicose veins or suffers from a general lack of tone in her muscular or ligamentary structures, this tendency to venous engorgement of the knees is much enhanced.”
“Under the influence of these mechanical factors and their associated circulatory disturbances, thickening and enlargement of the synovial fringes ensue. The inflammatory condition thus produced tends to increase automatically, as, owing to the articular incongruence, the enlarged fringes are very prone to become caught between the joint surfaces; in other words, a vicious circle is produced, as with the increasing villous hypertrophy the liability to internal traumatisms increases pari passu.”
In short, the joint disorder is fundamentally of static or mechanical origin, and, this being so, the results of anti-gouty treatment are open to a further misinterpretation. The victims, as we have said, exhibit very generally a tendency to obesity. Now, Ebstein and many others hold the view that obesity and gout have affinities. Ebstein, moreover, believes that treatment directed to the reduction of body weight will check the appearance of gouty arthritis or ameliorate the same when avowed. What happens is this: these corpulent subjects are placed on a special dietary. Hydrocarbon foodstuffs are limited, bread, amylaceous food and liquids being also restricted. Naturally, pari passu with reduction in their body weight, their overburdened joints become more equal to their office. But those who assume that the chronic arthritis is of gouty origin attribute, and, we think, wrongly, the beneficial results attained to correction of the underlying “gouty” habit.
We prefer to subscribe to the simpler or mechanical theory, and in view of the widespread and, as we believe, erroneous belief in the gouty nature of this arthritis, we take the liberty of appending the salient features of these cases, while adding further a few remarks on the differential diagnosis of other symmetrical affections of the knees which may also be wrongly attributed to gout.
The onset is gradual and insidious. Stiffness is the salient symptom, but sometimes the subject is more distressed by a sense of weakness, distension and unreliability. Pain is slight or absent, save when during walking pseudo-locking occurs. The mobility of the joints is usually unimpaired, and if any limitation exist it is the power of full extension that is usually restricted.
Objectively the joint shows either general enlargement or swelling localised to the supra- or infra-patellar regions. Intra-articular effusion which comes and goes is a very characteristic feature. On palpation a peculiar soft silken crepitus will be heard and felt as the patient alternately flexes and extends the limb. The enlarged fringes are also easily to be felt as knots or nodules which can be moved up or down on the underlying bone. The ease with which they can be appreciated depends upon the degree of effusion present at the time. Judging from their symptomatology, it seems probable that some of the cases included in Sir Dyce Duckworth’s category, chronic deforming gout, are of this description.
The diagnosis of villous synovitis should not be considered complete without skiagraphy being undertaken to reveal or exclude osteophytic outgrowths. For the subjective symptoms and signs of early osteoarthritis are practically identical with those of villous arthritis, and although the presence of osteoarthritic lesions elsewhere would be suggestive, skiagraphy alone will enable us to effect a differentiation with certainty. Indeed, Bassett Jones and myself are strongly of the opinion that the life history of osteoarthritis involves two stages: (1) a primary or pre-osteophytic phase, often of prolonged duration, whose clinical characteristics are those of villous hypertrophy; (2) a secondary or terminal stage, in which bony and cartilaginous outgrowths make their appearance.
Other symmetrical disorders of the knees that may be wrongly ascribed to gout are hydrarthrosis and gummatous synovitis.
Bilateral Hydrarthrosis.—Given effusion into both knees which is passive, copious, and persistent rather than recurrent, then its possible infective origin must be carefully canvassed. The common sources are gonorrhœa, syphilis, and tubercle. The history or presence of an urethral discharge and detection of the gonococcus will identify the first named. In syphilis the existence of other lesions, the response to Wassermann’s test and specific treatment are the points on which to rely, and in tubercle, the detection of visceral foci and the sero-reaction will give the clue.
As to the intermittent type of hydrarthrosis, the remarkable periodicity in incidence of the effusion will suffice to obviate any possibility of confusion.
Peri-synovial and Peri-bursal Gummata.—Affecting as they do commonly the knee joints of adults, these may, in the absence of a history of infection, be a source of error. The uneven and nodular swelling may quite easily be confounded with uratic deposits. Pain is slight and mobility but little impaired. The presence of neighbouring scars, a positive Wassermann reaction, and a favourable response to anti-syphilitic therapy will clear up the diagnosis.
The clinical portrait of tophaceous gout when of widespread distribution is one of the most striking to be met with in the whole domain of medicine, but for the broad outlines of the picture presented we would refer the reader to the chapter dealing with the clinical description of chronic articular gout.
In these polyarticular forms the most distinctive joint deformities are those met with in the hands or feet, more particularly the former. The excrescences produced are the outcome of successive uratic deposits. These latter when massive can scarcely be confused with any other disorder, for the superjacent skin, distended by the ever-increasing underlying uratic deposits, becomes thinned and purplish red in hue, and occasionally ulcerates. I have at present in my wards a case of this nature, and the subject hoards up the exuding “chalk” in a small bottle.
Fortunately such marked examples are relatively rare, though easily recognised; but it is the less marked types that occasion difficulty in diagnosis. The point at issue of course is the differentiation of moderate-sized or small tophaceous swellings from bony outgrowths. Frequently the task is impossible of achievement without resorting to puncture, when, if anything can be withdrawn, microscopic examination may reveal the presence of biurate crystals.
For the rest, attention to the following points will prove helpful in enabling us to differentiate clinically between gouty arthritis and other chronic joint disorders attended by deformities:—
(1) Tophi when of recent incidence are soft, and when of long standing are never so dense or so hard as bony outgrowths.
(2) The overlying skin is thin, and through its substance the subjacent white concretions may sometimes be discerned. It may be adherent, or the seat of ulcers.
(3) Uratic deposits are not located exactly at the level of the articulation. They do not adapt themselves to the contour or shape of the bone-ends.
(4) Unlike osseous growths, they may be slightly movable in lateral directions.
(5) Tophi may soften or disappear after exacerbations of arthritis.
The conditions likely to be confused with chronic polyarticular gout are osteoarthritis, rheumatoid arthritis, and the multiple arthropathies met with in affections of the central nervous system.
Its chief characteristics may be summarised as follows:—It is a disease rarely met with under forty years of age. The mode of onset is generally insidious, never really acute. In this respect it contrasts with gout, the initial outbreak of which is invariably acute. Osteoarthritis attacks both sexes equally. Although it may be polyarticular, its specific tendency is towards a mono- or, more accurately speaking, oligo-articular distribution, with no marked leaning to symmetry. It has a pronounced predilection for attacking the hip, the shoulder, and the spine—sites rarely, if ever, attacked by gout.
Unlike gout, constitutional symptoms, pyrexia and so forth, are generally absent; muscular atrophy is slight, hardly ever pronounced, likewise muscular spasm and contracture.
These are best appreciated in the small joints of the hand. Osteoarthritis has an affinity for terminal joints—the so-called Heberden’s nodes. Another favourite site is the carpo-metacarpal joint of the thumb, while the preference of gout is for the metacarpo-phalangeal joint thereof and for the same articulation in the other digits.
The overlying skin, as a rule, is unchanged, and never assumes, as in gout, a dusky red or purplish hue. The margin of the articular surfaces, instead of being smooth and rounded, is broken and irregular, its nodular contour being due to osseous outgrowths studding the line of junction of the bones entering the articulation.[42]
In this respect they contrast with tophi, which are located near to, but not at, the level of the joint fissure. Again, unlike tophi, bony outgrowths are fixed, immutable, undergoing no change save in the direction of progressive enlargement. While the tendency of an osteoarthritic joint is to expand and increase, still the enlarged and gnarled joints never attain the colossal bulbous appearance presented by inveterate examples of tophaceous gout.
This affection differs from the foregoing disorder as well as gout in that it is most commonly met with in persons under forty years of age. Moreover, it attacks women much more frequently than men. Of polyarticular distribution, it evinces a marked tendency to symmetrical invasion. Like gout, it has a pronounced preference for the smaller joints, while, similarly, it avoids the hip and shoulder.
Constitutional symptoms are conspicuous: pulse quickened, temperature raised, extreme wasting not uncommon. Intense and widespread muscular atrophy with contracture is a prominent feature, also trophic disturbances of varied nature and degree.
In early stages the skin over the joint is waxy white or semi-asphyxial in tint, outline of joint smooth, rounded, and spindle in shape, with, as a rule, no irregular bony projection at the level of the articulation. If seen at a later stage, the swollen joint will be found shrunken from atrophy of all the articular structures as well as the skin. Ultimately it becomes reduced even below its normal size, the small “end-joint” of atrophic or rheumatoid arthritis. The deformities due to muscular spasm are usually in the direction of luxation and hyperextension, and differ from those of gout and osteoarthritis, in which there is more generally lateral displacement.
The joint disorders incidental to tabes and syringomyelia do occasionally find their way to spas for treatment under the mistaken conception that they are instances of “gout,” “rheumatism,” or “rheumatic gout.” In the case of tabes the mistake is often referable to the confounding of its lightning pains with “gout” or “rheumatism,” with subsequent relegation of the swollen joints, whether single or multiple, to one or other of these categories. In the syringomyelic it is, I think, the close resemblance that obtains between the joint lesions and those of osteoarthritis or so-called “rheumatic gout” that accounts for their uncalled-for and utterly useless transference to spas. I have known a case of syringomyelia with multiple arthropathies in the hands sent to Bath under the mistaken idea that they were of “gouty” origin.
These remarkable joint affections will be distinguished by their fulminant onset with marked effusion and absence of pain, tenderness, and heat. In addition, associated phenomena will be present, viz., ataxic pupillary changes and lost knee-jerks in tabes, while syringomyelia is characterised by dissociated anæsthesia, trophic disturbances of bones, progressive muscular atrophy with paralysis.
It will be recalled that Rieken held the view that so-called “bleeders” were prone to attacks of gout, and that sometimes these alternated with intra-articular hæmorrhages. Nor was he devoid of supporters, for Sir Dyce Duckworth maintained that a definite hereditary relationship obtained between gout and hæmophilia, while that astute observer Jonathan Hutchinson also contended that the vascular weakness was the outcome of gout and aggravated by serial hereditary transmission. Wickham Legg, however, in his masterly contribution questioned the correctness of Rieken’s proposition.
Personally, I cannot out of my own experience confirm or rebut the view that “bleeders” come of gouty stock, nor have I ever met an avowed gouty subject who was likewise the victim of hæmophilia. Quâ its joint complications, hæmophilia to our mind would appear to display closer affinities with peliosis rheumatica than with gout; but, in view of Duckworth and Hutchinson’s claims, it were wiser on our part to withhold judgment, while paying them the deference of being alive to the possibility of there being some obscure connection, though not proven, between the two disorders. Again, as emphasising the necessity for discrimination, we would draw attention to the fact that Konig recognised three stages in hæmophilic arthritis: (1) hæmarthrosis; (2) an inflammatory process, with pyrexia and spindle-shaped swellings apt to be confused with tuberculosis; (3) extensive arthritic changes reminiscent of arthritis deformans. Confusion with gouty arthritis clearly is only likely in the second or third stages, and in the matter of diagnosis the personal and family tendency to hæmorrhages is the most important clue.