In the pathways of medicine, as in other walks in life, we are apt to become stereotyped, to fall into grooves, and sooner or later the inevitable rude awakening comes. Thus, so prone are we to think of gout as belonging, so to speak, to the foot, that when it erupts elsewhere it is often the last contingency to dawn upon us. If we diagnose it too often and too readily in the foot, we do so too seldom when it appears in joints remote.
Now, while in initial outbreaks of gout it is exceptional for more than one joint to be affected, it is not always so. For sometimes in those strongly predisposed by heredity not one, but many joints, may be implicated in the primary attack. Such cases, however, are extremely rare.
As a rule, this acute gouty polyarthritis occurs in individuals who have already experienced articular paroxysms at the classic site; but in the subsequent polyarticular attacks the toe joints are often unimplicated, and the disease is located in the larger articulations—the knees, ankles, wrists, or elbows. Herein resides the difficulty of diagnosis in these cases: the likelihood of confusion with other polyarthritides.
Confronted then with an acute polyarthritis of obscure nature marked by pain, redness, swelling, and pyrexia, what are the points necessary to establish it as being of gouty origin?
The sex and age should be noted, also the heritage, habits, and occupation. A history of previous attacks located in the big toe would be of prime value. The presence of a cardiac valvular lesion, while it would suggest a previous attack of acute rheumatism, would in no wise negative the possibility of the subject developing gout in later life. Here I may say that if the subject is over thirty-five and has never had acute rheumatism or acute gout, it is much more likely at his time of life that his acute polyarthritis is of gouty than of rheumatic origin.
As to the character of the pyrexia, it is usually of low grade; but if the condition be afebrile, it is even more suggestive of a gouty arthritis. But recollect, too, that the pyrexia in gonococcal arthritis is also of low grade or absent.
There is nothing distinctive of gout either in the character or distribution of the articular lesions. The ankles, knees, hands, wrists, are most commonly involved, much more rarely the elbows, shoulders, or hips. Naturally the local changes will differ according to the joint involved and the structures implicated; but these local variations in appearance, including œdema, may all be met with in any form of infective arthritis.
As to uric acid excretion, Osler, who was deeply interested in this type of arthritis, held that any lowering of the ratio of the uric acid to the urea excretion would be significant of gout. Also we should, as these cases of acute gouty polyarthritis are of the nature of successive paroxysms (“series et catena paroxysmulorum,” to use Sydenham’s expression), note any variations in the uric acid output ensuing pari passu with their rise and wane.
Last, but most important of all, a thorough search must be instituted for tophi, not only in the ears, but elsewhere. If anything could emphasise the indispensable rôle played by tophi in the diagnosis of gout, it would be our utter inability to effect in their absence a diagnosis of these acute types of gouty polyarthritis. The establishment of the existence in situ of such articular uratic deposits disposes forthwith of all possible doubts as to the true nature of the case; but if, as so frequently happens, the tophi when present are of ab-articular site, then we must withhold our decision pending the exclusion of certain other joint disorders, to the differentiation of which we now proceed.
The class of disorders that call for discrimination are those of infective origin. In the first place, acute articular rheumatism must be excluded; nor is it less necessary that we should eliminate gonorrhœal and syphilitic types; while, last, but not least, that vast group, the undifferentiated infective arthritides, is but too often a source of confusion.
Unquestionably many cases of acute gouty polyarthritis have been confounded with acute articular rheumatism, and vice versâ. Garrod on this point remarks: “That many cases of acute gout have been mistaken for acute rheumatism I do not doubt, and, on the other hand, that some few cases of acute rheumatism have been regarded as of a gouty nature I am no less certain. I may refer to the oft-quoted case related by Dr. Haygarth in which gout was supposed to have been transferred from the extremities to the heart as an example of the latter error.”
It is only, of course, with that type of acute gouty polyarthritis accompanied by pyrexia, and not the afebrile variety, that confusion with acute articular rheumatism is possible. What then are the points of discrimination?
| Acute Articular Rheumatism. | Acute Gouty Polyarthritis. | |
|---|---|---|
| Age and sex | Most common between ages of fourteen and thirty. Predominance of males after twenty. | Maturity and old age. Males. Females markedly exempt. |
| Heredity | Very disputable. | Very pronounced. |
| Onset | Usually abrupt and often with tonsillitis. | Insidious, with premonitory gastro-intestinal symptoms. |
| General symptoms | High fever, sometimes hyperpyrexia. Profuse acid sweats. | Moderate pyrexia. Marked daily remissions. |
| Distribution of lesions | Preference for large joints and markedly mobile. | Small joints, hand or foot often involved. Fixity typical. |
| Local characters | Joints exhibit slight reddish flush. No subsequent desquamation. No residual change. | Scarlet hue and œdema with later peeling of cuticle and itching. Tendency to involvement of bursæ and tendons. |
| Pain | Chiefly evoked by movement. | Spontaneous, more intense. |
| Duration | Twenty to thirty days, sometimes longer. | Six weeks to three months. |
| Associated phenomena | Cardiac lesions common. | Tophi. Occasionally glycosuria and albuminuria. |
| Therapeutic test | Salicylates a specific. | Not so in gout, but colchicum takes this rôle. |
This disorder, as we know, is sometimes of oligo- or poly-articular distribution. Moreover, as the attendant pyrexia may be slight or absent, it may readily be confounded with the afebrile variety of acute gouty polyarthritis. Osier, discussing diagnosis of the latter condition, observes: “A patient with three or four joints red, swollen, and painful in acute rheumatism has fever, and while pyrexia may be present, and often is, in gout, its absence is, I think, a valuable diagnostic sign.”
This is of course true, but it still remains necessary, for reasons above cited, to eliminate acute gonorrhœal arthritis. The tendency to such confusion has been emphasised by Sir Rose Bradford and Sir William Roberts, and I would urge the necessity of being alive to this possibility even in middle-aged men. One thing is certain, viz., we should be extremely chary of pronouncing any coincident urethral discharge to be a so-called “gouty urethritis”; nor should we translate any coincident conjunctivitis or iritis as further evidence of the articular affection being “gouty.” It is far more likely to be gonococcal. Apart from these inflammatory ocular affections, the relics also of previous attacks—viz., irregularity in contour or inequality in size of the pupils—have before now put me on the right track in obscure types of polyarthritis.
To sum up, the following are distinctive characters of generalised gonorrhœal arthritis:—
Etiology.—History or presence of urethral discharge and isolation of the gonococcus.
Onset.—Insidious, seldom acute.
General Symptoms.—Absent or slight relatively to extent and severity of joint mischief. Pyrexia, low grade or absent.
Distribution of Lesions.—Preference for large joints. Special liability of sacro-iliac, chondro-costal synchondroses, sterno-clavicular, tibio-fibular, and temporo-maxillary joints.
Local Characters.—Persistent passive effusion or peri-articular boggy swelling, with redness and local heat. No tendency to migrancy. Joint swelling very persistent.
Associated Phenomena.—Involvement of fasciæ, especially plantar, and of tendon sheaths, very distinctive, while coincident iritis or conjunctivitis is almost diagnostic.
The ease with which a subacute arthritis of this nature may be confounded with “gout” or “rheumatism” calls for comment. We have met with cases despatched to spas under this impression. The customary intermittent fever of secondary syphilis is usually present. The detection of periosteal nodes in addition to the joint swellings should arouse suspicion, while the presence of secondary syphilides and the rapid response to specific treatment will be confirmatory.
I well recollect some years ago a young farmer being sent to me by a medical man as suffering from gouty arthritis with gouty eczema. The eruption was a typical roseola, and the condition promptly cleared up under anti-syphilitic treatment.
While the old term “rheumatic gout” still clings to this affection, it has now achieved its isolation from gout on the one hand and rheumatism on the other. The fact that it occurs in young women in whom gout never occurs, and has a very marked clinical facies of its own, should almost preclude the possibility of its being a source of confusion. Still, for the sake of completeness, we append its chief characteristics.
Age and Sex.—Most common in young women.
Onset.—More or less acute.
General Symptoms.—Continuous low grade pyrexia, quick pulse, and rapid emaciation, and commonly concomitant gastro-intestinal derangements.
Distribution of Lesions.—Polyarticular. Beginning in the small joints, it spreads centripetally, with a tendency to symmetry. No migrant trend, but a steady, progressive involvement of joint after joint, including temporo-maxillary and cervical articulations.
Local Characters.—Overlying skin of affected joint white or semi-asphyxial in tint. Contour spindle-shaped, but in terminal stages shrinkage from atrophy of articular structures sets in. Muscular wasting and contracture conspicuous features.
Associated Phenomena.—Trophic and vasomotor changes prominent, but no tendency to cardiac lesions.
It were well in approaching any acute polyarthritis of obscure nature to bear in mind the axiom that any or all infections may be complicated by arthropathies, also that if the said polyarthritis does not respond quickly to colchicum or salicylate of soda we are almost certainly dealing with an infective arthritis either of specific or undifferentiated type. The specific forms of infective arthritis, as far as seems necessary, have been dealt with, but those rarer forms not referred to, viz., influenzal, pneumococcal, dysenteric, meningococcal, etc., have also to be borne in mind, if the history reveal any recent occurrence of these disorders.
Still far more common than any of these are the acute infective arthritides of undifferentiated type. As we before remarked, an extraordinary general clinical resemblance obtains between these types of joint disorder and acute gouty polyarthritis. Indeed, in the absence of tophi, their differentiation is well-nigh impossible. Even the blood picture in both types of the disorder is strikingly similar in the matter of leucocytosis and secondary anæmia.
Recently Dr. Henry A. Christian, lecturing at a clinic of the Harvard Medical School, emphasised this clinical similarity and the difficulty of discriminating between these two types of joint disorder. As he rightly says, “while there is a definite acute gouty polyarthritis (as evidenced by external tophi or deposits in bone or cartilage with variations in uric acid output) and also an equally definite infective arthritis, yet between those two there is a very considerable number of cases that present some of the factors suggestive of gout and other factors suggestive of an infectious arthritis, and there is where the difficulty comes.”
This is precisely the state of affairs, and one may well ask where gout ends and infection begins. Let us take an example. A man exhibiting tophi, the subject also of pyorrhœa alveolaris, develops an acute polyarthritis. What then is the nature of the joint disorder? There is a gouty element in his case, as attested by tophi, also an infective element, as evidenced by oral sepsis.
Now are we to regard such a case as one of infective arthritis of undifferentiated type occurring in a gouty subject, or are we to proceed on the assumption that the presence of tophi negatives the possibility of infection and forthwith to class it as a case of acute gouty polyarthritis of so-called metabolic origin?
This is no theoretical quibble. In the Royal Mineral Water Hospital, Bath, one constantly meets with cases in which the very elect would be puzzled as to whether they should be placed in the category of gouty or in that of infective arthritis. I have at present in my wards a middle-aged man, stout of body, rubicund of face, with well-marked auricular tophi and widespread arthritis. There are no tophi round his joints. On X-ray examination his phalanges show Bruce’s nodes, and his phalangeal joints show changes indistinguishable from those constantly met with in infective arthritides occurring in non-gouty subjects.
Indeed, this overlapping may proceed still further, the gouty and the infective characters neighbouring in such proximity as to suggest actual fusion, a community of origin. What else in truth can be the inference, when one meets with examples in which the peri-articular tissues are the seat of demonstrable uratic deposits, while the X-ray changes within the joint proper, the bone and cartilage, are typically those met with in infective arthritis?
Now, who will deny that if tophi were absent in such a case we should without hesitation hold the case to be one of infective arthritis? My own contention is that even in the presence of tophi the same appellation is indicated. In other words, I submit that acute gouty polyarthritis is itself but a form of infective arthritis which derives its specific character from the associated uratic deposits.
As to differentiation of the latter from these cryptic infective arthritides, this will rest mainly on—
(1) The presence of tophi;
(2) A history of previous attacks in the great toe;
(3) A swift response to colchicum.
In addition, acute gouty polyarthritis is confined to middle-aged males, while no period of life is immune from infective arthritis, and both sexes are equally liable.
Again, acute gouty polyarthritis may be afebrile. Pyrexia when present is moderate in grade, its curve undulating as the paroxysms rise and wane. In infective arthritis the temperature curve is irregular and erratic.
Lastly, the uric acid output in acute gouty polyarthritis drops a day or two before the paroxysm, rises markedly after its inception, then sinks again. Also we may add that occasionally glycosuria or albuminuria is present.
In conclusion, I would allow myself a brief digression regarding these infective arthritides of undifferentiated type. They constitute the bulk of the cases of arthritis that find their way to the Royal Mineral Water Hospital, Bath, under one or other of the appellations “gout,” “rheumatism,” and “rheumatic gout.” It is within this category that most of the cripples met with at spas fall, and their obduracy to “drug” treatment accounts for their belated despatch thereto.
I would that I could sufficiently emphasise the imperative necessity of early recognition of the true nature of these cases. Colchicum is a most valuable drug, and so is salicylate of soda. But they have their limitations. They act swiftly or not at all. Persistence with them in the absence of any response is worse than futile: it is definitely prejudicial. Because of our unreasoning devotion, our almost fetishistic addiction, to these drugs, I often feel that these agents, especially salicylate of soda, have made more cripples than they have saved. For, unfortunately, unqualified reliance on these drugs is apt to blind us to the surgical necessities of these cases. Foci of infection pass unnoticed, joints stiffen at unfavourable angles, and not infrequently a potential bread-winner is lost.
I make no apology for this digression, for it is, strictly speaking, wholly apposite, this in view of the fact that failure of quick response to the action of colchicum or salicylate of soda, say within a week, speaks in favour of the infection having ensued in a non-gouty as opposed to a gouty subject.