Acute Gouty Polyarthritis
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.