Gout, with a section on ocular disease in the gouty

by Llewellyn J. Llewellyn

Now in the case of the latter we regard the prodromal digestive phenomena as probably indicative of some infection located somewhere in the alimentary tract. It would be wiser, I think, to adopt the same attitude in regard to our “gouty” examples. Moreover, as we know, such dyspeptic symptoms recur from time to time throughout the life history of both rheumatoid and gouty arthritis. In the former disorder we regard them as indicative of recurring infection, followed as they so uniformly are by exacerbations of the joint trouble. Is it not time we adopted the same attitude towards the gastric or hepatic functional disorders that punctuate the course of chronic gout with a periodicity that rivals that of the articular paroxysms?

Unquestionably to my mind when we have regard to the extreme frequency with which local foci of infection, e.g., oral sepsis, etc., are found in gouty subjects, this would be the more rational attitude, the one more in conformity with modern medical thought.

But if we would condemn those who, in the presence of unequivocal tokens of gout, label antecedent or intercurrent dyspepsias, etc., as “gouty,” what are we to say of those that even in patients who have never had regular gout or exhibited tophi yet presume to classify their associated digestive troubles as “gouty”? This, I contend, is wholly unjustifiable. I would say more, that such conjectures are hazardous in the extreme, this both in the overtly gouty as well as in the non-gouty. I recall the instance of an individual who suffered from classical articular gout which palpably alternated with attacks of abdominal pain, but the clue to the true nature of the latter symptoms, as revealed at operation, was a chronically inflamed appendix. If so in this case, how many so-called “gouty” acidities have resolved themselves into appendicular or gall-bladder dyspepsia!

My conclusion then is that the gastro-intestinal disorders attributed to gout cannot legitimately be regarded as examples of irregular gout. They should not be held “symptomatic” of, but etiologically related to, gout, a view more calculated to lead to exact diagnosis and rational therapy, and incidentally to elucidate the true nature of gout.

In respect of other organs and the symptoms connected with them in “gouty” persons the case is very much the same. Always and ever are we confronted with the same difficulty, inability to determine whether antecedent, co-existing, or consecutive affections in certain examples of gout, are not associated merely by coincidence.

Disturbed cardiac action is not uncommon in gouty subjects, palpitation and arrhythmia and syncopal threatenings, and frequently symptoms difficult of differentiation from true angina pectoris.

I am reminded of an old physician whom I saw in consultation some years ago, who suffered from alarming attacks of precordial anxiety. He was well on in the sixties, and very obese. He was convinced that his cardiac irregularities, etc., were of gouty origin, and often exclaimed regretfully: “If I only dared to take two bottles of port, and got it in my toe, all would be well.” He had never had an articular outbreak, and based the diagnosis of his case on the fact that from time to time his urine for long since contained excess of urates. Having suffered much of many physicians, he at last grew restive, took the bit between his teeth, rushed to a spa, and forthwith embarked on a very strenuous course of “waters and baths.” At once he got a severe attack of acute polyarthritic gout, and mirabile dictu, all his cardiac troubles straightway ceased.

Retrospectively viewed, many would regard the preceding cardiac condition as of “gouty” source. That the old gentleman, of florid countenance, plethoric build, and lethargic habit, was potentially “gouty,” there is no doubt. But he was also abnormally fond, not of alcohol, but, curiously enough, of sweetmeats and cakes of all sorts, hence “dyspeptic.” He had a feebly acting heart, but no detectable valvular lesion, though mural degeneration seemed likely. My own diagnosis was flatulent dyspepsia with secondary cardiac disturbance, and finally acute gout, the exciting cause of which, as I have so frequently seen, was a course of hydrotherapy. The patient never regretted his venture, and, I am glad to say, lived for some years.

Such cardiac paroxysms are not uncommon in the “gouty,” and, alarming though they are, I question if purely functional disturbances of this nature ever prove fatal. As to the valvular lesions and mural degenerations observed in the “gouty,” there is little or no evidence that they are dependent on gout. Indeed, the lack of a tendency to endocarditis is one of the criteria distinguishing gout from acute rheumatism. I note that in one textbook pericarditis is classed among the cardiac manifestations of irregular gout. But it must not be forgotten that renal disease, a frequent concomitant of gout, predisposes to pericarditis, which, indeed, occurs in granular kidney even when unassociated with gout.