Other Irregular Manifestations
The more dramatic examples of retrocedent gout, as before stated, occur mainly in the acute varieties of the disorder. But the same visceral metastases are occasionally linked up with the less severe articular manifestations, or with that vague clinical entity known as “goutiness,” the same being frequently known as “wandering” or “flying” gout. Most of the examples met with in the present day belong to the last category. This may possibly find its explanation in the growing infrequency of the more acute or sthenic types of gout.
Both of the mild and of the severe forms of metastasis the same pathological interpretation is hazarded. The gout is described as “suppressed” or “retrocedent.” According to the former conception, the gouty process itself suffers inhibition, while the latter term signifies deflection of the materia peccans of gout from the joint into the viscera. Of the twain the former hypothesis seems to me the more plausible. Thus, given an acute gout at its inflammatory zenith, it is conceivable that, if abruptly checked, the same might reflexly precipitate the occurrence of internal lesions in structures undermined by insidious and pre-existing degenerative changes. In other words, the aborted attack is not the cause, but the occasion, of the cardiac failure, the apoplectic stroke, the uræmia, etc.
On the other hand, given that such were due to actual transference of the gouty poison, one would expect that it would induce the same inflammatory phenomena in the viscera as in the joint. But there is no anatomical proof that such occurs, no evidence of an actual invasion of the impeached viscus by the gouty inflammation. Uratic deposits have, it is true, been found post mortem at the site of visceral lesions, but, be it noted, generally in degenerating tissue altered by other morbid processes. Some, however, affirm that in such the gouty process has quâ the uratic deposits left, so to speak, its attestation behind it.
But any degenerative focus may in a gouty subject become the seat of such a deposition. Yet it would be presumptuous to infer its gouty origin from this fact alone. Such are common in chronic nephritis, and this apart from gout. What need for wonder then that the same should occur in gouty subjects, with their blood surcharged with uric acid?
Were such uratic deposits located at the site of inflammatory as opposed to degenerative visceral foci, it would to our mind give more colour to the assumption that they were the outcome of a true gouty process; in other words, that, as in the joints, they were the sequel or concomitant of acute gouty inflammation. But it is not so.
As for the structural or organic degenerations met with in gouty subjects, very many, if not all, as Longstreth rightly says, “belong to some one of the great general classes of tissue changes, some of which are due to special causes, but the most of them own many causes. One of these many causes can be under certain circumstances gout, but there is really nothing special in the appearances by which we can unequivocally pronounce them of gouty origin.” With this view few would join issue, save only the reservation that the scleroses so commonly met with in gout, if due thereto, must owe their origin to some more vital agent than uric acid, a few milligrammes more or less in the blood content thereof.
It will be seen then that the anatomical evidence that gout can affect the internal organs is wholly lacking. The criteria then upon which the assumption is based that this or that functional disturbance is a manifestation of irregular or visceral gout are wholly clinical.
Doubtless the conception of irregular gout was derived from “the unaided operation of custom.” Thus, when one clinical event, A, was noticed frequently to precede another, B, the idea of an association between A and B was generated, and by virtue of this association A was said to be the cause of B. But obviously the fact that B has followed A does not establish any necessary connection between the two clinical events. In other words, the idea of a causal relation is in a sense a purely intellectual feat, a clinical inference presumptive and retrospective.
The evidence that a relationship exists between irregular and regular manifestations of gout rests upon the following sequences and alternations of clinical events:—
(1) The subsidence or disappearance of functional visceral derangements following the development of articular gout;
(2) Their occurrence directly after an articular paroxysm has been apparently suppressed;
(3) Their recurrence and alternation with arthritic outbreaks, this in some instances repeatedly;
(4) Lack of any appreciable cause for the functional derangements and their indefinite anomalous character;
(5) Their favourable response to specific gouty therapy.
As before noted, digestive troubles frequently precede the initial outbreak of articular gout. The same likewise are frequent in chronic cases between the intervals of arthritic seizures.
Now it has been customary to regard the alimentary or other disturbances that precede an initial articular attack as “gouty,” and likewise those that intervene between the gouty paroxysms in long-standing cases. In other words, in light of the subsequent articular outburst, what was mysterious ceases to be a mystery. All the vague “acidities, flatulencies, megrims, and biliousnesses, of whatever occult kind,” are forthwith hailed as “gouty,” this merely upon the ground of the sequence of clinical events, because the symptoms have disappeared from, e.g., the stomach to reveal themselves in the joint or joints, or vice versâ.
Now my own view is that the antecedent hepatic or digestive disturbances that so frequently precede initial attacks of gout are in all probability, nay assuredly, not gout. They should rather be regarded as the cause, the foundation, of the malady than its effect, a cause inoperative save in the presence of individuals victimised by inherent morbid tissue potentialities. For similar symptoms are but too common in the non-gouty. They are very common antecedents of, e.g., rheumatoid or atrophic arthritis. Nevertheless we do not when the arthritic disorder subsequently manifests itself talk of the preceding digestive disturbances as “rheumatoid” dyspepsia. Then why this presumptive and retrospective diagnosis of similar prodromal phenomena as “gouty” dyspepsia? For there is pending the articular outbreak nothing distinctive in the digestive derangements, nothing that would enable us to diagnose them as “gouty.” They might, for aught we know, be significant of oncoming rheumatoid arthritis.
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.
As to the respiratory organs, such chronic maladies as bronchitis and asthma are very frequent in the “gouty,” but I question if they are more so than in non-gouty subjects. In any case their symptomatology and course are the same whether gout be present or not. Much, too, has been made of the fact that asthmatic and arthritic manifestations may alternate. But we must recollect that asthma per se has a paroxysmal tendency; it has a tendency to periodicity and a liability to be excited or aggravated by much the same factors as favour outbreaks of gout. It is said, too, that there is a “gouty” pneumonia, and that the same has been replaced by an acute articular paroxysm. But, in respect of all these alleged “gouty” respiratory disorders, would it not be more scientific to cease talking of them as “gouty” and instead to speak of them as bronchitis and asthma occurring in “gouty” subjects? This, I may remark, is not to say that we should take no count of the reigning diathesis in our treatment of all associated affections.
Of the nervous phenomena relegated to gout we hear nowadays less and less. “Gouty” headaches are almost a thing of the past. The acute “gouty” delirium of older writers in many cases was but an euphemism for alcoholism, and likewise the spinal paralyses; while the convulsions and comas were certainly almost always attributable to uræmia. It would be held rash to-day to speak, like our forefathers, of “gouty” cystitis, urethritis, or orchitis, for there is no evidence of any pathological connection between them; and the same stricture is also applicable to the many cutaneous affections affiliated without sound pretext to the materies morbi of gout.
In the early part of the nineteenth century the French school were most insistent on the prevalence and variety of the cutaneous manifestations of l’arthritisme; but even by them the all-pervading influence of gout in the etiology of skin disorders is no longer held even as a working hypothesis.
Conclusions.—The sum of my experience and reflections on so-called “irregular” gout leads me to regard it as an “abstraction” rather than as a proven clinical fact. Moreover, if I may judge by the “admission certificates” to the Royal Mineral Water Hospital, Bath—a fair test, as I maintain—many are of the same mind as myself, for during the past ten years I do not recall a single instance in which a patient sought admission thereto as suffering from “irregular” gout.
But some writers on gout—indeed, I think I may say all—whatever doubts they entertain as to the propriety of retaining the term, yet qualify their pronouncement in favour of some particular variety of anomalous gout, visceral, cutaneous, or other. Still, in justification of my own uncompromising attitude, I must say that dispassionate analysis of their eclectic claims, in light of present day knowledge, to my mind fails to show any adequate reason for the faith that is in them. Of some of them I feel sure that sub-consciously they have been influenced by a respect for tradition, forgetful of Pliny’s sentiment,—
“Quamvis enim cedere auctoritati debeam, rectius tamen arbitror, in tanta re, ratione quam auctoritate superari.”—Lib. i., Ep. 20.
But, to resume, this much at any rate may be affirmed, viz., that there is no proof that visceral disturbances or cutaneous disorders are due to uric acid. On the other hand, in view of my contention that the inherent morbid potentialities of the “gouty” demand for their fruition the intervention of an infection, the reader may rightly ask whether the same agent may not be capable of evoking the visceral or cutaneous, as opposed to the arthritic, manifestations of gout.
Trousseau, a whole-hearted advocate of irregular gout, drew an analogy between gout and syphilis. Somewhat contemptuously he observes: “To those physicians in whose eyes localisation constitutes the particular disease the differences in appearances are so many different diseases, while to those who consider that the disease consists much more in the aggregate of the general phenomena, in their evolution, in their progress (and that, thank Heaven! is the direction in which sound observation leads), these affections, differing in appearance, are only multiplied expressions of the same species of morbid action. To the real physician exostosis, alopecia, psoriasis, roseola, bubo, and chancre are always syphilis—syphilis in different garbs.” In the same way he held that the infinitely varied manifestations of irregular gout were all affiliable to one and the same morbid agent. He claimed, too, that visceral gout was “the result of a sort of imperfect inflammation analogous to that which manifests itself in the joints.”
Unfortunately for the cogency of the argument, there is no proof that such visceral inflammations as do occur in the “gouty” are of gouty origin. Unfortunately, too, the microbic agent that we postulate as responsible for “gouty” arthritis is as yet unisolated. If this disability be removed, it might be found that the said organism was capable of originating, not only the arthritic, but the alleged visceral, forms of gout. But pending such discovery I am of opinion that the term “visceral” gout should be abandoned, in other words that we should cease to talk of, e.g., bronchitis, dyspepsia, etc., as “gouty,” and should talk of them as bronchitis or dyspepsia occurring in the gouty. In this way we may escape, or, better, render uncalled for, the scathing criticism of Pye Smith:—“It has become common to ascribe bronchitis, dyspepsia, gastralgia, iritis, gravel, cystitis, and even psoriasis to the ‘gouty’ diathesis; but the evidence is very slight, and the ‘gout’ to which such evidence as there is applies is the distillation of morbid humours which belong to a bygone pathology.... There is no reason to believe that gout ever flies to the stomach, but over-indulgence at the table may produce acute dyspepsia as well as inflammation of the great toe. Elderly people are liable to gravel, gout and cough; and while lead and drink may lead to gout and chronic Bright’s disease, cirrhotic kidneys favour an attack of gout.”