The very disparity between the local lesions seems to exclude the possibility of their being due to one and the same cause: in the joint, acute inflammation; in the heart and brain, degenerative changes. Where then the nexus? Surely it is but a time relation, a coincidence, the outcome of, concurrent though unrelated cardiac and vascular lesions. In short, the cases of so-called retrocedent “cardiac” and “cerebral” gout usually resolve themselves into cardio-mural degeneration, arterio-sclerosis, or renal disease.
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.