The term retrocedent or suppressed gout still lingers in medical nomenclature, largely, we think, as a tribute to tradition, for rarely indeed is it invoked in current literature. Known since the days of Galen and Aretæus, it originally signified a condition in which sudden inhibition of the acute joint affection is followed by or coincides with the development of serious internal symptoms referable either to the gastro-intestinal, cardio-vascular, or nervous system. Thus, there may be, e.g., vomiting, diarrhœa, dyspnœa, cardiac arrhythmia, cerebral hæmorrhage, delirium or coma.
Naturally for our forefathers the abrupt subsidence of the joint disorder with the incidence, as fulminant, of severe and alarming visceral symptoms appeared to be an example of true metastasis. That death, tragically sudden, so often ensued, but rendered more imperious the necessity for explanation; and, in the then state of knowledge, the proffered assumption could hardly be regarded as anything other than a perfectly legitimate and useful hypothesis.
The retrocession of the articular affection in acute examples of gout ensues abruptly, but in chronic types it usually transpires more gradually. Often no cause is assignable, but frequently the so-called metastasis has followed exposure, chill, or the imprudent application of cold to the inflamed joints. The late Dr. Parry, of Bath, in one winter saw two instances of apoplexy follow “the removing of gout in the extremities by immersing the feet affected in cold water.” In some, following the same revulsive procedures, severe cardiac pain has ensued with syncopal attacks, sometimes fatal, while in others gastro-enteric symptoms of like gravity have developed.
It is the asthenic types of gout that, according to Duckworth, are most prone to metastasis. When the phenomena occur rapidly, flitting from place to place, they have been designated “flying gout.” Nevertheless, as before said, the most dramatic examples arise in acute sthenic gout, though in their instance less likely to occur spontaneously than in sequence to depressing external agents, e.g., cold lotions, etc.
Reviewing the recorded examples of retrocedent gout in the light of latter day experience, it is, we think, most significant that no such dramatic examples apparently occur nowadays, at least none to which the term “retrocedent gout” appears applicable. The designation, indeed, bids fair to become obsolete. What then is the explanation? That even to-day cases of acute articular gout yield to, or are replaced by, functional visceral disturbances, of varying degrees of gravity, is certainly true. But, partly through increase of knowledge and partly through the growth of a more critical attitude, we seldom, if ever, feel justified in ascribing them to gouty metastasis.
Take “gout in the stomach,” to which organ, in the days of the Regency, it appeared to fly on the slightest pretext, a “vulgar belly-ache taking rank by courtesy” as such, before Sir Thomas Watson pricked the bubble of these pretentious ailments by his suggestion that “gout” (so called) in the stomach sometimes turned out, under the test of an emetic, to be nothing more than pork in the stomach. A caustic stricture, but doubtless well merited. For the symptoms held typical of “gout in the stomach” are but those of gastric irritation, with nothing to suggest that they are of “gouty” origin.
Again, as Brinton in his classic exposure of this clinical myth observes, some of the recorded instances doubtless derive their melodramatic aspects from unrecognised biliary colic. As he rightly says, some of the cases instanced by Scudamore were jaundiced usque ad unguem. Gallstones, too, are among the many derivatives of the so-called “gouty” habit. The age incidence of both disorders is identical, whence doubtless the conception of the relationship. But what of the abdominal catastrophes attached to gallstones, all wholly unguessed at in those days? What, too, of the unrecognised and doubtless frequently coincident renal disease, with its menace of uræmia—pain, vomiting and prostration, not to mention Buzzard’s reflection that some cases of gout in the stomach were probably referable to gastric “crises,” i.e., tabes dorsalis?
If we recall that none of these sources of fallacy—and we have named but the more common—were eliminated, and also the absence of any anatomical proof post mortem of gastric lesions, one may well ask with Brinton, “Is there any ‘gout in the stomach’ left after the subtraction of these various affections?” Personally, I can say with Brinton that “I know of no such case; have never seen one; have never been able to get trustworthy evidence of one from some of the most accomplished physicians living, or from the best records.”
Reverting to the cardiac and cerebral phenomena that have sometimes followed the retrocession of acute gout, the same difficulties confront us. The conclusion that they are examples of retrocedent gout is drawn from premises which really do not support it. Strictly speaking, there is nought but the time relation to go upon, and the laconic comment “Non sequitur” is obvious.
To continue, the more we know of the causes and effects of disease, the less relevant becomes the time relation, and the nearer do our conceptions of cause and effect approximate to the more truly valid conception of ground and consequence. But what grounds have we for assuming that the anginal, the syncopal attack, or the apoplexy is the consequence of gout, that it is exclusively due to the materies morbi of gout?