Prodromal Symptoms
While we recognise that local inflammatory reaction in the joints is more particularly characteristic of gout, it is no less necessary that we take cognisance of the general precursory symptoms that often, if not always, usher in its onfall. Gout begins in a disorder of function.
Uncomfortable sensations may obtain days and weeks before the incidence of the fit. To old time sufferers they are sufficiently alarming. But their significance, as heralds of an initial attack, by victim and too often by physician also, is usually only appreciated when the threatened fit becomes an actuality. Speaking of premonitory phenomena in gout, Sydenham remarked, “Its only forerunner is indigestion and crudity of the stomach, of which the patient labours some weeks before,” and doubtless this is in the main true.
As Trousseau long since observed, the patient’s appetite often becomes capricious. He likes his meat strongly spiced, and craves for acids. But his satisfaction is short-lived. For eating is followed by drowsiness, feelings of oppression and fulness, with unpleasant eructations, or more rarely definite retching. The bowels are generally costive, but in exceptional instances diarrhœa has been noted. The state of the urine is variable. Generally scanty and high-coloured, it may in some be copious and pale.
Uneasiness in the right hypochondrium and even slight swelling of the liver was noted by Trousseau and also by Scudamore. Such congestion of the portal system and hepatic enlargement may be only fugacious, but often the same is permanent, a penalty of the same cause—free living—which leads to the production of gout. For in many instances but too true is it that “for years together,” as Sydenham said, “a man has drunk and feasted, has omitted his usual exercise, has grown slow and sluggish, has been over-studious or anxious, in short, has gone wrong in some important point of life.”
But more palpable to his friends than to himself are the concomitant changes in his disposition and character. From being good-natured and easy-going he becomes morose and irritable. The irascibility of the gouty is proverbial, and the explosive mental outbursts to Duckworth appeared at times to be “a metamorphic substitution for a more overt and regular attack,” or, as Sydenham expressed it, “Non rectius podagræ quam iracundiæ paroxysmus omnis dici potest.”
Sometimes his mental vagaries are exchanged for or accompanied by neuralgia, painful cramps in the limbs, etc. In truth, the premonitory phenomena of gout are protean, inasmuch as, given any prior weakness or functional derangement of any viscus, the symptoms of oncoming gout are masked by aggravation of the same, it may be by cardiac irregularities, vesical irritability, or in an old bronchial subject by increase of cough, etc.
But it may be objected, there is nothing specific about these various functional disturbances. They are not more common in the gouty than in others. Moreover, the habits of life productive of gout favour the development of gastric and hepatic derangements. The mental irritability, the gastric disturbances, etc., may be quite as well accounted for by overeating and overdrinking as by gout.
Now, if there be nothing specific of gout in these so-called prodromata—“heartburn, acidity, flatulence, etc.”—then what is their true significance? For, obviously recognition of their true import is most essential. Now to my mind the said “dyspeptic” symptoms should be regarded not as symptomatic of gout, but as etiologically related thereto.
For, though the etiology of gout is still much debated, the same obscurity will certainly not be clarified, if we merely content ourselves with dubbing such “dyspeptic” symptoms as “gouty.” On the other hand, if we, at this early stage, endeavour to elucidate the true origin of the “dyspeptic” symptoms, who will deny that this is the more rational and scientific mode of procedure? The timely elimination of septic foci in the mouth, tonsils, and naso-pharynx conjoined with modification or restriction of food intake and recognition betimes of the signs of intestinal infection and constipation would perhaps stave off or avert the threatened articular outbreak.
It has been suggested that there is some statistical evidence that “acute rheumatism” has declined in frequency since the introduction of tonsillectomy. In the same way, I cannot help thinking that the growing infrequency and attenuation of gout is in part due to increasing appreciation by the laity and the profession of the vital importance of oral hygiene and timely and radical treatment of local foci of infection. The fact that in children, victims of so-called infantile gout, the purin metabolism may show those same derangements held typical of the subjects of gout, is surely an indication that the disorder begins betimes, and that we too must not tarry if we would prevent these evil potentialities coming later to fruition.
Now, if there be nothing specific of gout in the “dyspeptic” derangements held prodromal thereof, the reader may well ask the pregnant question, Are there any symptoms or signs that will enable one to identify the victim of these minor discomforts as being “actually” or “potentially” a “gouty” subject? In attempting to answer this reasonable query one would emphasise the fact that tophi in the ears or at other sites sometimes antedate articular outbreaks.
Now given that an individual exhibits auricular tophi, one or many, can anyone deny that he is “gouty,” nay more, that he has gout, this even though he never has had, or may never have, an articular outbreak? In truth, the eruption of a tophus in the ear is as essentially a “fit of gout” as if it had occurred at the classic site, the big toe.
How vivid the light then thrown upon the import, the etiological significance, of otherwise inexplicable functional derangements! How grim the potentialities of, e.g., “dyspeptic” symptoms as revealed by detection in the subject of a tophus! Whether viewed from the diagnostic or prognostic aspect, its importance cannot be overestimated. For let us not forget that the tophus is the one incontrovertible token of the “gouty diathesis.” This morbid localisation is the sole outward expression of the inward and dominant pathological trend.
The great Charcot did not despise its aid. He narrates the case of a man thirty-five years of age, a sufferer for some months from “acid dyspepsia,” in whom he predicted a fit of gout from noting an uratic concretion in one ear. Is not the moral obvious that in an individual complaining of gastric or hepatic disturbances, etc., we should, at any rate, examine the ears for tophi?
For, far more often than is currently realised, their eruption antedates the articular outbreaks.[27] Moreover, they may not be solitary, but numerous, the cutaneous gravel of older authors. In truth, these cases of tophi, uncomplicated by articular lesions, seem to merit some distinguishing term, representing as they do a purely ab-articular form of gout.[28] They constitute what might be termed primitive elemental gout, of which the subsequent articular outbreaks are but an extension, a further manifestation of the “gouty diathesis.” For it is just this same tendency to uratosis or deposition of sodium biurate, and this alone, that to our mind constitutes gout, this “primordial vice of nutrition,” not the congeries of distempers that with the passing ages have clustered around the primitive gout, well-nigh submerging its identity.
Premonitory Symptoms of Tophus Formation.—While tophi may antedate articular attacks, we do not always meet with them as mature concretions easily recognisable as such. We must have regard therefore to the symptoms and signs indicative of their impending eruption. Consequently in a patient complaining of the various functional disturbances that so frequently anticipate gout we should never dismiss as trivial any complaints of pricking or tenderness in the ears.
Sometimes the pain in the ears is acute, the tenderness such as forbids their pressure on a pillow. Graves, of Dublin, not only noted that the pain in some instances was agonising, lasting a few hours, but he himself suffered also from such attacks of auricular pain, which only disappeared when gout supervened in his fingers. I have myself frequently known the pain and soreness referred to chilblains, though later their tophaceous nature was disclosed.
Given such auricular pain and tenderness, we should examine the pinna for small red swellings.[29] These, when definitely localised, should be punctured and the thick white fluid which exudes examined microscopically for urate of soda crystals. In some instances the creamy-like exudate does not yield a crystalline deposit, and Dr. Munro and I are inclined to believe that there is a pre-uratic stage in the evolution of tophi. We have observed this absence of crystalline deposits in apparently unmistakable tophi, as evidenced by the usual pearly white concretions in the rim of the ear. I recollect that the late Sir William Osler, when visiting our laboratory, was deeply interested in this possibility, as suggested by Dr. Munro, of a pre-uratic stage. Needless to say, all local sources of fallacy—Woolner’s tip, fibroid nodules, sebaceous cysts—were excluded, while, in the lack of crystalline proof, the evidence in favour of the associated arthritis being gouty rested on its being at the classical site, the great toe. Moreover, as an alternative explanation we have the possibility of reabsorption. We may recall Duckworth’s well-known example where a man had two attacks of gout in the right great toe joint, yet autopsy revealed no speck of uratic deposit. We know, too, that, following an acute attack, tophi may diminish in size or even disappear, while coincidently fresh tophi form at other sites.
Premonitory Articular Pains.—Again, when, in association with indigestion or other premonitory symptoms, twinges in the toe recur from time to time, especially after consuming wines or certain articles of food, these same are very suggestive of impending gout. Garrod is very definite on this point: “I have no doubt that many persons experience extremely slight attacks of gout before the development of the affection in an acute form, and several of my patients have assured me that for years before their first severe attack in the great toe they have felt slight periodic twinges. I am of opinion that when such twinges occur deposition has already taken place.”
In conclusion, we would urge that, given gastric or hepatic disturbances, etc., in a subject predisposed by heredity or habits to gout, we should note the presence or absence of the following:—
(1) Pain, pricking, or tenderness in the ears, with or without small red swellings.
(2) Similar sensations at site of finger joints, with dorsal swellings over which the skin may be red or unchanged.
(3) The existence or not of pearly white concretions, i.e. mature tophi (as tested microscopically), at the above sites or elsewhere.
Further signs that may be sought for in cases of doubtful nature, i.e. unevidenced by tophi, would be:—
(4) The presence of uricæmia.
(5) A lowered or sub-normal output of uric acid in the urine.
(6) Diminution or retardation of the output of exogenous purin.
To take up the thread of our narrative regarding the prodromal symptoms which at any moment may give place to an articular outbreak. The determinants or exciting causes having been already dealt with in the section on etiology, we shall here only note those symptoms or signs that portend the imminence of the paroxysm. These are very variable. But it is suggestive if without any change in the habits the “dyspeptic” symptoms abate somewhat or disappear.
Indeed, it is well recognised that, whatever the nature of the prodromal phenomena, they all tend to cease just before the oncoming attack. Occasionally a pre-existing depression gives way to a feeling of exuberant health or well-being. We recall the instance of a celebrated physician whose lectures always just prior to an attack took on an added brilliance.
Reverting to more definite harbingers, it has been noted that the urine becomes scanty, and its content of uric acid much diminished, some three or four days before the paroxysm, though such is not invariable. Easier of note and widely recognised is the fact that in those exhibiting tophi pricking pains or tenderness are experienced at their site. Scudamore, Garrod, and Duckworth are all agreed on this point. Another sign noted by Sydenham was that the veins of the part about to be affected become engorged—a feature confirmed by Trousseau and others.[30]