Acute Localised Gout

If we would clarify somewhat the obscurity that enshrouds the genesis of disease, our watchword must here, as in other spheres, be “Despise not the day of small things.” We know not the proximate cause of gout, it is true, nor the exact modus operandi of those agents, infective or other, which bring to fruition the latent morbid potentialities of its victims. But, even if so handicapped, we should be quick to descry those portents of the coming storm, those minor backslidings from physiological righteousness, that doubtless foreshadow the outbreak of the disorder.

For it cannot be doubted that the evil potentialities which make for gout are for long in operation before their definite installation in its chosen seat, the joints, ensues. As Trousseau puts it, “The diathesis is in action before there is time for the local affection to show itself in a precise form.” In short, given imminence of an attack, the whole system is charged with gout, or, as Sydenham laconically expressed it, “Totum corpus est podagra.”

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:—

Further signs that may be sought for in cases of doubtful nature, i.e. unevidenced by tophi, would be:—

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]

The Acute Paroxysm

A brief interlude, lasting a few hours or a day, frequently intervenes between cessation of the prodromal discomforts and the onset of the attack. This delusive sense of well-being deceives none but the uninitiated, for to the old time sufferer it is but the truce before the threatened assault.[31]

Still the subject feels better and more placid than his wont, seeks his bed, and sinks to sleep (“sanus lecto somnoque committur”). But suddenly, more commonly an hour or two after midnight, he awakes to a pain in the foot, usually in the ball of the great toe, though more rarely in the heel, instep, or ankle. Simultaneously he becomes chilly, shivers, or has a rigor. But as the pain, at first bearable, grows in intensity, these feelings lapse, giving way to feverish restlessness. Posture after posture is renounced, but, toss as he will, he strives in vain to find a place of ease for the tortured limb. Even the pressure of the bedclothes is intolerable. But towards morning (“sub galli cantu”) the pain remits as suddenly as it began. Anon the sufferer breaks into a gentle sweat, falls asleep, and wakes to find the painful part red, swollen, tense, and shiny, surrounded with œdema and turgid veins.

The same series of events recurs, though often in mitigated form, for some days and nights. During the day his pain is lulled, but towards evening it gathers in intensity to cease or diminish towards morning. The cycle continues from eight to ten days; then pain ceases, redness fades, œdema subsides, and the inflamed cuticle peels, with itching. The temperature meanwhile has sunk to normal, the local tenderness and stiffness gradually pass off, and health is restored. “Gout is the cure of the gout,” said Mead long since, and certainly recovery from the first attack of gout is usually speedy and complete. A renewed sense of bien-être ensues, free from the discomforts that led up to the outbreak. Indeed, in exceptionally rare instances the disease seemingly exhausts itself in a single paroxysm, or decades may pass before another visitation. Sir William Roberts tells of a Yorkshire squire who sustained a classical attack in his twenty-seventh year, the next in his eighty-ninth year. Frequently a second attack may not occur for one, two, or even three years. But the tendency to recurrence usually becomes more and more pronounced as the years roll on, and eventually the gouty man resigns himself to the doleful expectation of an attack once or twice a year, during spring or fall, with some approach to periodic regularity.

Initial attacks of gout are usually monarticular, but consideration of the polyarticular variety will best be postponed until we come to consider acute gouty polyarthritis. Also we think it will be more convenient for us to defer discussion of retrocedent gout to the chapter dealing with the irregular or anomalous types of the disorder. Meanwhile we will now proceed to detailed description of the individual phenomena that make up the clinical content of acute gout.

Detailed Consideration of Phenomena

Onset.—From Sydenham’s classical account it might be inferred that the onfall of gout is always fulminant. But this is far from being the case. For I find myself in agreement with Hilton Fagge that in many, if not the majority of instances, even the initial outbreak of the disorder is installed in a far less dramatic manner. Certainly in not a few cases its manner of approach is insidious, not to say stealthy. At onset then the nature of the case is therefore frequently misinterpreted both by victim and physician. The free liver, fearing that Nemesis has overtaken him, is fertile in suggestion. He has overwalked, his boot pinched him, or it is a sprain. Local appearances may be non-committal. There may be no swelling nor redness, and no access of pain at night. Still there is discomfort when he walks. The so-called sprain lingers, and one morning the great toe, instep, or ankle, is swollen, tender, flushed, and the victim’s fears and the physician’s suspicions are converted into certainty: it is gout!

Still in this matter of the onset I must not overlook the findings of my colleague James Lindsay. In 569 cases, the onset was sudden in 458, and in the remaining 111 examples gradual. It was noted that only 14·5 per cent. of the male cases were of gradual onset. But no less than 47·1 per cent. of the female cases developed after this fashion.

Again to resume, it is by no means invariably the case that the onset is nocturnal. For, as Duckworth has pointed out, many attacks begin during the day, and this is perhaps more often the case after the disorder is fully established.

Locality.—Gout in its classical form is monarticular in distribution. In 375 out of 512 initial seizures, Sir Charles Scudamore found that the metatarso-phalangeal joint of the great toe of one or other foot was the joint affected. Garrod, too, noted that, excluding the great toe, in not more than 5 per cent. were other joints implicated. As to the frequency of incidence in joints other than the big toe, opinions differ. For Scudamore it is the ankle, for Garrod the instep, and afterwards the outer side of the foot and the knee. In contrast, Hilton Fagge holds that next to the great toe gout vents its initial fury with greatest frequency upon the metacarpo-phalangeal joint of the index finger, adding, “certainly not the thumb.” Most authorities however agree that gout in its early stages rarely attacks the joints of the upper limb, and even in its most inveterate form the shoulder and hip joints are immune. Personally, I have never seen a case of gout in the shoulder or hip; such cases are usually examples of osteo-arthritis.

Exceptionally, even in first seizures, more than one joint may be affected. Thus it may migrate from one big toe to its fellow, or travelling further afield, may invade ankle, knee, wrist, or elbow, or small joints of hand. W. Gairdner held that in gout the joints of the left were more commonly attacked than those of the right limb. But James Lindsay’s figures would appear to indicate precisely the reverse, viz. a predilection for the right side of the body.

Pain.—If we may accept the lurid imagery of its victims, even the tortures of the Inquisition failed to transcend in agony the—

Sydenham said that at its onset the pain was as that of a dislocation (ossium dislocatio). At its zenith it was as if the flesh was being gnawed, squeezed in a bootscrew, or scalded by molten lead or boiling water. Sensory perversions are superadded, and, as Ambrose Paré said, “some patients say they burn, while others complain of icy coldness.”

Its peculiarly exasperating nature is well illustrated by Hosack, an old time Professor of Medicine of New York, who thus delivered himself: “Some compare it with the gnawing of a dog, the pressure of a vice, or the pain of the actual cautery; this probably is not far from the truth, judging from the anecdote I have heard of a man subject to gout. This man falling asleep barefooted before a large fire, the fire fell, and a large coal found its way to his foot; half awake and half asleep, he cried out: ‘There’s that d——d gout again!’ He at length awoke, when he found a large coal frying his great toe. The sensation of the two evils was probably the same.”

The pain is aggravated in that frequent “startings” of the limb prevent the victim keeping the foot at rest. The slamming of a door, or the incautious shaking of the bed, so quickens its throbbing intensity as provokes a literal frenzy of rage. But fortunately it is not always so. For though the pain of gout is unquestionably severe, at times excruciating, yet it presents infinite grades of severity. Also one must recollect that but too many of its victims are already in a high state of irritability before the outbreak. Moreover, their powers of self-control are too often sapped by unbridled self-indulgence, and they have but slight reserves of patience and fortitude to draw upon.[32]

Apart from the personal factor, in subacute cases the pain is notably less severe than in the acute sthenic form. The pain of gout, as a rule, is more intense than that of acute rheumatism, and, I fancy, than that of all other varieties of acute arthritis.[33] Sir Thomas Watson in his fascinating lectures tells of a witty Frenchman who, comparing acute gout and acute rheumatism in respect of pain intensity, remarked: “Screw up the vice as tightly as possible, you have rheumatism; give it another turn, and that is gout.”

Lastly, in respect of the duration of the pain, it is not always true that it wholly intermits at the approach of dawn. It does so frequently, it is true, but in some instances pain, more or less severe, continues during the day as well as the night. Occasionally, on a crescendo scale, it continues increasing almost up to the crisis. Generally speaking, too, the shorter the duration of the paroxysm the more intense the pain, and the more prolonged the less the degree of suffering.

Following the crisis, the pain gradually becomes less and less, giving place to a feeling of numbness of the toe, which in older subjects may endure for some days.

General Phenomena.—Symptoms, other than those referable to the affected part, vary widely in different cases. In this respect the acute sthenic forms contrast with the acute asthenic types. In the former the pulse quickens; the temperature rises, but rarely exceeds 101°-102°, though Garrod saw it reach 104°. The tongue is furred, the breath foul, with anorexia and thirst. Though the appetite is frequently impaired or lost, yet in some instances it is retained. Dyspeptic symptoms, hiccough, eructations, etc., are sometimes prominent, but often wholly lacking. The bowels are constipated, as a rule, the stools pale, or dark and extremely offensive. The urine is generally scanty, high-coloured, with a lateritious sediment on cooling. It may contain a trace of albumen. Severe cramps affecting muscles of the leg, thigh, and upper parts of the body, are more or less prominent symptoms in a considerable number of instances.

The pyrexia appears to be symptomatic, more or less in proportion to the acuteness of the local phenomena. Comparably the highest temperatures are usually met with in sthenic forms in relatively young or robust middle-aged subjects. Duckworth noted the interesting point that “a preliminary rise is commonly noted for one, two, three or four days before a joint is actively involved.” With the articular outbreak the febrile movement becomes more active. The temperature runs up to 100° or over, but with the morning abatement sinks to normal or nearly so. The following evening it rises again frequently to a higher level, 102° with a morning remission, and so it continues for a variable number of days, it may be only two or eight to ten. It then subsides, and frequently for a few days remains sub-normal. Lastly, the acute asthenic forms, that occur often in women (Garrod), may be wholly afebrile.

Changes in the Blood.—Apart from its increased content of uric acid, further morbid changes take place in the blood in gout.

Neusser in 1894 described what he termed “perinuclear basophilic granules” over and about the nuclei of the leucocytes in the blood of gouty patients. He held that the dark granules constituted the mother substance from which uric acid was derived, and that their presence in the blood was distinctive of the “gouty diathesis.” Subsequent researches, however, by Futcher and others appear to have shown the absence of any interrelationship between the amount of these granules and uric acid elimination, though Neusser claimed that cases showing them excreted uric acid in excess.

More significant, however, is it that the blood in acute gout may show a high grade leucocytosis with secondary anæmia.

In a case under my care of acute gout at classic site, though by no means of unusual severity, the following was the content of the blood picture:—

Uric Acid Excretion.—If when on a purin-free diet a gouty subject develops a paroxysm, the curve of uric acid excretion in the urine is so characteristic as to be almost pathognomonic of the disorder. As His pointed out, immediately before the onset of the paroxysm the endogenous uric acid sinks to a lower level (termed by Umber the anacritical stage of depression). With the onset of the attack the uric acid content of the urine quickly increases, to reach its zenith on the second or third day. F. Pfeiffer, who first noted this point, termed it an uric acid wave. Subsequently, with the gradual subsidence of the paroxysm, it again drops into what Umber termed the post-critical stage of depression. While this curve of endogenous purin excretion may be modified by oft recurring exacerbations, still Umber holds that nevertheless it is of decided value in differential diagnosis.

Local Phenomena.—The site and character of the pain having been dealt with, we now pass on to consider the objective changes in the affected part. The local engorgement of veins that precedes the articular outbreak becomes more pronounced, extending from the vicinity of the painful joint as far as the leg. The overlying skin of the joint quickly becomes red and tumid. It is not a bright, but a dark red, the superjacent skin taking on a shining smoothness that has been compared to the peel of an onion. Indeed, in its more violent form it resembles but too closely the ordinary appearance of an abscess, over which the skin is becoming thin. The redness is not strictly confined to the surface of the joint, but spreads a little beyond, and where it ceases œdema is perceptible.

The redness in its intensity attains its zenith in from twenty-four to forty-eight hours, and then in hue becomes more violaceous. On the other hand, the œdema may go on increasing for some days. At first, owing to tension, the presence of œdema may not readily be elicited. But with the subsidence of inflammation the swollen parts readily pit on pressure. It is scarcely possible to detect intra-articular effusion unless it be the ankle joint that is involved.

According to Duckworth, in the more sthenic forms there may be local ecchymoses. With the crisis the redness, œdema, and venous turgescence die down. The previously distended skin becomes wrinkled, and with complete subsidence of inflammation desquamation ensues. This process is generally attended with troublesome itching. It is most noticeable about the feet and hands, but more rare at other sites. Scudamore said that in seventy-eight out of 234 cases no peeling occurred, but, as Garrod observed, it may readily be overlooked unless especially sought for.

The exquisite sensitiveness of the parts, as before noted, gives way to numbness. The diminished sensibility, coupled with stiffness of the joint, renders walking difficult for some days, and, indeed, a month or more may elapse before the joint, even in favourable cases, recovers its customary mobility.

In acute asthenic forms great contrasts appear. Pain and tenderness in the toe may be moderate, but there may be little local heat or redness and no pyrexia. But œdema is generally in evidence, and the usual desquamation of skin follows.

Tophus Formation.—To the local changes that mark their eruption at ab-articular sites we have already alluded. Here we would only reiterate that their formation follows the local joint inflammation. Consequently if a few days after the attack local pain or tenderness, with or without swelling in the vicinity of the joint, should be complained of, it should not be dismissed as of no account, but the affected parts should be scrutinised carefully and, where possible, at short intervals. This in the interests of diagnosis of a joint affection which may at the time have been of doubtful nature, more especially if the primary attack occur elsewhere than at the classical site. Some observations of Trousseau are well worth quotation: “Physicians who have watched the progress of the evolution of tophus believe that it is formed during the paroxysm of gout. They are mistaken: the deposit appears during the interval between attacks, or at least when the attacks have not been of long duration, and when they do not recur in such rapid succession as to run into one another, in which cases their secretion has commenced during the preceding and continued during the succeeding attack.”