Chronic Articular Gout

In delineating the features of the acute polyarticular variety, we have to a certain extent trenched on the clinical territory of the chronic form; this is scarcely avoidable, inasmuch as the line drawn between acute and chronic gout is purely arbitrary. Thus one authority remarks of acute gout: “If the disease continue beyond three or four weeks, it is to be considered as persistent or chronic” (Flint). Trousseau, again, discussing the acute variety, more particularly the acute polyarticular type, states that it “may last for some weeks, or even for three months,” adding: “Should it extend beyond that period, it is no longer acute gout; it is chronic gout.”

The truth is that articular gout in this respect is very prone to vagaries. Thus, in rare instances an attack of acute or sub-acute gout, more particularly the latter, may merge without break into the chronic form of the disease.[35] Far more commonly the tragedy is more slowly played out. The unfortunate victim, after passing through several more or less classical attacks, finds that the intervals become shorter and shorter until they merge, as it were, one into the other. Fortunately its course is not one of continuous uniform severity. Remissions, but not complete intermissions, occur, and every now and again intercurrent acute attacks take place.

But, the reader may observe, surely this is very reminiscent of acute gouty polyarthritis, with its serial content of acute paroxysms?[36] Quite so; but there is this difference, that, although such may last six weeks or three months, still there is a period put to the sufferings. A respite of months or years of immunity, and relative health may then supervene.

Not so, unfortunately, when such paroxysmal waves sweep over the subject of long-standing or chronic gout. Not only do the recurrent acute outbreaks occur with increasing frequency, but also with increasing length of duration. It is here no longer a question of the intercurrent acute attack lasting days, but weeks. Also during such exacerbations either four, five, or six joints are simultaneously attacked, or in such rapid sequence that before one joint is free another is involved.

But a word here as to the variations in distribution of the articular lesions in chronic gout. The well-marked penchant of acute gout for the great toe continues throughout the life history of the disorder, the predilection for this site being equally a characteristic of the chronic type. As to the subsequent articular involvement, Garrod held the sequence to be as follows: heels; ankles; knees; the smaller articulations of the hands; lastly, the shoulders and hips. It has never been my lot to see either the shoulders or hips involved; but I have seen osteo-arthritis of the hip in men displaying auricular tophi, and I am inclined to think that, in the presence of the latter, it has sometimes been assumed that the hip mischief was of gouty nature—the “hip gout” of the older authors.

Moreover, the order of sequence is by no means invariable, for oftentimes a local circumstance, i.e., injury or sprain, determines the location. Again, chronic gout is very erratic in respect of the number of joints implicated. In some almost all the joints may be affected, while in others, no matter how ancient the disorder and how oft its recurrence, it remains localised to but a few joints; or it may progress after a leisurely fashion, with each attack invading different joints in succession.

Naturally, if the disorder confine itself to a few joints, and these, and these alone, are the seat of the oft-recurring attacks, permanent changes sooner or later make their appearance. Nor are the morbid effects limited to the joints, but they invade the continuity of the limb, for the oft-repeated inflammatory reactions lead to engorgements of persistent nature. The contour of the affected members is distorted by the œdematous tumefaction, which, more pronounced at the level of the joints, extends in lesser degree beyond their confines. The skin, too, especially over the fingers, undergoes a change in texture, often becomes smooth and glossy, and through its dusky pink subjacent uratic deposits may be discerned.

Old gouty subjects are often of sallow or parchment-like complexion. The blood in these cases of polyarticular gout conforms in attenuated degree, in the matter of leucocytosis and secondary anæmia, to that observed in the more acute types, as witness the following blood pictures.

All were males, the subjects of chronic articular gout of many years’ standing. They all exhibited tophi, which were verified microscopically. The examinations were conducted during the inter-paroxysmal periods.

(1) Blood Count.

Differential Count.

(2) Blood Count.

Differential Count.

(3) Blood Count.

Differential Count.

In these chronic forms, save during exacerbations, there may be little or no febrile movement, and local pain, heat, and redness may be slight or wholly lacking. But the articular swellings never wholly disappear, and the mobility of the joints is never entirely regained. The articulations, few or many, become stiff, ankylosed, and deformed, by the growth of tophaceous deposits. But to detailed description of these latter we shall return later.

In inveterate cases of this nature the victim grows more and more crippled and infirm, the inroads of the disease upon the constitution more and more palpable. Pelion is heaped upon Ossa, as one ailment sets in after another, now of the digestive organs, now of the heart, or of the kidneys. These subjects of chronic gout are more often than not dyspeptic, show signs of arterio-sclerosis. Their blood pressure is raised, their vessels tortuous and thickened, and the left ventricle enlarged.

As to the variations in uric acid excretion, these, as before remarked, show no appreciable deviation from normal. Occasionally, however, there is a tendency to uric acid gravel. Of more sinister significance, albeit, is the fact that in many of these cases the urine is copious, of low density, paler than normal, and shows a trace of albumen with hyaline casts.

As the disease marches to its fell end the appetite becomes impaired, gastric catarrh and diarrhœa may sap the waning strength, or palpitations, fits of dyspnœa, or angina-like attacks, sometimes fleeting, but often of organic source, may portend a fatal issue. Ripe for the sickle, a kindly “stroke” perchance puts an end to his protracted misery. Or symptoms, long since manifest, of progressive renal failure may usher in the closing scene, and happy the victim if he pass muttering, half conscious, into that dream-like stupor drifting by insensible graduations to death.

So much in attempted portraiture of the long-drawn-out tragedy of inveterate chronic gout. But, fortunately, it is not always thus, and nowadays, at any rate, the evils wrought on the constitution by the malady are seldom so malignant. For not only, as before stated, has gout become less frequent, but its virulence also much attenuated. States of so-called “gouty cachexia” were, however, more familiar to our forefathers. It more commonly ensues in subjects of strongly hereditary tendency, and particularly in those in whom the initial attacks ensue before thirty years of age. I recall the instance of a colonel who sustained his first attack of gout when a subaltern of but eighteen, brought on, as he thought, through exposure while shooting snipe in Peshawur. It is in such cases that this so-called “gouty cachexia” may overtake a man while yet in his prime, and vest him untimely “with all the characters of age.”

As to the milder types of regular chronic gout, such usually arise, not in youth, but in men past the meridian of life. In their instance the recurrence of gouty paroxysms is often erratic. Periodicity becomes less pronounced or wholly lost. The life history of the disease may be summed up in a few sporadic outbreaks, occurring irregularly throughout a long life. Even when at first the attacks occurred regularly in the spring and fall the rhythm of incidence becomes broken. An attack comes before its time, is belated, fails of appearance wholly, or an intermediate paroxysm comes as a surprise. Moreover, in many such the gouty manifestations with the passing years tend to become more and more attenuated, maybe even to extinction. Thus, a man who in the middle decades was a martyr to gout in old age gains freedom from its visitations, the disease having apparently exhausted its vicious potentialities.

Reviewing articular gout as a whole, one cannot but realise that it does in respect of the recurrence of gouty paroxysms exhibit inexplicable vagaries, inexplicable in that, as Sir William Roberts long since said, “in many instances they are dependent neither upon medical treatment nor upon altered dietetic habits, but are due to spontaneous changes in the constitution. They form part of the natural history of gout; and it is important to bear their existence in mind when we seek to estimate the value of therapeutic means in order to prevent ourselves from becoming the dupes of misinterpreted sequences.”

Albeit, we would not end on too sombre a note. For, in respect of the graver consequences of gout, it is unquestionable that right living, aided by efficient therapy, may arrest the course or mitigate the severity of the disorder. Moreover, as long as the attacks do not follow quick upon each other, but are separated by long intervals, there is little fear of a cachectic condition supervening. Life may not be appreciably shortened, and such textural degenerations as may ensue, though frequently attributed to gout, may often with at least equal plausibility be assigned to advancing years, but this with reservation, for, as Duckworth says, “the wilful libertine is likely soon to become cachectic, while the prudent man may altogether avoid this state or avert its evils for many years or decades of years.”

The Joint Deformities of Chronic Gout

The palpable changes in the affected joints differ widely in different cases, and why is not apparent. Thus, the first attack, if of prolonged duration, may bequeath a legacy of crippledom comparable to that met with after repeated paroxysms. On the other hand, some, although they have suffered from the disorder off and on throughout their lives, yet escape those consecutive deformities which in others deform and cripple the hands and feet, though the disease may be of relatively brief duration.

But in the less fortunate cases the continued ravages of gout lead to a pitiful disablement of the affected limbs, reaching its acme in the hands and individual fingers, flail-like and semi-paralytic as they so frequently become.

Not only are the digits variously distorted, their joints more or less ankylosed, but the overlying skin, distended by the ever increasing subjacent uratic deposits, becomes thinned and purplish red in hue, and occasionally ulcerates. Similarly at ankle, knee, wrist and elbow thickening and deformity ensue as the concretions accumulate in and around the affected joints, these further accentuated by the correlated inflammatory and degenerative processes. Coincident deposits in the tendon sheaths and related bursæ contribute their quota, and at knee and elbow the bursal masses may reach extraordinary dimensions. Not only do the joints become deformed, but distorted also, through reflex muscular spasm and instinctive adoption of unnatural attitudes for the avoidance of pain.

So much for the broad outline of the picture presented, but a still closer scrutiny is called for. The deformities produced are the outcome of uratic deposits, which, as Charcot long since pointed out, take on the shape of “irregularly rounded or ovoid swellings, bunched, and either large at the base or just the opposite, i.e., provided with a pedicle.”

As shown in the coloured plate, the favourite site for their development is the dorsum of the hand or the vicinity of the metacarpo-phalangeal or mid-phalangeal joint. The resultant disfigurement of the hand is very characteristic. Irregular tuberous swellings surmount the knuckles, and spreading laterally, obliterate the fossæ between them and their fellows. The same extend forward over the first phalanges, from nigh the distal end of which again arise similar bossy excrescences over the mid-phalangeal joints. Encroaching thus upon the length of the first phalanx from either end, but little of its shaft is ultimately left exposed. In like fashion the mid-phalanx may be buried in uratic deposits, its contour wholly lost; and, the terminal phalanx participating, the digits become almost pedunculated, the nails projecting from the ends thereof—the “parsnip hand” of Sydenham. Such is the appearance presented in inveterate chronic gout.

Fortunately such examples are relatively rare, and a study of the condition in its earlier stages reveals some interesting features. The uratic deposits, it is important to note, are not located exactly at the level of the articulation. Unattached as they are to the articular ends, they are not compelled to, nor do they in any way, adapt themselves, as it were, to the contour or shape thereof. In short, the tophaceous formations are erratic, are not like osteo-arthritic nodules, erupted from and continuous with the articular bone ends. Again, relatively independent of the contiguous tissues, they, unlike osseous outgrowths, are slightly movable in lateral directions.

When of recent incidence, their consistence is soft, and, be they never so ancient, they do not attain the density and hardness of bony outgrowths. The overlying skin, to which they are sometimes adherent, takes on a peculiar glossy and satin-like texture, its dusky pink blotched with spots of dead white colour, i.e., subjacent uratic deposits.

In other particulars also they differ from bony outgrowths. The tophaceous masses may soften and disappear after exacerbations of arthritis, and others may form at different sites. Following such absorption or difference in their location, some increase in joint mobility may happily ensue. This same fortunate occurrence may follow discharge of the uratic masses through ulceration and perforation of the skin.

Tophi: Their Evolution and Distribution

In our chapter on Uratosis we dealt with the chemical nature and mode of formation of tophi. Also we affirmed our belief that tophi, whether articular or ab-articular in site, were always preceded by local inflammatory reaction, and to the clinical tokens of their impending eruption we need not recur. Albeit this point, i.e., antecedent inflammation, is of such prime importance that we have not hesitated to append to our text a lengthy footnote,[37] this because, as Garrod, who quotes the same in extenso, rightly claims, the genesis and evolution of tophi has never been so graphically depicted as in Moore’s description.

It will be seen that this observer holds that tophus formation “is usually preceded and accompanied by inflammation.” Garrod, as we know, believed uric acid to be the cause, and not the consequence, of gouty inflammation. But he emphasises the fact that the phenomena attendant on the eruption of auricular tophi are “exactly the same as when a joint is affected, and constitute, in fact, a true gouty paroxysm, commencing with infiltration of the tissue and subsequent inflammation.” Still, though venturing to differ as to the sequence of events, we gladly invoke this authority’s observations in proof of the fact that the inflammation even in the ear is not always of negligible grade: “I have seen many cases in which the ear symptoms have proved very annoying, so that patients have been unable to rest their ears on the pillow.” Subacute gout sometimes occurs in the ears, says Duckworth, who furthermore believed that the indurations in the cartilage observed by him in gouty subjects were the outcome of such attacks. Laycock, too, long before noted that the ears of gouty subjects often appeared to be “soldered.”

Pain or discomfort in auricular tophi often presages an oncoming articular paroxysm. “Those gouty persons,” said Scudamore, “who are affected with concretions (chalk-stones), experience for a short time before the fit pricking pains in the parts where they are situated. This is described even by those who have minute points of concretions in the lobes of the ears and in no other parts of the body.” Hence tophi have a prognostic as well as diagnostic valency in that the incidence of pain at their site may foretell the oncoming of articular outbreaks.

While, as before emphasised, the eruption of tophi may antedate the occurrence of articular gout, on the other hand tophi may be present at the joints, but lacking in the ears and all other ab-articular sites. Auricular tophi, extracted occasionally by patients, are sometimes shed spontaneously. According to Duckworth’s statistics, in one-third of all well-marked cases of gout the ears present tophi in the helix, the anti-helix and its fossa and the lobule, and in some cases they may be situated on the posterior surface of the pinna.

Other Sites of Tophi

Apart from the external ears, tophi are apt to form in various localities. Most frequently they are situated in the vicinity of the joints and bursæ, especially that over the olecranon. As attack follows attack at short intervals the tophaceous matter is heaped up around the joint, and in this way many articulations may be involved, even all of them, says Trousseau, “as happened to Gordius, who composed on himself the following jocular epitaph:—

Uratic deposits sometimes attain a prodigious size. I have seen them the equivalent of a small hen’s egg. The largest tophi are invariably found in the neighbourhood of some joint, and the upper extremities furnish the most marked examples. But even when of considerable magnitude they may be non-adherent, the skin gliding freely over their surface. As John Hunter wrote: “The chalk shall remain for years without producing inflammation, and seldom produces it at all but from quantity.”

Often, however, their presence at length induces irritation of the overlying integument. As they approach the surface the skin assumes a purple hue, becomes thin, and ulcerates. The uratic ulcers thus formed have generally an indolent fungous base. As the deposits extrude or are removed they are continually redeposited, and in this manner ounces of urates may be discharged. The same is followed by great relief and diminution of deformity.

Discussing such lesions, John Hunter tells us that “when the interior surfaces are exposed they hardly take on common inflammation and suppuration, healing more readily than a sore of the same magnitude from any other cause; even a joint shall be exposed, yet common inflammation shall not come on, nor shall it suppurate: only a watery fluid shall come out, bringing the chalk with it occasionally, and it shall heal up kindly.”

A glance, too, at the preceding footnote shows that Moore also agreed with Hunter as to the absence of common inflammation and suppuration. Moreover, even of recent years it has been suggested that, because gouty tophi do not suppurate even when ulcerated through the skin, the urates have antiseptic properties. But Bendix (Zeit. klin. Med., 1902) failed to demonstrate such qualities experimentally. The truth would appear to be that, though gouty inflammation never ends in suppuration, yet abscess formation very commonly occurs in the peri-tophal tissues. Such more often ensues in subjects of frail health or of definitely cachectic type. Garrod saw as many as five or six open at one time in each hand, and others on the feet. In his experience they give rise to but little constitutional disturbance. Scudamore, speaking of the same, says the sores produced are “unusually tender, aching, and sometimes very painful as the fit is making its approach.”

Ultimately the gouty ulcers thus formed dry up, and this indifferently whether or not the uratic deposits are wholly extruded in the discharging pus. The wound then closes, leaving a small scar, which, however, given a fresh attack of gout, is but too likely to break down, and this process may occur repeatedly. Bursal sacs containing tophi not infrequently suppurate, constituting abscesses containing urates.

An interesting fact noted by Garrod was that so long as such abscesses were discharging freely the subjects enjoyed comparative immunity from overt gout. But, given healing of the same, in several instances he had seen it the signal for a sharp outbreak. Duckworth, too, states that “whenever ulceration and flow of tophaceous matter occurs it is rare to meet with paroxysmal attacks anywhere in the body. With the cessation of the discharge renewed fits may intervene.”

While they tend to aggregate themselves round the joints, yet tophi sometimes invade the integument of the limbs. They have been seen in the skin over the ulna and tibia, and commonly over the olecranon and patella. Pye Smith recalls the instance of a man in whom a number of small ulcers, discharging urate of soda, formed in the middle of his thighs and legs. The case is not an isolated one, but the incidence of subcutaneous uratic deposits in the limbs, save over articulations, is exceptional.

In the palms of the hands and the pulps of the fingers, the knuckles and phalanges, tophi are found not infrequently; and Trousseau tells of a lady of sixty in whom the cutaneous palmar folds of both hands were “marked with radiating white lines such as are seen in those who have long been employed in tempering plaster.”[38] Similar deposits have been noted in the plantar surface of the feet.

Reverting to the trunk, uratic deposits have been found in the scapular region, also in the perineum. I have twice seen tophi in the corpora cavernosa of the penis. In the face, apart from the ears, they have been found in the alæ of the nose. In the eyelids Duckworth noted uratic deposits in streaks resembling xanthoma; they were chemically tested, and proved to be of this nature. Speaking of “gout in the eye,” Garrod states: “I have witnessed many cases in which conjunctivitis and sclerotitis appear to be distinctly connected with the gouty diathesis, and in two cases there existed deposits of urates on the surface.”

As before stated, we recognise only one type of gout, viz., the tophaceous variety. But even so it must be noted that in some instances the process of tophus formation is greatly accentuated. In other words, the tophi may not only be of prominent size, but of unusually widespread distribution. Indeed, poetic exaggeration has it that one Baylas and one Acragas were entombed while alive in their own uratic deposits. But, apart from such imaginative flights, there are unquestionably some cases in which tophi are most widely diffused. Thus Plater tells of a patient whose whole body, even the eyelids, was studded with them: “ex toto corpore, per poros, adeo ut etiam palpebræ oculorum non exemptæ fuerint, ejusmodi materia gypsœa, circa poros cutis mox in tophos mutata, prodisset.”

These cases of multiple tophi are far more common in men. Duckworth met with some well-marked cases in women. They may occur also in persons who have been lifelong abstainers. Sometimes trauma seems to have played a part in determining their localisation. Garrod held that, given prodigious uratic deposition, the kidneys might be held as unsound and undergoing sclerosis; and, according to Duckworth, the rule commonly holds good.

Affinities Between Gout and Other Diseases

Whatever be the explanation, no fact in practical medicine is better established than this, viz., that certain disorders are peculiarly liable to arise in gouty subjects. Of these the more noteworthy are glycosuria, phlebitis, certain cutaneous disorders, and nephritis. While, for myself, I prefer to regard these affections as merely diseases to which the gouty are especially subject, nevertheless each and all of them, by one authority or other, have been classed as among the irregular manifestations of gout.

This, on the assumption that these several morbid entities may precede, alternate with, or follow arthritic seizures, frequently also on the basis of their alternation in hereditary transmission with arthritic gout. Thus, in a family of marked gouty proclivity, while one son, despite a temperate life, may have severe articular gout, on the other hand his brother may suffer only with irregular manifestations, i.e., phlebitis, eczema, etc.

As to whether these particular disorders, phlebitis, glycosuria, etc., are directly caused by the toxin of gout, or whether their not infrequent association with gout is merely accidental, is a moot point. But to the sources of fallacy in this connection we shall allude more in detail when dealing later with irregular gout. Meanwhile extended knowledge of the intimate etiology of phlebitis, glycosuria, etc., tends to an attitude more critical than that of our forefathers, who, faute de mieux, relegated a large number of conditions whose pathology was inexplicable to the nebulous domains of irregular gout.

Gout in Relation to Glycosuria

That some obscure link existed between glycosuria and gout was long since suspected. Prout noted it as far back as 1843, and Bence Jones discussed the subject under the title “Intermitting Diabetes” (1853), while in the following year Gairdner announced that he had long surmised the kinship between the two disorders. About the same time Claud Bernard remarked that gout and glycosuria might alternate, and so did Trousseau, and many since that day have ranked glycosuria as one of the forms of irregular gout, whether legitimately or not is an open question, but at any rate it does not affect the established clinical fact that glycosuria occurs with significant frequency in gouty individuals.

Gouty glycosuria is more common in males than females. The subjects are usually robust, middle-aged, and of full habit. Sugar is found intermittently in their urine in small amounts, but no acetone bodies. It is as a rule unaccompanied by thirst or wasting. It quickly responds to dietetic restrictions. As Gull long since observed, gouty glycosuria does not “discover itself,” but is “not uncommonly discovered.” This tersely sums up the clinical difference between this affection and true diabetes, albeit, as in all glycosurias, there is always the risk that carbohydrate excess, mental strain, or other adverse circumstances may aggravate the disorder and the case merge into one of true diabetes.

Following the installation of glycosuria, the tendency to paroxysmal articular outbreaks often ceases. The converse also has been observed, viz., that when, in sequence to dietetic restrictions, the sugar disappears, the articular pains may reappear. The fact that attacks of glycosuria may alternate with attacks of gout led to the assumption that a positive antagonism existed between the two disorders. Hence the phrase “the more sugar the less gout,” and vice versâ. This, however, with reservations, for a fugitive glycosuria has been seen during an acute articular paroxysm, and a classical outbreak in the toe has been known to supervene in the course of a well-established glycosuria.

It is generally held that glycosuria is most commonly associated with irregular forms of gout. But, in view of our ignorance of the intimate nature of even regular gout, I should myself deprecate affixing the prefix “gouty” to any glycosuria other than one that has supervened in sequence to, or alternates with, gouty arthritic seizures. Moreover, the glycosuria of gout is usually the alimentary glycosuria of fat elderly people, in whom the sugar excreted represents the unconsumed surplus of carbohydrate food. But fat elderly people are not necessarily “gouty,” neither is every so-called benign glycosuria inevitably linked on to a gouty diathesis. In fact, the relegation of glycosuria to the gouty category is but too often not a matter of diagnostic certainty, but rather an inference. Hence my plea that the prefix “gouty” would best be restricted to glycosurias occurring in individuals who suffer regular attacks of gout, or those displaying those objective tokens pathognomonic of the disorder, i.e., tophi.

Again, James Taylor has recently reminded us that, if nerve affections are relatively common in true diabetes, the same may be met with in gouty glycosuria, even when of temporary duration. Thus symptoms indicative of peripheral neuritis may occur, i.e., lost knee jerks, paræsthesiæ, and paresis of the lower limbs. Now, as this authority pertinently observes, the subjects of gouty glycosuria are frequently given to alcohol. Consequently the question whether or not the symptoms are due, not to sugar, but to alcohol, arises forthwith.

In some undoubtedly the alcoholic factor plays a rôle, but such symptoms may, on the contrary, arise in very abstemious individuals. This notwithstanding, James Taylor holds that the clinical complex differs substantially from that met with in true alcoholic neuritis. It is slighter in degree, the paresis usually restricted to lower limbs, while the exquisite tenderness to pressure on nerve trunks so typical of alcoholic neuritis is little or not at all in evidence. Nor is there the same tendency to contractures in muscles as met with in the alcoholic variety, and withal there is an absence usually of the mental changes—loss of memory—associated therewith. Accordingly Taylor holds that we must recognise the existence in the gouty of a true glycosuric peripheral neuritis quite independent of alcoholic peripheral neuritis.

Other concomitant nerve troubles noted in this association are severe intercostal neuralgia and, even more commonly, neuralgia of the fifth nerve, and to this may be added migraine and that other neurosis asthma. Intense mental irritability and depression is not an infrequent sequel in gouty glycosuria. According to James Taylor, melancholia even may result, especially if the glycosuria have merged into true diabetes—a sequel, he says, especially prone to occur in Jewish subjects.

Having seen and suffered many painful disillusionments through too flippant relegation of neuralgias or neuritides to diatheses “gouty” or “rheumatic,” I would emphasise the necessity for great caution. In other words, before labelling a neuralgia or neuritis as “gouty,” all possible causes, infective or other, should be excluded, this always, but pre-eminently so in brachialgia, sciatica, and trigeminal neuralgias. Nor even, should there be a history of classic outbreaks or blatant tophi present, should we be less vigilant.

By all means recognise the gouty diathesis. It often avails much in treatment, but not if, e.g., dental caries, antral disease, cervical rib, or pelvic growth be overlooked, not to speak of recent or concurrent sources of infection or toxic absorption.

Lastly, we should always recollect that gouty glycosuria, as Gull said, “does not discover itself”; it is not writ large on the subject like true diabetes. But given the incidence of nerve troubles in a gouty person, i.e., a paræsthesia, itching, neuralgia, etc., we should always suspect its presence.[39] Incidentally our search may reveal not only sugar, but also albumen, and the latter may explain much that appeared inexplicable.

Gout in Relation to Phlebitis

It is to Sir James Paget that we are indebted for recognition of the fact that phlebitis occurs with significant frequency in gouty subjects. This great surgeon held that the disorder was the outcome of a modification or transformation of gout, the result of “morbid conditions changing and combining in transmission from parents to offspring.” At the present time some regard it merely as a complication of gout, others as one of the irregular manifestations of the disease.

It occurs most commonly in men, women being rarely the subjects of gouty phlebitis. It may install itself insidiously with but mild local discomfort, and yet on examination a cord-like hardness is detected. In others it announces itself with pain, in rare instances intense, this more commonly if the deep veins of the calf are its seat.

Its predilection is for the veins of the lower extremity, the superficial rather than the deep vessels. If the former, a faint blush over the affected veins may be seen, but if the deep veins, then œdema and tenderness may be the sole token of its presence.

Frequently the phlebitis is patchy in distribution and migratory. Thus, as Paget says, it may on one day be located in a short length of the saphenous vein, flitting the next day to some other portion thereof, or, it may be, to the corresponding vein of the opposite limb. This tendency on its part to metastasis and symmetry led Paget to the conclusion that “the essential and primary disease is not a coagulation of the blood, but an inflammation of portions of the venous walls.”

Its duration is not uncommonly prolonged, and it displays a marked tendency to recurrences, the latter determined by blows, unusual exertion, or, according to some, exposure to cold. Most cases end favourably, but death from embolism sometimes occurs. Occasionally, given occlusion of the large veins, some degree of swelling lingers permanently.

The instances most indicative of a gouty origin are those in which the veins of a limb, the seat of acute gout, are simultaneously attacked by phlebitis. In three cases of this nature recorded by Garrod, the subjects, despite their suffering from acute articular gout, persisted in leaving their beds to record their votes in the parliamentary election of 1884. This type of case, according to Garrod, is usually confined to men, and, with the exception of the cases above noted, a varicose condition of the veins of the legs of long standing existed in his series of examples.

Garrod recognises in addition a second type, in which phlebitis, “usually of a much less acute character, ensues without the previous development of gouty inflammation in the neighbourhood of the part.” Here we may recall that, according to Paget, the incidence of phlebitis in an elderly person without any external cause warrants the suspicion of gout. Perhaps the chief justification for such an assumption rests on the fact that phlebitis appears sometimes to be hereditary. Paget cites the instance of a man who suffered from phlebitis of both saphenous veins during an attack of acute gout. On the maternal side his mother, two uncles, a grandmother, and two cousins had been the subjects of phlebitis.

In conclusion, for myself, I would suggest that the term “gouty” phlebitis be restricted to those instances in which a limb, the seat of acute articular gout, is complicated by phlebitis of the veins of the affected part. Here we are dealing with what is palpably an extension of the gouty inflammation from the affected joint to the veins, and which, I venture to assert, is strongly confirmatory of the view that an infective element intrudes in “gouty” arthritis. We may recall that, e.g., gonorrhœal phlebitis of the lesser saphenous veins is not so uncommon, while the frequency with which phlebitis complicates infections calls for no emphasis.

Leaving aside these rare instances of acute gout complicated by acute phlebitis, I think there is a too flippant tendency to regard any phlebitis occurring in middle-aged or elderly subjects as being of this nature, this often in the absence of any evidence, hereditary or other, of a gouty element in the case. Frequently, too, the subjects are women with varicose veins of long standing, and ipso facto potentially liable to phlebitis. But why, in the absence of ancestral or acquired gout, dub such cases forthwith as “gouty”? We may, it is true, as in Paget’s classical instance, elicit a familial tendency to phlebitis, but even so I doubt the legitimacy of the inference that the phlebitis is necessarily “gouty.” Is it not equally true that the tendency to varicose veins is hereditary, and ergo predicates an enhanced liability to phlebitis?

Cutaneous Disorders

The incidence of tophi in the skin naturally engendered the conception that gout was responsible for many and diverse types of cutaneous affections. In accordance with this, every effort was made to prove that they were the outcome of uratic infiltrations, but in vain.

Objective proof of this nature being lacking, the older clinicians found their justification in the alternation of arthritic attacks with cutaneous disorders, and their alternation in inheritance was laid great stress upon, this especially by French dermatologists, notably Bazin, but at the present day Jacquet’s non-committal pronouncement is probably representative of the attitude of the French school as a whole towards “arthritic” affections of the skin: “Le lien admis entre le groupe de maladies dites arthritiques est très mal connu dans son essence, mais il serait tout aussi contraire à l’esprit scientifique de le nier avec rigueur que de l’affirmer avec presomption.”

As to the skin disorders associated with acute types of gout, perhaps the most interesting and well ascertained is herpes. It may precede an acute attack, may alternate with it, or be a sequel thereof. Rendu noted that acne, boils, and carbuncles also might occur prior to, in alternation with, or in sequence to acute attacks, and Scudamore noted the same in respect of erysipelas.

The noteworthy liability of the gouty to these disorders is but another proof that gout predisposes its victims to infections. The fact that acute gouty arthritis might follow acne, boils, etc., lends colour to our contention that the same may be of infective origin. But unfortunately the suspicion also intrudes that some of the arthritides occurring in such association may, on insufficient grounds, have been diagnosed as “gouty,” this especially if the joint disorder were located anywhere save at its classic site, the big toe.

Passing to skin affections associated with chronic gout, it must be admitted that as a whole the contention that they are “gouty” in origin is, to say the least of it, doubtful. French dermatologists claimed that the cutaneous eruptions of the “gouty” might be recognised by their polymorphism, circumscribed location, etc., but these are no more distinctive peculiarities than the concomitant pricking, hyperæsthesia, and hyperalgesia upon which Bazin laid such emphasis in their diagnosis.

In short, sequences, coincidences, and alternations are the basis of much that has been written upon so-called “gouty” cutaneous affections, criteria all of them fruitful sources of fallacy.

As to psoriasis, I have met with it so frequently in association with non-gouty arthritides that I have never felt justified in claiming any example as “gouty.” So-called “gouty” pruritis and prurigo, these when they occur in the “gouty” are frequently referable to an associated glycosuria, and when this is not the case, it is frequently a senile prurigo. The claim that urticaria is “gouty” may be dismissed without comment.

As to frequency of incidence in the “gouty,” eczema undoubtedly must be awarded the palm. But whether the scaliness of skin on extensor surfaces of arms and legs and back of neck, which ultimately, under the influence of skin infection through scratching, develops into a dermatitis which assumes the character of eczema, can be, strictly speaking, held as of “gouty” origin, is questionable. Certainly, whatever be the origin of the pruriginous scaliness of the skin, there can be no doubt that the later dermatitis is the outcome of infection by skin organisms. Frequently the presumption that the eczema is “gouty” rests upon general rather than specific grounds, on “goutiness” rather than “gout.” Accordingly I think it would be wiser to regard eczema as an occasional complication of gout rather than an integral element thereof.

Lastly, there can be no doubt that many of the so-called “gouty” cutaneous disorders ensue at what may be called the arterio-sclerotic stage of life. It is when renal and cardio-vascular changes are present that we meet with exudative erythema, pityriasis, exfoliative dermatitis, and purpuric eruptions. All these have at one time or another been foisted upon gout, whereas they are far more closely related to the cardio-vascular and renal changes with which the disorder is so frequently associated.

Gout and Nephritis

The association between gout and renal disease is admittedly intimate, in so far as gouty subjects often have granular kidneys, while gout is a frequent complication of this type of renal disorder. Nevertheless, the clinical relation between the two diseases is ill defined and, moreover, somewhat erratic. In most instances the renal defect is engrafted upon the antecedent gout, or the sequence is reversed; and, again, the two conditions may arise contemporaneously. Lastly, in sharp and disconcerting contrast to this mutual overlapping of the two disorders, we have the awkward fact that more commonly gout and granular kidney run to their fell end quite independently of each other.

Thus, Sir William Roberts observed: “It is quite common to see articular gout, even of chronic and inveterate character, run its entire course without any accompanying signs of structural disease of the kidneys.” The same, to be sure, is equally true of granular kidney, which may pass to its close without any suspicion of gout.

Now, as we have seen, the primary renal origin of gout fails of demonstration. Is gout, then, causally related to granular kidney, or is there some less direct relation between them?

As to this, to begin with, it is extremely rare that a “gouty” subject develops acute nephritis. In the exceptional instances when it does occur it is either purely accidental or else the outcome of an exacerbation of a previously existing interstitial nephritis.

The question then arises, Can gout when long continued originate per se the condition we are pleased to term “gouty kidneys”? As seen above, such renal lesions are by no means an inevitable sequel or concomitant of long-standing gout. Moreover, there is nothing specific of gout in the so-called “gouty” kidney. It is an interstitial nephritis, which may assume the appearances of the ordinary “contracted kidney” or the “arterio-sclerotic” type. There may be uratic deposits at the apex of the pyramids, or even an uric acid calculus; but even so that of itself constitutes no proof of the renal changes being “gouty” in origin. In short, the prefix “gouty” as applied to these types of renal lesion is just as unscientific and unwarrantable as used in regard of “phlebitis,” “eczema,” and so forth.

Nor, quâ gout as a causal factor, are we in better case if the renal disorder be of the “arterio-sclerotic” type. No direct relationship is established between gout and arterio-sclerosis beyond the fact that both are usually met with in middle-aged or elderly people. Moreover, a man may develop arterio-sclerosis and arterio-sclerotic kidneys, yet never have any vestige of gout.

There being nothing specific of gout in the lesions of so-called “gouty” kidneys, we must revert to the clinical findings to refute or establish any causal connection between gout and the renal disorder. Now, gout is a disease of middle and late life, and rarely of itself proves mortal. On the other hand, it appears increasingly probable that the seeds of granular kidney are laid in earlier life, and, on the average, its course is shorter than that of gout. Also the two disorders have clinical facies absolutely distinct the one from the other.

From the above considerations it is, I think, clear that, whatever the hidden nexus between gout and “granular kidney,” it is neither essential nor constant. It is rather, I believe, of the nature of a coincidence. Furthermore, as applies to so many problems pertaining to gout, and, for that matter, to “granular kidney” also, we labour under the grave disability that both terms are, especially “gout,” very vaguely applied and when used are often a matter of personal opinion. Consequently, as Samuel West shrewdly observes, “it is difficult to discuss satisfactorily the relation of two conditions to each other when neither condition admits of precise definition, for some authorities are more easily satisfied in the diagnosis of gout than others; and, while some place all forms of chronic interstitial nephritis in one and the same category, others are not so comprehensive, and regard granular kidney as a definite clinical disease, of which the interstitial nephritis is only a part.” Under these circumstances, the need for further and more exact researches in this sphere is but too obvious.

Meanwhile, accepting the general opinion as to the frequency of the co-existence of gout and granular kidney, is there any explanation thereof? For myself, I am inclined to believe that the common overlapping of the two disorders is in large measure due to this, that the factors, i.e., excess in alcohol, overeating, etc., that make for the eruption of gout, are largely identical with those that promote the development of granular kidney. Hastings Gilford holds “there is very little doubt that syphilis, lead, and gout do not so much originate Bright’s disease as excite it into activity when it already exists in a smouldering or latent condition.”

With this view I feel much in accord, and if to the malign effects of gout be superadded the effects of alcohol or, haply, lead also, how incalculably greater the chances of fanning into flame any latent tendency to nephritis—a legacy, perhaps, of some long bygone infection.

Prognosis in Gout

Gout per se rarely, if ever, proves fatal. Certainly, as Sir Thomas Watson long since said, “gout in the extremities is not a mortal disease.” When death did occur during or in close relation to an acute paroxysm, it was by our forefathers attributed either to its retrocession or to some misplaced or irregular manifestation. Indeed, their attitude was very much that of the French physician who observed: “La goutte articulaire est celle dont on est malade, et la goutte interne est celle dont on meurt.”

But, as we shall see later in our chapter on Irregular Gout, most, if not all, of their instances of the assumed translation of the materies morbi of gout to some vital organ are without foundation. The demise, often dramatically sudden, was not due to gout, but to some insidious, unguessed-at organic degeneration, or to one of the accidental intercurrent maladies to which these subjects seem especially liable. To sum up, the immediate danger to life from regular gout when uncomplicated is slight.

Not that gout is salutary, lessens the liability to other diseases, or promotes longevity. Very much the reverse—“a tendency to recurrence is a law of the disease.” Broadly speaking, the more pronounced the tendency to recurrence of articular outbreaks, the more protracted the isolated paroxysms, the worse the outlook, the more sombre, too, the greater the number of joints involved. Conversely, if the disease, though it recur, restrict itself to the classic site, the big toe, the longer, as a rule, the intervals of freedom, the brighter the prospects of long life. Lastly, the more the subject is crippled, the more pronounced the tendency to tophaceous deposits, the more likely is the disease to pursue a downward course, the greater the risk of associated degenerations in renal and vascular tissues.

While these reflections are in the main, we think, justifiable, we must recollect that in gout, as in other maladies, the elements of prognosis reside in the individual, not the disease. Does he come of a long-lived stock?—not uncommonly a feature of gouty families. If so, the outlook is favourable. If he come of a short-lived breed, then in all probability, no matter how carefully he lives, he will not likely make “old bones,” this, certainly, if the gout makes its appearance early in life, say under thirty.

As to the axiom, generally accepted, that the earlier in life gout makes its début, the more unfavourable the outlook, there are exceptions. Where longevity marks the stock, they usually are true to type. Thus, even if the first outbreak occurs in the twenties, I have known them reach the allotted span and over. Nor if their urine show traces of albumen is this necessarily of grave import, for these gouty veterans may for many years, even to old age, exhibit traces of albumen without apparently developing genuine Bright’s disease.

“There dies not above one of a thousand of the gout, although I believe that more die gouty,” wrote Graunt long years since; and this contains a kernel of truth, for the prognosis of gout rests in the main not on the gout, but the conditions correlated therewith—the absence or not of complications. For, be it always remembered, gout, though it may appear in youth, is chiefly an appanage of the middle and later decades, in short of the regressive period of life.

This last is, I think, apt to be forgotten, and gout vicariously saddled with all the infirmities of age. Thus, out of 2,680 examples of arterio-sclerosis Huchard held gout and lithiasis responsible for no less than 693. An appalling indictment, but what of the long arm of coincidence? For age unquestionably is the chief factor in the production of arterio-sclerosis, though many allot gout a dominant rôle in its genesis. This certainly is by no means proven. Still, whatever be the relationship, gout and arterio-sclerosis are very often found in association. If so, the prognosis will obviously rest, not on the gout, but on the vascular disease—the pulse tension. If therewith be correlated albuminuria and a displaced apex beat, the outlook is unfavourable.

Again, is the subject lean or obese? If the former, so much the better, for corpulency and gout are a sinister combination. Gout in itself, as previously observed, favours microbic invasion, and obesity accentuates the liability. Moreover, the gouty obese are prone to arterio-sclerosis and granular kidneys, with sometimes a superadded glycosuria, or even true diabetes. In such subjects also the presence or absence of signs of cardiac mural degeneration must enter into our forecast, which at best is but gloomy.

Apart from arterial degeneration, we have to recollect the tendency to phlebitis of recurrent type. This when present always carries with it the risk of embolism and sudden death. Cases therefore displaying this proclivity to phlebitis must be judged accordingly. The gouty glycosuric, too, is always subject to the risk that the condition may develop into one of true diabetes. The absence of response to dietetic restrictions, viz., persistent sugar in the urine, the onset of thirst, polyuria, or other concomitants of diabetes, will darken the prognosis.

Also I myself believe that the presence of local foci of infection gravely prejudices the course of gout, accentuates any tendency to recurrence of the attacks, and incidentally reinforces any latent proclivity to vascular and visceral degenerations.

Last, but not least, what of the subject’s habits? The “internal environment” of the tissue cells of the gouty is presumably of itself none too good; but if to this be added the poison of alcohol, lead, or the toxic products of gluttony, it is incalculably worse. The painter or the plumber, if he can, would be wise to change his calling. If the alcoholic be deaf to remonstrance or the glutton continue to gorge, their chances of life dwindle proportionately, and if given to both vices, still more so.

In conclusion, the prospects of long life in gout depend in the main on the presence or absence of associated morbid states. If there be no complications such as I have indicated, the disease, in my experience, is not likely to shorten life materially, always provided that the victim is amenable to what should be the watchword of the gouty,—