XVIII. CLINICAL ACCOUNT (continued)
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.
Red corpuscles, per c. mm. 4,832,000 = 96·6 per cent. Hæmoglobin = 64 ” Colour index = ·66 ” Leucocytes, per c. mm. 11,000
DIFFERENTIAL COUNT.
Lymphocytes 42 = 4,620 Large mononuclears 4 = 440 Polymorphonuclears 52·5 = 5,775 Eosinophils 0 = 0 Mast cells 1·5 = 165
(2) BLOOD COUNT.
Red corpuscles, per c. mm. 5,040,000 = 100·8 per cent. Hæmoglobin = 72 ” Colour index = 0·72 ” Leucocytes, per c. mm. 13,400
DIFFERENTIAL COUNT.
Lymphocytes 15 = 2,010 Large mononuclears 2·5 = 335 Polymorphonuclears 78 = 10,452 Eosinophils 1 = 134 Mast cells 3·5 = 469
(3) BLOOD COUNT.
Red corpuscles, per c. mm. 4,280,000 = 85·6 per cent. Hæmoglobin = 66 ” Colour index = 0·77 ” Leucocytes, per c. mm. 12,000
DIFFERENTIAL COUNT.
Lymphocytes 23 = 2,760 Large mononuclears 3 = 360 Polymorphonuclears 74 = 8,880 Eosinophils 0 = 0 Mast cells 0 = 0
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.
“The life of all his blood Is touched corruptibly, and his pure brain (Which some suppose the soul’s frail dwelling-house) Doth by the idle comments that it makes Foretell the ending of mortality.”
Shakespeare.
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:—
“‘Nomine reque duplex ut nodus Gordius essem.’”
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,—
“The rule of not too much, by temperance taught In what thou eat’st and drink’st, seeking from thence Due nourishment, not gluttonous delight.”
Milton.
XIX. ETIOLOGICAL AND CLINICAL DIAGNOSIS
ARTICULAR GOUT
The intimate cause of gout is unknown—a humiliating reflection, albeit salutary, if it but engender a more catholic attitude on our part when seeking to unravel the nature of this obscure joint affection. For, to secure ideal ends, diagnosis must be, not only clinical, but etiological. This is the more likely to be attained if we shed all preconceived ideas and prejudices.
ETIOLOGICAL DIAGNOSIS
Confronted, then, with a suspected case of gout, whether acute or chronic, what shall be our way of approach? Not the easy and hazardous path of lightning diagnosis affected by those who plume themselves on their so-called clinical “instinct,” but the slow, laborious route of clinical “observation,” that leads more surely to the vantage ground of truth, this assuredly in all diseases, but in none more so than in joint disorders, whose outward resemblances so oft hark back to inward disparities.
First, as to the manner of man, while one would not decry the hints obtainable from physiognomical peculiarities, it is often hard, if not impossible, to fit the subject to the so-called “gouty diathesis.” They are not all of the John Bull type; not a few are spare in build. Hence the danger of too ready inference from so-called “gouty” traits, to be regarded rather as ancillary to, but not substitutes for, more exact criteria.
Now, as to heritage, for, despite the fallacies that surround inquiries into family predispositions, they often furnish valuable hints as to the metabolic trend of the stock. True, ancestral stories often prove indefinite, but fortunately less so in the “gouty” than in those of “rheumatic” tendency. For, as Sir Dyce Duckworth points out, even the laity are quick to recognise what they term “chalky” gout, and so “if a history be given of ancestors or relatives thus affected, there need be no hesitation in pronouncing for true gout amongst them, and for the probably gouty nature of such arthritic ailments as may be complained of by the patients under examination.”
Turning to the individual himself—for the subjects of regular gout are rarely women—what is his age? If he is over thirty-five and has never previously had an arthritic disorder, it is much more likely to be gout than rheumatism, this only as a broad generalisation.
What occupation does he follow? What are his habits? Is he of the “idle rich” who “fare sumptuously every day”? Is he a plumber, a painter, or a butler, coachman, or club waiter, these last being men who, as Sir Thomas Watson observes, “often live more luxuriously and more idly a great deal than their masters”? In short, we must search for any evidence of overeating, overdrinking, and indolence. For of this triad of vices is gout too oft begotten.
As to illnesses, his past may tell of classic outbreaks, one or more in the great toe, and if to this be added a visible tophus, we stand face to face with a “gouty diathesis.” More eloquent this than a “cloud of witnesses” as to previous attacks of migraine, asthma, eczema, etc. All these and more may emerge during the subject’s recital, and by all means let them be ascertained. But forget not that they often arise in the non-gouty. Above all, though, miss not the significance of heightened blood pressure, a cardiac lesion of degenerative type, sugar or albumen in the urine. For these are of the things that will out, but let it not be to our discomfiture!
Even presuming that all facts and observations up to now point to a “gouty” origin of the arthritis, the end is not yet. What has evoked the arthritis? We seek a cause. For to call an arthritis “gouty” is but to restate the problem. How clear the need then for a meticulously careful investigation, in the hope of achieving not a merely nosological, but an etiological, diagnosis.
To narrow our field, we should, in the first place, exclude gonococcal infection, and failing this, influenza, syphilis, or any of the zymotic or other disorders prone to be followed by or associated with joint affections.
If none of such be forthcoming, we should search for local foci of infection. The mouth and its accessory cavities first claim attention. It should be closely scanned for the presence of oral sepsis, the most fruitful source of which is pyorrhœa alveolaris. If dentures are worn it is wise not to take the subject’s word that all his teeth have been extracted. Like others, I have in such found the broken-off stumps still in situ. The condition of “bridges” should be noted, fruitful sources of sepsis as they are. Clinical examination of the mouth may prove inadequate, as buried roots, cysts, or abscesses, not to mention alveolar rarefaction, etc., demand for their detection radiographs.
The pharynx and tonsils should be thoroughly investigated, for disorders of these same are by no means uncommon in “gouty” subjects. Any history of aural or nasal discharges demands the same careful local examination; and, needless to say, the same course must be pursued in regard of any local infections of the genito-urinary passages. In short, in gouty, as in non-gouty, forms of arthritis, thorough and routine examination of every patient by modern bacteriological methods is imperative.
Ignorant of the precise etiology of gouty arthritis, we can ill afford to overlook any associated infective foci which may prejudice the well-being of the victim, as, for aught we know to the contrary, we may be overlooking the very fons et origo mali. Compare our attitude towards other arthritides of cryptic origin, how systematic our search for infective foci, and what a light has thereby been shed on their intimate etiology!
Here may we lodge a plea for routine examination of the blood in all cases of gout? For, as shown, the findings, leucocytosis, etc., have doubtless some profound significance. Apart from this, the routine employment of complement-fixation tests for the organisms responsible for local infections might illumine the obscurity that overhangs this complex problem of their relationship to remote pathological lesions.
If up to now our search for local foci prove futile, it remains for us to note the presence or absence of functional derangements of the alimentary tract, or its accessory glands. We must not, because we think perhaps that the patient “looks gouty,” assume that his dyspeptic symptoms are of like origin. It is our duty to ascertain, if possible, the precise nature and origin of the dyspepsia.
We know that, given oral sepsis, sequential infections of the appendix and gall bladder are not uncommon. Recently it has been remarked that many gouty patients suffer with attacks of pain in the region of the appendix, and simultaneously tenderness over the gall bladder. That the subjects of gout enjoy no immunity from appendix or gall bladder disorders is certain, and at this we need not be surprised, seeing the frequency with which they suffer from alleged causes thereof, i.e., dental sepsis, etc.
But what we would insist upon is that we should not be content merely with dubbing these symptoms “gouty,” as they are much more likely to be, not symptomatic of gout, but etiologically related thereto. If then we are to arrive at the exact nature of the underlying lesion, the probable site of infection or toxic absorption, we must invoke all modern methods of investigation. Thus, how valuable the existence of an X-ray barium or bismuth meal in furnishing positive evidence of gastric or duodenal ulcer on the one hand or of gall bladder or appendix disease on the other. What an aid to the location of adhesions the demonstration of ileal and cæcal stasis, etc.!
In obscure cases the fæces may have to be scrutinised for evidences of pancreatic inefficiency, viz., bulky pale stools, undigested meat fibres, and excess of neutral fat. Their bacterial content, too, if abnormally high, should be noted. As in other arthritides of unknown origin, the results following the administration of vaccines prepared from the predominant organisms have been such as to suggest a causal connection.
The urine should be subjected to chemical and bacteriological examination. As to uric acid, the delusion still widely prevails that gouty subjects excrete large amounts thereof. How frequently is “the degree of acidity” of the urine or “its content of uric acid” held to justify a diagnosis of gout. The deduction is quite unjustifiable. Equally so the assumption that the reverse, a defective excretion of uric acid, is an invariable feature of the gouty diathesis. For though when on a purin-free diet the output of uric acid in the gouty is low, it rarely, if ever, falls below the level of normal. The truth is that we cannot on the mere basis of the variations in uric acid excretion in the urine presume to diagnose gout.
To have any semblance of diagnostic value, the patient should be on a purin-free diet, and a long series of exact quantitative examinations made. C. v. Noorden, to gauge the limit of tolerance of his patients, gives them increasing amounts of purin, and so determines the quantity the subject can deal with without showing retention. But, as Von Fürth satirically observes, “when a physician allows a quantitative analysis to be made of any arbitrarily collected specimen of urine of his patient and then makes a diagnosis of the presence or absence of a ‘gouty diathesis’ after a glance at the list of data of the analysis, he is really not proving by his actions his possession of diagnostic acumen as much as he is laying bare his total ignorance of bio-chemical matters.”
So much for the diagnostic valency of uric acid estimates in chronic gout, but if the patient be on purin-free diet, and an acute attack ensue, the curve of uric acid excretion is fairly characteristic. In other words, for a day or two preceding the outbreak, the uric acid output falls below the usual level, but early in the attack rises markedly, to be followed by a secondary fall.
Some aid in diagnosis has been afforded by the fact that after ingestion of purin-containing food the gouty individual does not, like a normal person, eliminate the excess of uric acid, but the excretion is “spread out over a number of days.” But this retardation and diminution in the excretion of exogenous purins has been seen in non-gouty forms of arthritis, not to mention some cases of nephritis and chronic alcoholism. Hence delayed nuclein exchange, though highly suggestive of gout, is not infallibly diagnostic thereof.
As to uric acid in the blood, it will, I fear, not for long, if ever, be easy to prevail on patients to submit to withdrawal of the amount of blood necessary, even by modern methods, for its estimation. Fortunately, our American confrères appear to be more successful in securing such opportunities. Pratt states that in his twenty-one cases of genuine gout the uric acid content of the blood, irrespective of diet, was 3·7 mg. per 100 grams, as opposed to 1·7 mg., the average amount in 156 non-gouty cases studied by Adler and Ragle. Still Pratt noted that in a few cases of undoubted gout the uric acid content of the blood was within normal limits, though it never fell, even on a purin-free diet, below 1·4 mg. Nevertheless he holds that there is conclusive evidence that the uric acid content of the blood is in gouty individuals notably increased both in the intervals and during attacks.
He has found the sweetbread meal an aid in diagnosis, and the following is his method of procedure: “The patient is placed on a purin-free diet, and the daily output of uric acid in the urine determined. After having been on this diet for at least four days the blood is analysed for uric acid, and 150 to 300 grams of sweetbread (weighed raw) are fed. The purin-free diet is then resumed. The blood of gouty subjects forty-eight to seventy-two hours after the sweetbread meal has shown in every case examined an abnormally high amount of uric acid, while in control subjects this was not found. It is not improbable that this rise in the uric acid content of the blood may occur in certain cases of nephritis and other pathological conditions.”
A bacteriological examination of the urine should be undertaken. Trautner held mucous colitis as one of the initial manifestations of gout, and believes that the bacillus coli communis is the primary agent in gouty affections. He suggests that it produces a reducing substance which during its passage through the body is transmuted into xanthin and uric acid. Be this as it may, there is increasing evidence that an etiological potency may attach to coliform bacilli, streptococci, and other organisms. Dr. Munro in his researches at the Royal Mineral Water Hospital, Bath, noted that the blood serum in one of my cases of acute gout agglutinated B. coli. He has also found streptococci in the urine in acute gout, and these subjects certainly enjoy no immunity from other forms of bacteriuria.
It is beyond the scope of this volume to outline the methods of differentiating and determining the exact organisms which may be responsible for gouty arthritis. But if we aim at rational as opposed to purely haphazard serum or vaccine therapy, we must effect a differential specific diagnosis in a bacteriological sense. How searching our investigations must be in these cases we learn from Adami’s brilliant address on sub-infection when he laid down the axiom that in all cases “there ought to be routine blood cultures, routine examination and reports on the stools and their predominant bacterial types, blood counts, hæmoglobin examination, in fact the full clinical study of each case, so that nothing is neglected.”
No apology is needed for our insistence on the imperative necessity of routine systematic investigation from all sides of these cases of gouty arthritis. For its origin still remains hidden, and who can doubt that, to remove this long-standing reproach, we must approach our study of these cases in a more catholic attitude of mind, one bent on etiological, not merely nosological, diagnosis?
CLINICAL DIAGNOSIS
Introductory Remarks
The word gout itself is void of offence, innocent of scientific pretensions, neither expressing nor violating any article of pathological belief. But let us not forget that the term is neither self-explanatory nor final. Derived through the French goutte from the Latin gutta, it but expresses laconically the fanciful doctrine of those who so christened it.
What the old humoralists saw was the tophus, and would that they had clung more steadfastly to this as their sheet anchor in diagnosis! but casting their moorings, they launched forth on the uncharted seas of abstract philosophy. Even in the writings of the nineteenth century physicians we trace the influence of their disquisitions, and we are tempted to think that some even of our day still bide beneath their thrall.
But, with the advance of pathology to the dignity of a natural science, we must assert our independence of misty hypotheses, rendering obeisance only to facts. What then, may we ask, is the outstanding fact of the “gouty diathesis”? It is, in a word, the tophus! Even as the vague and shadowy constitutional warp known as the “rheumatic diathesis” finds expression, or rather becomes incarnate, in fibrous nodule and induration, so also does the equally nebulous “gouty diathesis” become objective, crystallised in the tophus.
THE DIAGNOSTIC STATUS OF TOPHI
This problem calls for more critical consideration than is usually accorded thereto. The tophus is, in truth, the touchstone of gout, yet not a little controversy obtains as to the frequency of its incidence in “gouty” subjects.
At one extreme we find Sir Charles Scudamore maintaining that tophi have occurred in only a few individuals “of particular ‘gouty’ idiosyncrasy,” in, according to him, less than 10 per cent. of the victims. At the other Sir Alfred Garrod, discussing these figures, observes: “From my own experience I consider these numbers far below the real proportion, from their being deposited in parts of the body scarcely to be expected.”
Now as to these distinguished physicians, who shall doubt that of the twain Garrod stood on firmer ground than his predecessor? In arriving at their diagnoses of gout, Scudamore rested on clinical “instinct,” Garrod on clinical “observation.” To the more scientific mind of the latter the tophus appealed with all the insistence of a fact, while the former was yet in bondage to abstract philosophy, dominated too much by crude and unproven hypotheses.
Given the presence of tophi, the diagnosis of a “gouty diathesis” is assured; in their absence it is but speculative.
It is upon this dictum that we would take our stand, and this without depreciating in any way the pioneer researches of Garrod. For it must be recognised that the increasing differentiation of joint diseases has proceeded apace. How many are now affiliated to specific germs, not to mention the undreamt-of light thrown on their inward characters by X-rays! Scudamore’s work appeared exactly a century ago, Garrod’s in 1876. The conclusion then seems inevitable that many of their alleged cases of gout—at any rate, those unattested by tophi—would now be relegated to widely different categories.
But this zeal for infinite cleavage and subdivision, so characteristic of the modern school, far from diminishing, does but accentuate, the diagnostic valency of the tophus. It still remains the infallible criterion of diagnosis, and, for myself, I feel convinced that infinitely more good than harm would ensue if we refuse to recognise any individual as being of the “gouty diathesis” unless he exhibit these objective stigmata thereof.
Of course to some such a rigid attitude will spell anathema. I hear them say in oracular tones: “Never forget gout, or awful indeed will be your awakening.” More harm, say they, is wrought by failure to recognise gout than by diagnosing gout where none is. Doubtless they are right in counselling us not to forget gout, but not to the exclusion of all else. For, at issue with them, I hold it better to miss gout than to miss syphilitic, gonorrhœal, and other forms of arthritis.
“A name being so readily found for an obscure disease, the practitioner considers himself as excused from the difficult task of nicer discrimination.” Thus wrote Scudamore a century since, a rebuke and a warning for all time.
TOPHI IN RELATION TO ARTHRITIS
How elated we are, and rightly, when in an obscure form of arthritis we pounce on these objective criteria of gout, how apt to deem our diagnostic quest as ended, and with what fatal glibness the time-worn “gout” slips from our lips, sure, alas, of ready and almost complaisant acceptance. Fallacious inference, all too prevalent, that the presence of tophi stamps any concomitant arthritis as “gouty.”
True, tophi are pathognomonic of gout, but their existence does not confer on their host immunity from all other forms of arthritis. In view of the increasing light shed upon joint disorders, who can doubt that (and this not only for our forefathers) the tophus has too often proved a veritable snare, allaying all diagnostic doubts, lulling us into false security? For an individual may, for example, exhibit auricular tophi and be the victim also of an arthritis, but the latter is not inevitably “gouty.” All that can be assumed at sight is merely that the joint disorder, whatever its nature, has ensued in a subject of “gouty diathesis.”
For it may be of specific infective origin, gonococcal, syphilitic, pneumococcal, etc. Quâ a concomitant arthritis, then, the diagnostic significance of tophi, at any rate when of ab-articular site, must not be overrated. It is at once a beacon and a warning. In other words, the diagnosis of a co-existent arthritis as “gouty” should not be entertained pending the exclusion of all other forms of arthritis.
Conversely, in the absence of tophi, the diagnosis of an arthritis as “gouty” is not absolute, but presumptive.
For in the lack of these objective stigmata how can the authenticity of our diagnosis be established? Is it not when achieved a nosological rather than a diagnostic feat? Put otherwise, is not our diagnosis, especially in initial attacks, largely topographical? Not that we would for one moment decry the advantage of realising the predilection of certain organisms for this or that particular joint: of the gonococcus for the sterno-clavicular, of typhoid for the hip, post-scarlatinal rheumatism for the phalangeal joints, etc. But we would drive home the fact that our diagnosis in initial attacks of “gout” is very largely topographical. Let but inflammatory trouble ensue in the big toe, and forthwith we assume it gout, as if, forsooth, this particular joint were immune from all other forms of disease, this, too, while in the same breath we comment on its extreme liability to injury. So, indeed, we maintain, is the marked predilection of gout for the toe joint explained. Is not this a little crude? Does not the same circumstance increase its liability to infection and, we may add, not less important, its proneness to static deformities? But to this we shall recur when discussing differential diagnosis.
To return, how often, apart from the above pitfalls, is the diagnosis “gout” arrived at without any search for tophi wherewith to support the assumption. Our contention is that even in primary attacks of gout our search for tophi should be exhaustive. If undiscoverable, why not be honest with ourselves and recognise that our diagnosis is presumptive pending their development?
Sir William Roberts on this point observes: “As a rule, diagnosis of acute articular gout is easy, but exceptional cases of difficulty occur. The gouty character of the inflammation is affirmed by the discovery of uratic concretions in the rim of the ear or elsewhere.”
Again, Sir William Osier, discussing the diagnosis of acute gouty polyarthritis, remarks: “We have had of late years several cases admitted for the third or fourth time with involvement of three or four of the larger joints. The presence of tophi has settled the nature of a trouble which in previous attacks has been regarded as ‘rheumatic.’”
One may, we think, gather from these two statements the inference that both these distinguished authorities hold tophi to be the only infallible criterion upon which to base a diagnosis of gouty arthritis. In my own practice I must affirm that I never feel justified in christening any arthritis as gouty unless I have discovered tophi, and then only when to the best of my ability all other known causes of arthritis have been excluded.
FREQUENCY OF TOPHI IN TRUE GOUTY ARTHRITIS UNDERESTIMATED
In reviewing the statistics of authors as to the frequency of the incidence of tophi in their cases of assumed gouty arthritis I am inclined to think their relative infrequency is apparent rather than real, in other words that many of their cases of alleged “gouty” arthritis which lack tophi would, if investigated by modern methods, have been shown to be due to other causes of arthritis, this especially as regards their assumed cases of chronic gout. For who can doubt that prior to the discovery of X-rays many cases of osteoarthritis, etc., were thus erroneously labelled? Nor indeed, as we hope to show later, is it improbable that similar fallacies obtained even in regard to acute types of gout, particularly when of polyarticular distribution.
It will be noted that we confine our criticisms to those examples of “gouty” arthritis unassociated with tophi. But if, as we maintain, our scepticism be justifiable, then it follows that it diminishes to an unknown extent the percentage of cases of genuine “gouty” or uratic arthritis which lack tophi.
DIFFICULTY OF DETECTING TOPHI
Apart from the probability of such erroneous relegation to the “gouty” category of non-gouty arthritides, there remains this further consideration, the ease with which tophi, even when superficial, may be overlooked. We look for pearly white concretions, and if none are seen we straightway assume that tophi are absent. This, I am sure, is a very common pitfall. At their inception tophi are neither white nor hard. They are largely fluid and soft to touch. The skin over them may be unchanged in colour or reddened. Only when mature, and the overlying skin is thin, do they assume the ordinary aspects of a tophus. These observations apply not only to tophi in the ears, but to those in the vicinity of the small joints of the hands and feet or elsewhere. I would urge that in the case of all soft localised swellings of dubious nature in the neighbourhood of the phalangeal joints aspiration with a hypodermic syringe will often prove very helpful. If fluid can be withdrawn and the same microscopically examined, it will more often than is supposed reveal the presence of biurate crystals.
More information is badly needed as to the relationship of their formation to acute attacks of gout. Garrod on this point remarks: “The deposits are probably formed during an attack of gout, but occasionally they appear shortly afterwards. In one case, of which I have notes, the ears were carefully examined without result when the patient left the hospital, but within ten days, on re-examination, a deposit was found. Perhaps some fluid was effused during the fit, but being at first transparent, could not be easily distinguished.” Sir Dyce Duckworth, too, observes: “After acute attacks of gout have passed off there may follow renewed pain in the neighbourhood of the joint, and later there is discovered a nodular or soft swelling. In the latter case there may be fluctuation, indicating a liquid collection of urates. This should never be opened. In a few weeks this tumour tends to indurate, grow more compact, and a so-called ‘chalky’ concretion is established.”
Reflection upon the foregoing considerations leads me to the conclusion that not only was Garrod right in his affirmation that “gouty inflammation is invariably attended with the deposition of urate of soda,” but more that examples of true uratic arthritis which lack tophi are exceptional, and that in their absence their diagnosis as such cannot be with certitude established.
We have now, we trust, sufficiently defined our attitude towards the tophus, the salient objective stigma of a “gouty diathesis,” and the indispensable rôle it plays in enabling us to establish the diagnosis of articular gout.
XX. CLINICAL DIAGNOSIS (continued)
ACUTE ARTICULAR GOUT—LOCALISED VARIETY
The nonchalance with which not a few writers dismiss the diagnosis of acute gout when located in the great toe or elsewhere in the foot is, to say the least of it, somewhat remarkable. “It is a very easy matter,” say they, and as an earnest of their good faith are silent as to the many pitfalls that await the unwary. Should they deign to differential diagnosis, they are at pains to discriminate between it and acute articular rheumatism, which re classical outbreaks in the toe seems a little superfluous! But not a word of traumatic lesions, infective processes and static deformities, all infinitely more likely stumbling-blocks.
Did all cases conform to the classic type, acute sthenic gout, it might be held relatively easy. But such are not, to say the least of it, common nowadays. More often than not our examples are, as Garrod terms them, of acute asthenic character. As he observes: “There may be indeed pain and tenderness in the toe, and some amount of swelling, but accompanied with little heat or redness, and all febrile disturbance may be absent; still œdema is generally observed and itching and desquamation follow.”
That diseases, like their victims, alter with environment is but too clear. Who can doubt that the gout of the Regency has to-day assumed a milder clinical facies? Physicians of those days were haunted with the fear of confounding it with erysipelas and phlegmon. Still, while no such fears apparently beset us to-day, it were well to walk circumspectly.
Thus, recently a friend of mine came across an instance of what he deemed acute gout in a metacarpo-phalangeal joint. Its failure to respond to colchicum and the growing intensity and extent of the local inflammation suggested incision, when, lo, pus issued, to the subject’s comfort, but to his own chastening!
There are, however, many more likely sources of fallacy, these, too, of the most diverse type, inasmuch as they differ according to the exact location in the foot of the assumed gouty process. For while the big toe is the site of predilection for the initial manifestation, it is not always so. The primary outbreak may be located in any of the smaller joints of the foot, or outside them in related structures: in the heel, the sole, or the tendo Achillis. These vagaries greatly enhance the difficulties of diagnosis. For the process of differentiation will vary according to the particular joint or structure involved, the predilections of certain infective processes, not to mention the marked liability of the foot to painful disturbances of static origin.
DIFFERENTIAL DIAGNOSIS
Inasmuch as the primary outbreak may be located in any part of the foot, we purpose, for reasons just cited, dealing seriatim with gout in (1) the big toe; (2) the instep; (3) the heel; (4) the sole.
GOUT IN THE BIG TOE
Infections.—There is no â priori reason why any of the infections may not find a nidus in the first metatarso-phalangeal joint. Thus, Garrod, as we know, held gouty subjects specially liable to pyæmia. In rare instances, the primary focus has been in or near the great toe, and has consequently been mistaken for gout. The rapid progress of the disease would of course soon clear up the nature of the case. But if the subject has previously suffered from gout, such a diagnostic error at first sight is quite excusable. Accordingly, as a safeguard in all doubtful cases, inquiry should be made as to the existence of bladder troubles, piles, etc., especially any recent operation in this or other regions.
Again, while gout in its articular form is rarely, if ever, met with in children, it must be recalled, on the authority of Sir James Goodhart, that rheumatism in their instance is occasionally limited to one joint. Moreover, this distinguished physician actually saw it localised in the great toe, “in a case in which the subsequent course of the disease showed that it was acute rheumatism.”
Acute Gonococcal Arthritis.—We may recall that Van Swieten, a disciple of Boerhaave, held that sometimes a wife while nursing her gouty husband had contracted the same disorder. A tribute, we fear, to Van Swieten’s diplomacy rather than to his clinical acumen—an euphemism for gonorrhœal rheumatism!
Of course in adolescents or in young adults monarticular pain, with or without swelling, heat, or redness, should not suggest “gout,” but an infective disorder either in the joint or the related bone-ends. At the same time middle-aged men enjoy no immunity from gonorrhœa, and we may add that gonococcal infection of the metatarso-phalangeal joints is not so uncommon. When located in that of the great toe, it is easy to see how readily the acute arthritis may be confused with gout. But, unlike the latter, its duration is measured by months or weeks rather than by days. It is well to recollect, too, that “gouty” persons are more prone to develop arthritis following gonococcal infection. Given therefore a history even remote, we should in doubtful cases recall the longevity of the organism, its persistence in the prostatic recesses, and the need for bacteriological investigation.
Traumatic Lesions.—Its exposed situation renders the big toe very liable to trauma. Often, too, the injury being slight, and not followed by any immediate consequences, the connection may easily be overlooked. A blow or a fall may readily bruise the synovial membrane without at first any external sign. But given trivial hæmorrhage into the cavity or subjacent tissues, an acute synovitis with effusion is induced.
Again, joint disorder following injury is usually monarticular, whereas the same when the outcome of so-called “constitutional” causes is generally oligo- or poly-articular. The relevancy of this is obvious when we recall that initial attacks of gout are monarticular. Accordingly, given a history of definite injury to the toe joint, the question arises, Is it acute gout or acute traumatic arthritis? this especially if the subject has not had a previous attack of gout at this site.
Here I would lay stress on the fact that indirect rather than direct traumatisms are more common antecedents or determinants of gout, viz., sprains or strains. Moreover, in reviewing the writings of the older physicians one is driven to the conclusion that frequently a septic cellulitis, synovitis, or a frankly traumatic arthritis was confused with acute gout.
The following examples cited by Scudamore are, we contend, susceptible of such an explanation: “A gentleman much subject to gout, when considering himself unusually well, underwent the slight operation of having the nail of the great toe cut on account of its improper growth. The toe was much pressed, and gouty inflammation was the immediate consequence.” In another case “the patient, never before having suffered the gout, tore off a broken portion of the thumb-nail, so as to make the part tender. Very soon the thumb and part of the hand put on a swollen and shiny appearance, and was exquisitely painful. A poultice was applied. Suddenly on the third evening the pain quitted the thumb and seized the toe, next the ankle, then the knee, and lastly the great toe of the other foot. Throughout he secured ease and sleep till the first light of the morning appeared, and hence facetiously observed that the gout in this respect assumed all the behaviour of a ghost.” Was not this probably a case of septic absorption with cellulitis and a mild degree of sapræmia, evoking arthralgic pains?
In conclusion, without denying the potentialities of trauma, whether direct or indirect, in determining an outbreak of gout, we would submit that its diagnosis under such circumstances should not be hastily arrived at, but by the slower process of elimination, this especially if the trauma has involved slight abrasions with the possibility of sepsis. A quick response to colchicum would of course be highly suggestive of gout.
Acute Osteoarthritis.—It is perhaps not so widely recognised as it should be that osteoarthritis not uncommonly attacks the metatarso-phalangeal joint of the great toe. It becomes enlarged owing to the hypertrophy of the articular ends. Like similar lesions in the small joints of the hand, the big toe joint from time to time undergoes exacerbation, with increased vascularity and local heat, which, though of minor degree, may by a superficial examiner be readily misinterpreted as gout. The parts are painful, somewhat swollen, hot, and tender, but the local symptoms are never intense, and constitutional disturbance is lacking. The presence of osteoarthritic lesions elsewhere and the revelations of skiagraphy will suffice for differentiation of such cases from asthenic articular gout.
STATIC FOOT DEFORMITIES
Hallux Valgus with Inflamed Bunion.—Scudamore in his “Treatise on Gout” observes that “the bursal disease over the first joint of the great toe, which is familiarly known as bunion, is a very common complaint with gouty persons.” In view of the fact that no reference is made in the context to the absence or presence in such cases of a condition of hallux valgus, one is led to believe that Scudamore overlooked the deformity and regarded the local bursitis as the outcome of a gouty inflammation of this structure.
Bradford and Lovatt, discussing hallux valgus, observe: “There may be pain and irritability in the great toe joint, and in severe cases extreme pain and difficulty in walking, which is usually attributed by the patient to gout.” We would only qualify this statement by the fact that the local heat, redness, and swelling that in this condition so often follow slight injuries or excessive walking is not only so interpreted by the patient, but far too frequently also by his medical attendant.
Routine examination of the bare foot will minimise the chance of such a fallacy, though of course it must be borne in mind that a gouty subject may present this deformity. But when we recollect that hallux valgus of slight degree “is almost universally present after middle childhood,” we see that, given the presence of this static foot deformity, any inflammatory process in the superjacent structures is infinitely more likely to be due to an inflammatory bursitis than to a gouty arthritis.
Given an inflamed bursa with cellulitis spreading over the dorsum of the foot, confusion with acute sthenic gout is all too easy. But in our experience, mirabile dictu, the ordinary more or less chronic circumscribed redness over the bunion is but too commonly misinterpreted as gout, this particularly in women, despite the rarity with which gout attacks their toe and the frequency with which their footgear is precisely adapted to produce hallux valgus. Given therefore the presence of this static foot deformity, we should in the absence of objective stigmata of gout, viz., tophi, suspend our diagnosis pending observation of the results obtained by local treatment of the displaced toe.
Hallux Rigidus.—This deformity is but too often overlooked, and if marked by pain and more or less rigidity of the first metatarso-phalangeal joint, it may, in lack of adequate examination, be flippantly dismissed as “gout,” this more particularly in its later stages, when, in addition to pain and stiffness therein, the joint is swollen, tender to the touch, and the bony ends actually enlarged. Here again local examination, if carefully carried out, will suffice to obviate such errors, while the quick response to rest and appropriate applications, with correction of the frequently associated sunken arch, will sufficiently attest its true nature.
Metatarsalgia.—As pointed out in our previous work on Fibrositis, “this painful condition is more often than not confused with rheumatism or gout.” We have known subjects wander to nearly every spa on the Continent under such a misconception. Not to mention the financial expense, the dietetic penances imposed, the consequences of such faulty diagnosis, are by no means trivial, for the intensity of the suffering may reduce the walking capacity to a minimum.
The neuralgic pain radiates into the toes and often upwards into the leg, usually comes on while walking, and is relieved by the removal of the boot. For its detection any altered relationship in the position of the third, fourth, and fifth metatarsals, especially their displacement to a lower level than normal, should be noted, and any limitation of the power of dorsal flexion of the foot likewise estimated. The presence of callosities under the heads of the metatarsals is very suggestive of this painful condition.
GOUT IN THE INSTEP
Next to the metatarso-phalangeal joints, the tarsal articulations are the most frequent site of initial attacks of gout. Here again we would insist on the necessity of excluding infections of the tarsal joints or shafts and even more important, static foot deformities.
Gonococcal Arthritis.—In a table compiled by Garrod from those of Foucart, Brandes, Rollet, and Fournier, the relative frequency of the implication of individual joints in gonorrhœal arthritis shows that out of a total of 119 the tarsus and metatarsus were attacked in five instances. In the more acute cases the periarticular swelling, local heat, and pink blush may be confused with acute gout. The resemblance is enhanced in that, as in gout, the overlying tendon sheaths are liable to become inflamed and distended with fluid.
Tuberculous and Syphilitic Disease of the Tarsal Joints or the Related Joints.—In cases of obscure pain and inflammatory trouble in the instep the possibility of arthritic and bony lesions of this nature should not be overlooked, especially if there be suggestive lesions elsewhere, or if the history afford evidence of the possibility of such contingencies.
Pes Planus.—In all cases of pain and swelling, with or without redness, in the instep, it is well to recollect that, though flatfoot may for a long time exist without giving rise to symptoms, it frequently happens that, in sequence to some unusual strain on the plantar arch, the static disturbance in the foot enters quite abruptly on a painful phase. Congestion and swelling of the foot is common, and actual teno-synovitis of the tibial and peroneal muscles is not infrequent. Tenderness, too, at points of ligamentary strain is almost always present, and more or less constant pain.[40]
The frequency with which the local and referred pains of flatfoot are misinterpreted as “gout” and dietetic restrictions and other useless and uncalled-for methods of therapy enjoined is well exemplified by a case which has just left our consulting room.
The subject, a middle-aged spinster of lean kind, came to Bath for treatment of her supposed gout, and for which indeed she had previously received spa therapy. Her feet when bared showed a condition of double hallux valgus with related bursal thickenings. The occasional inflammation of these latter structures and the recital of doubtful ancestral proclivities were the sole evidence on which was based the diagnosis of gout. In addition, as is so frequent in hallux valgus, there was associated therewith a bilateral flatfoot, and it may be added that in the left foot a hammer-toe had been removed some years since. Unfortunately the neglected symmetrical flatfoot had, as so frequently happens, initiated, through the erroneous deflection of a body weight, a condition of chronic villous synovitis in both knees. This again was misinterpreted as but another proof of her assumed “gouty” diathesis. Reflecting upon human nature, how curious the reluctance with which such subjects elect to part with their “gout.” Women especially hold tenaciously thereto, even those of austere type, clinging to the taint handed down to them from some far-off ancestor whose “superfluity of naughtiness” was a by-word among his generation. To exchange gout, morbus dominorum, for “flatfoot” and inflamed “bunions,” savours of degradation, and to couple it with aspersions on their footgear is well-nigh insupportable. Nor are the “lords of creation,” we fear, exempt from this failing. We recall during the War being consulted by a highly placed officer who complained of gout. A well-preserved man of nigh sixty years of age, he obviously prided himself on being immaculately booted. As such patients frequently do, he brought his own diagnosis of “gout.” Removing his footgear, manifestly too small, his crucified toes stood out with bunions in a state of hot resentment. But impeachment of his boots was too much for him. Persuasion and argument were futile, and I doubt not he walks to-day stiff, a martyr to his vanity. “Il faut souffrir pour être belle.”
GOUT IN THE HEEL
In some instances the first manifestations of gout occur in the heel, while in others the sheath of the neighbouring tendo Achillis is the part first invaded. Probably there is no region of the foot in which there exist more pitfalls, and doubly careful should we be before concluding that any painful or inflammatory condition thereof is one of “gout.”
Referred Pain.—Pain in the heel affords many loopholes for misinterpretation. It may, as Sir James Paget pointed out many years ago, be symptomatic of a renal calculus. In my own experience it is sometimes complained of by the subjects of internal hæmorrhoids, the pain waxing and waning with the variations in the rectal trouble, and only disappearing permanently when the piles have been radically treated. It is, again, a symptom sometimes complained of by the victims of enlarged prostate.
LOCAL SOURCES OF FALLACY
If the pain and tenderness be located on the under-surface of the os calcis, there are several misconceptions possible.
(1) Careful examination may reveal a tendency to flatfoot, the pain being referable to strain on the posterior insertion of the plantar fascia.
(2) The root of the trouble may be a gonococcal inflammation of the plantar fascia, or of the periosteum covering the os calcis.
(3) A skiagram may show the existence of a bony spur on the inferior surface of the os calcis.
(4) The bursa under the os calcis may be inflamed.
(5) Also, as Tubby has pointed out, pain in the heel may be referable to shortening of one leg or constant standing, and more rarely to tuberculous disease of the os calcis.
If the pain and tenderness be located on the posterior surface of the os calcis, or in the tendo Achillis, the following should be excluded before assigning the trouble to “gout”:—
(1) Post-calcaneal Bursitis.—Inflammation of the bursa lying between the os calcis and the tendo Achillis is not uncommon. It may be uni- or bi-lateral, and in the majority of instances is attributable to violent exercise, or chafing of the heel by ill-fitting boots. The local swelling and tenderness at the site of the inflamed bursa and its aggravation by plantar flexion of the foot will afford a clue to its true nature. (An exostosis projecting from the hinder surface is sometimes a cause of post-calcaneal bursitis.)
(2) Synovitis of the Tendo Achillis.—Symptoms very similar to those above described have been met with in a teno-synovitis of the tendo Achillis, as evidenced by swelling of the sheath, tenderness, and silky crepitus.
GOUT IN THE SOLE
There is a wide disposition to regard all painful or unpleasant sensations in the sole of the foot as evidences of “goutiness.” It may be recalled that Strabo, according to Plutarch, apostrophised heat or itching of the feet at night as “the lisping of the gout.” Duckworth, too, emphasised the frequency of this symptom in the gouty, and Sir Charles Scudamore also held heat and dryness of the sole as frequent harbingers of acute attacks. Now, did we but confine our hazards as to gout only to cases marked by heat or itching in the sole, possibly little harm might result; but unfortunately there is a flippant readiness to relegate all obscure pains or abnormal sensations in the sole to the “gouty” category. Needless to say, this is quite unjustifiable. We need not reiterate the bounden necessity of excluding all static foot deformities, but we should in addition recall the various types of plantar neuralgia.
Plantar Neuralgia.—Occasionally, as we have pointed out elsewhere, the pain is of almost unendurable severity. It constitutes one of the types of so-called partial sciatica, the pain and paræsthesia being confined to the plantar nerves. Indeed, pain, numbness, hyperæsthesia, or sweating of the sole are often symptomatic of a definite neuritis. Such may follow typhoid fever or caisson disease, and in this latter be of aggravated type. When we realise that the pain in these cases may be limited to the tips of the toes or the ball of the great toe, we see how readily it may be confused with “gout.” Fortunately plantar neuralgia is exceptionally rare; but even after exclusion of the foregoing causes we should, before pronouncing any such neuralgia to be “gouty,” recollect that plantar neuralgia or hyperæsthesia is very common in alcoholism and hysteria.
Erythromelalgia.—Among the exceptional cases that find their way to spas are examples of this rare disorder. Almost invariably they come under the diagnosis of “gout” or “rheumatism.” When we reflect that in the majority of instances the initial burning pain typical of the disease is located in some part of the sole of one foot, and that the associated redness and vascularity may be delimited to the ball of the great toe, the heel, or outer or inner side of the foot, we see the danger of its being too easily referred to “gout.”
If seen at the zenith of an attack, the severe pain, the local heat, the intense purplish redness, the distension of the veins, and in some instances œdema, how close the resemblance to gout! Precisely also, as in gout, the simulation of a deep-seated inflammatory process is very pronounced. Indeed, in not a few examples of erythromelalgia fruitless incisions have been made. Accordingly in all cases of pain, redness, and swelling in the sole of the foot, we should canvass the possibility that we may be face to face with an instance of erythromelalgia, a disorder which, like gout, is most frequently met with in men of middle age.
In drawing to a close our remarks on the diagnosis of acute gout in the foot, we would emphasise the fact that in all such cases the bare feet should be thoroughly examined. For, apart from infective and traumatic lesions, the frequency with which the various static foot deformities are confused with “gout” is incredibly common. That gout may co-exist with hallux valgus or other distortion we readily admit, but this does not absolve us of our responsibility—correction of the static deformity. Combine this, if you will, with constitutional treatment if there be evidence, i.e., tophi, of a “gouty” diathesis, but, we repeat, correct the mechanical defect. For gout may come and go, but static errors remain. In so doing, the victim will be saved much preventable suffering, and, for aught known to the contrary, the removal of irritation and local congestion may haply minimise the chances of subsequent gouty outbreaks.
ANOMALOUS SITES FOR INITIAL OUTBREAKS
While primary attacks are in the vast majority of instances localised to the foot, if not actually to the toe, it is well to recollect that very rarely the knee, the wrist, elbow, or ankle may be the chosen spot. In such cases there is need for exceptional caution before committing oneself to a diagnosis of gout. Certainly not until all other known causes of acute arthritis of monarticular type have been excluded.
If in the knee or wrist, any possibility of injury or strain should be thoroughly canvassed. To make assurance doubly sure, a radiograph should always be taken. Specific infective forms of arthritis then call for careful elimination—i.e., gonococcal, etc. If there be no history of such, a painstaking search should be made for any local foci of infection, e.g., mouth and accessory cavities. If any be found, they should be radically treated, as it is much more likely that the arthritis is due thereto than to gout.
If, notwithstanding a meticulously careful investigation, no cause can be assigned, we may entertain the possibility of its being gout, the more legitimately if the subject be a middle-aged man coming of gouty ancestry and exhibiting himself tokens of this diathesis, i.e., tophi. It would be confirmatory, too, if, apart from its exceptional localisation, the joint disorder in its course conformed to that typical of gout in the toe, in other words if it was of sudden nocturnal onset, showed marked daily remissions in temperature and pain, responded swiftly to the action of colchicum, and was not protracted beyond the usual week or ten days.
Sir Hale White, discussing the diagnosis of acute gout of unusual localisation, remarks: “The real difficulty in acute cases comes when it is suggested that an acute arthritis with pyrexia and swelling and redness of a joint other than that of the great toe is caused by gout. I have recently seen the difficulty in one patient in the wrist, in another in the knee. Such cases, if they are not gout, are some bacterial arthritis.”
XXI. CLINICAL DIAGNOSIS (continued)
ACUTE GOUTY POLYARTHRITIS
In the pathways of medicine, as in other walks in life, we are apt to become stereotyped, to fall into grooves, and sooner or later the inevitable rude awakening comes. Thus, so prone are we to think of gout as belonging, so to speak, to the foot, that when it erupts elsewhere it is often the last contingency to dawn upon us. If we diagnose it too often and too readily in the foot, we do so too seldom when it appears in joints remote.
Now, while in initial outbreaks of gout it is exceptional for more than one joint to be affected, it is not always so. For sometimes in those strongly predisposed by heredity not one, but many joints, may be implicated in the primary attack. Such cases, however, are extremely rare.
As a rule, this acute gouty polyarthritis occurs in individuals who have already experienced articular paroxysms at the classic site; but in the subsequent polyarticular attacks the toe joints are often unimplicated, and the disease is located in the larger articulations—the knees, ankles, wrists, or elbows. Herein resides the difficulty of diagnosis in these cases: the likelihood of confusion with other polyarthritides.
Confronted then with an acute polyarthritis of obscure nature marked by pain, redness, swelling, and pyrexia, what are the points necessary to establish it as being of gouty origin?
The sex and age should be noted, also the heritage, habits, and occupation. A history of previous attacks located in the big toe would be of prime value. The presence of a cardiac valvular lesion, while it would suggest a previous attack of acute rheumatism, would in no wise negative the possibility of the subject developing gout in later life. Here I may say that if the subject is over thirty-five and has never had acute rheumatism or acute gout, it is much more likely at his time of life that his acute polyarthritis is of gouty than of rheumatic origin.
As to the character of the pyrexia, it is usually of low grade; but if the condition be afebrile, it is even more suggestive of a gouty arthritis. But recollect, too, that the pyrexia in gonococcal arthritis is also of low grade or absent.
There is nothing distinctive of gout either in the character or distribution of the articular lesions. The ankles, knees, hands, wrists, are most commonly involved, much more rarely the elbows, shoulders, or hips. Naturally the local changes will differ according to the joint involved and the structures implicated; but these local variations in appearance, including œdema, may all be met with in any form of infective arthritis.
As to uric acid excretion, Osler, who was deeply interested in this type of arthritis, held that any lowering of the ratio of the uric acid to the urea excretion would be significant of gout. Also we should, as these cases of acute gouty polyarthritis are of the nature of successive paroxysms (“series et catena paroxysmulorum,” to use Sydenham’s expression), note any variations in the uric acid output ensuing pari passu with their rise and wane.
Last, but most important of all, a thorough search must be instituted for tophi, not only in the ears, but elsewhere. If anything could emphasise the indispensable rôle played by tophi in the diagnosis of gout, it would be our utter inability to effect in their absence a diagnosis of these acute types of gouty polyarthritis. The establishment of the existence in situ of such articular uratic deposits disposes forthwith of all possible doubts as to the true nature of the case; but if, as so frequently happens, the tophi when present are of ab-articular site, then we must withhold our decision pending the exclusion of certain other joint disorders, to the differentiation of which we now proceed.
DIFFERENTIAL DIAGNOSIS
The class of disorders that call for discrimination are those of infective origin. In the first place, acute articular rheumatism must be excluded; nor is it less necessary that we should eliminate gonorrhœal and syphilitic types; while, last, but not least, that vast group, the undifferentiated infective arthritides, is but too often a source of confusion.
ACUTE ARTICULAR RHEUMATISM
Unquestionably many cases of acute gouty polyarthritis have been confounded with acute articular rheumatism, and vice versâ. Garrod on this point remarks: “That many cases of acute gout have been mistaken for acute rheumatism I do not doubt, and, on the other hand, that some few cases of acute rheumatism have been regarded as of a gouty nature I am no less certain. I may refer to the oft-quoted case related by Dr. Haygarth in which gout was supposed to have been transferred from the extremities to the heart as an example of the latter error.”
It is only, of course, with that type of acute gouty polyarthritis accompanied by pyrexia, and not the afebrile variety, that confusion with acute articular rheumatism is possible. What then are the points of discrimination?
ACUTE ARTICULAR RHEUMATISM. ACUTE GOUTY POLYARTHRITIS.
Age and sex Most common between ages Maturity and old of fourteen and thirty. age. Males. Predominance of males Females markedly after twenty. exempt.
Heredity Very disputable. Very pronounced.
Onset Usually abrupt and often Insidious, with with tonsillitis. premonitory gastro-intestinal symptoms.
General symptoms High fever, sometimes Moderate pyrexia. hyperpyrexia. Profuse Marked daily acid sweats. remissions.
Distribution of Preference for large joints Small joints, hand lesions and markedly mobile. or foot often involved. Fixity typical.
Local characters Joints exhibit slight reddish Scarlet hue and flush. No subsequent œdema with later desquamation. No residual peeling of cuticle change. and itching. Tendency to involvement of bursæ and tendons.
Pain Chiefly evoked by movement. Spontaneous, more intense.
Duration Twenty to thirty days, Six weeks to three sometimes longer. months.
Associated Cardiac lesions common. Tophi. Occasionally phenomena glycosuria and albuminuria.
Therapeutic test Salicylates a specific. Not so in gout, but colchicum takes this rôle.
ACUTE GONOCOCCAL ARTHRITIS
This disorder, as we know, is sometimes of oligo- or poly-articular distribution. Moreover, as the attendant pyrexia may be slight or absent, it may readily be confounded with the afebrile variety of acute gouty polyarthritis. Osier, discussing diagnosis of the latter condition, observes: “A patient with three or four joints red, swollen, and painful in acute rheumatism has fever, and while pyrexia may be present, and often is, in gout, its absence is, I think, a valuable diagnostic sign.”
This is of course true, but it still remains necessary, for reasons above cited, to eliminate acute gonorrhœal arthritis. The tendency to such confusion has been emphasised by Sir Rose Bradford and Sir William Roberts, and I would urge the necessity of being alive to this possibility even in middle-aged men. One thing is certain, viz., we should be extremely chary of pronouncing any coincident urethral discharge to be a so-called “gouty urethritis”; nor should we translate any coincident conjunctivitis or iritis as further evidence of the articular affection being “gouty.” It is far more likely to be gonococcal. Apart from these inflammatory ocular affections, the relics also of previous attacks—viz., irregularity in contour or inequality in size of the pupils—have before now put me on the right track in obscure types of polyarthritis.
To sum up, the following are distinctive characters of generalised gonorrhœal arthritis:—
Etiology.—History or presence of urethral discharge and isolation of the gonococcus.
Onset.—Insidious, seldom acute.
General Symptoms.—Absent or slight relatively to extent and severity of joint mischief. Pyrexia, low grade or absent.
Distribution of Lesions.—Preference for large joints. Special liability of sacro-iliac, chondro-costal synchondroses, sterno-clavicular, tibio-fibular, and temporo-maxillary joints.
Local Characters.—Persistent passive effusion or peri-articular boggy swelling, with redness and local heat. No tendency to migrancy. Joint swelling very persistent.
Associated Phenomena.—Involvement of fasciæ, especially plantar, and of tendon sheaths, very distinctive, while coincident iritis or conjunctivitis is almost diagnostic.
SECONDARY SYPHILITIC ARTHRITIS
The ease with which a subacute arthritis of this nature may be confounded with “gout” or “rheumatism” calls for comment. We have met with cases despatched to spas under this impression. The customary intermittent fever of secondary syphilis is usually present. The detection of periosteal nodes in addition to the joint swellings should arouse suspicion, while the presence of secondary syphilides and the rapid response to specific treatment will be confirmatory.
I well recollect some years ago a young farmer being sent to me by a medical man as suffering from gouty arthritis with gouty eczema. The eruption was a typical roseola, and the condition promptly cleared up under anti-syphilitic treatment.
ACUTE RHEUMATOID OR ATROPHIC ARTHRITIS
While the old term “rheumatic gout” still clings to this affection, it has now achieved its isolation from gout on the one hand and rheumatism on the other. The fact that it occurs in young women in whom gout never occurs, and has a very marked clinical facies of its own, should almost preclude the possibility of its being a source of confusion. Still, for the sake of completeness, we append its chief characteristics.
Age and Sex.—Most common in young women.
Onset.—More or less acute.
General Symptoms.—Continuous low grade pyrexia, quick pulse, and rapid emaciation, and commonly concomitant gastro-intestinal derangements.
Distribution of Lesions.—Polyarticular. Beginning in the small joints, it spreads centripetally, with a tendency to symmetry. No migrant trend, but a steady, progressive involvement of joint after joint, including temporo-maxillary and cervical articulations.
Local Characters.—Overlying skin of affected joint white or semi-asphyxial in tint. Contour spindle-shaped, but in terminal stages shrinkage from atrophy of articular structures sets in. Muscular wasting and contracture conspicuous features.
Associated Phenomena.—Trophic and vasomotor changes prominent, but no tendency to cardiac lesions.
INFECTIVE ARTHRITIS OF UNDIFFERENTIATED TYPE
It were well in approaching any acute polyarthritis of obscure nature to bear in mind the axiom that any or all infections may be complicated by arthropathies, also that if the said polyarthritis does not respond quickly to colchicum or salicylate of soda we are almost certainly dealing with an infective arthritis either of specific or undifferentiated type. The specific forms of infective arthritis, as far as seems necessary, have been dealt with, but those rarer forms not referred to, viz., influenzal, pneumococcal, dysenteric, meningococcal, etc., have also to be borne in mind, if the history reveal any recent occurrence of these disorders.
Still far more common than any of these are the acute infective arthritides of undifferentiated type. As we before remarked, an extraordinary general clinical resemblance obtains between these types of joint disorder and acute gouty polyarthritis. Indeed, in the absence of tophi, their differentiation is well-nigh impossible. Even the blood picture in both types of the disorder is strikingly similar in the matter of leucocytosis and secondary anæmia.
Recently Dr. Henry A. Christian, lecturing at a clinic of the Harvard Medical School, emphasised this clinical similarity and the difficulty of discriminating between these two types of joint disorder. As he rightly says, “while there is a definite acute gouty polyarthritis (as evidenced by external tophi or deposits in bone or cartilage with variations in uric acid output) and also an equally definite infective arthritis, yet between those two there is a very considerable number of cases that present some of the factors suggestive of gout and other factors suggestive of an infectious arthritis, and there is where the difficulty comes.”
This is precisely the state of affairs, and one may well ask where gout ends and infection begins. Let us take an example. A man exhibiting tophi, the subject also of pyorrhœa alveolaris, develops an acute polyarthritis. What then is the nature of the joint disorder? There is a gouty element in his case, as attested by tophi, also an infective element, as evidenced by oral sepsis.
Now are we to regard such a case as one of infective arthritis of undifferentiated type occurring in a gouty subject, or are we to proceed on the assumption that the presence of tophi negatives the possibility of infection and forthwith to class it as a case of acute gouty polyarthritis of so-called metabolic origin?
This is no theoretical quibble. In the Royal Mineral Water Hospital, Bath, one constantly meets with cases in which the very elect would be puzzled as to whether they should be placed in the category of gouty or in that of infective arthritis. I have at present in my wards a middle-aged man, stout of body, rubicund of face, with well-marked auricular tophi and widespread arthritis. There are no tophi round his joints. On X-ray examination his phalanges show Bruce’s nodes, and his phalangeal joints show changes indistinguishable from those constantly met with in infective arthritides occurring in non-gouty subjects.
Indeed, this overlapping may proceed still further, the gouty and the infective characters neighbouring in such proximity as to suggest actual fusion, a community of origin. What else in truth can be the inference, when one meets with examples in which the peri-articular tissues are the seat of demonstrable uratic deposits, while the X-ray changes within the joint proper, the bone and cartilage, are typically those met with in infective arthritis?
Now, who will deny that if tophi were absent in such a case we should without hesitation hold the case to be one of infective arthritis? My own contention is that even in the presence of tophi the same appellation is indicated. In other words, I submit that acute gouty polyarthritis is itself but a form of infective arthritis which derives its specific character from the associated uratic deposits.
As to differentiation of the latter from these cryptic infective arthritides, this will rest mainly on—
(1) The presence of tophi;
(2) A history of previous attacks in the great toe;
(3) A swift response to colchicum.
In addition, acute gouty polyarthritis is confined to middle-aged males, while no period of life is immune from infective arthritis, and both sexes are equally liable.
Again, acute gouty polyarthritis may be afebrile. Pyrexia when present is moderate in grade, its curve undulating as the paroxysms rise and wane. In infective arthritis the temperature curve is irregular and erratic.
Lastly, the uric acid output in acute gouty polyarthritis drops a day or two before the paroxysm, rises markedly after its inception, then sinks again. Also we may add that occasionally glycosuria or albuminuria is present.
In conclusion, I would allow myself a brief digression regarding these infective arthritides of undifferentiated type. They constitute the bulk of the cases of arthritis that find their way to the Royal Mineral Water Hospital, Bath, under one or other of the appellations “gout,” “rheumatism,” and “rheumatic gout.” It is within this category that most of the cripples met with at spas fall, and their obduracy to “drug” treatment accounts for their belated despatch thereto.
I would that I could sufficiently emphasise the imperative necessity of early recognition of the true nature of these cases. Colchicum is a most valuable drug, and so is salicylate of soda. But they have their limitations. They act swiftly or not at all. Persistence with them in the absence of any response is worse than futile: it is definitely prejudicial. Because of our unreasoning devotion, our almost fetishistic addiction, to these drugs, I often feel that these agents, especially salicylate of soda, have made more cripples than they have saved. For, unfortunately, unqualified reliance on these drugs is apt to blind us to the surgical necessities of these cases. Foci of infection pass unnoticed, joints stiffen at unfavourable angles, and not infrequently a potential bread-winner is lost.
I make no apology for this digression, for it is, strictly speaking, wholly apposite, this in view of the fact that failure of quick response to the action of colchicum or salicylate of soda, say within a week, speaks in favour of the infection having ensued in a non-gouty as opposed to a gouty subject.
XXII. CLINICAL DIAGNOSIS (continued)
CHRONIC ARTICULAR GOUT
If the diagnosis of acute types of articular gout often presents difficulties, these same are, if anything, accentuated when we approach its chronic manifestations. For, apart from uratic deposits, the anatomical lesions that ensue in joints the seat of long-continued gout have no specific character. In short, there is nothing pathognomonic of gout in the changes produced, and which, as a matter of fact, we know to be capable of production, by many different morbid agencies. Surely this lack of specificity in its structural lesions should make us very chary of admitting to the category of chronic articular gout any examples of arthritis destitute of uratic deposits.
In our chapter on classification we emphasised the desirability of restricting the usage of the term chronic articular gout to that type long since known as tophaceous gout, this because there is little, if any, doubt that that variety known as chronic deforming gout (syn. arthritis deformans uratica) is largely made up of examples of rheumatoid or atrophic arthritis and hypertrophic arthritis or osteoarthritis.[41]
As to osteoarthritis, I do not for a moment deny that uratic deposits may be met with in its victims. One frequently meets with patients, the subjects of osteoarthritis of the hip, who at the same time exhibit tophi in the ears.
But such to our mind are to be regarded as merely instances of osteoarthritis occurring in subjects of “gouty diathesis.” This apparent blending of the two disorders must not be allowed to impair the clarity of our conception as to the essential distinctness of gouty arthritis and osteoarthritis.
Sir W. Hale White has some pregnant observations on this point. Many patients, he says, “with chronic arthritis are quite wrongly said to have gout; usually they have osteoarthritis. The presence of bony outgrowths is strongly against gout, though it is not conclusive, for such may occur in true gout either more or less all round the joint or in the form of little nodules, but they never attain the considerable size common in arthritis,” and he adds: “If no urate of soda is visible anywhere the diagnosis may be very difficult.”
To proceed, the general and local phenomena of chronic articular gout are such as scarcely lend themselves to succinct definition, and for their description we would refer the reader to the chapter dealing with its clinical aspects. As that careful observer Sir Alfred Garrod states: “Chronic gout is at times confined to one or two joints, but sometimes numerous articulations are involved.” In other words, chronic articular gout may be mono-, oligo-, or poly-articular in distribution; and naturally the process of differentiation is modified accordingly.
This being so, I purpose dealing in the first instance with chronic monarticular gout, and in succession with the types of oligo- and poly-articular location.
CHRONIC MONARTICULAR GOUT
Occasionally gout in its recurrences clings obstinately to the great toe and tarsal joints. But since the advent of radiography there should be little or no difficulty in differentiating a chronic gouty arthritis of the great toe from the only other arthritic lesion with which it is likely at this stage to be confounded, viz., osteoarthritis. But at the same time we would refer the reader back to the chapter dealing with the differential diagnosis of the localised variety of acute gout, as therein we dealt fully with other possible sources of fallacy, i.e., static deformities, etc. We shall therefore now proceed to discuss those exceptional cases in which chronic gout is located not in one of the small, but in one of the larger, articulations.
MONARTICULAR GOUT IN LARGE ARTICULATION A RARITY
Given a chronic arthritis of one of the larger joints, say the ankle, knee, or elbow, we should be careful not to jump too readily to the conclusion that it is of “gouty” nature. The more obscure it appears the more need for caution. Needless to say, if the objective changes be but minimal and the condition be, so to speak, practically a mere arthralgia, there rests upon us the paramount necessity of careful discrimination before labelling it as “gouty” in kind.
Thus, if it be the knee, it may be a referred pain due to hip disorder, e.g., osteoarthritis or tuberculous disease, or it may be symptomatic of an inflammatory process, or, having regard to the usually mature or advanced age of the subject, it may be a neoplasm in the bones.
On the other hand, suppose the subject come complaining not much of pain in his joint, but more troubled because of its enlargements. If now on examination we find also that there is little or no tenderness, but simply a condition of peri-articular thickening or intra-articular effusion, what shall be our method of procedure? Certainly not to leap forthwith to the conclusion that it is gouty. No, not even if he exhibit tophi in his ears.
Now, as to pain and tenderness, it is a blessed feature of gouty arthritis that, generally speaking, in the chronic forms pain becomes much attenuated. But let us at the same time recollect that syphilitic arthritis, both secondary and tertiary, is relatively painless. But it is the much rarer tertiary form, be it remembered, which is usually monarticular. By the bye, too, we should never forget that a Charcot’s joint is also painless.
Coming now to the objective phenomena, is the case predominantly one of peri-articular infiltration or intra-articular effusion? As to the former, while you never know, still tuberculous joint disease is exceptionally rare at the age at which we usually meet gout. On the other hand, gummatous synovitis, with or without osteoperiostitis, is occasionally met with. It is just such a case as this that may be confounded with gout, the irregular lumpy thickening of the sub-synovial tissues with effusion being wrongly attributed to a gouty process with uratic deposits. Do not be misled if a history of injury be forthcoming in such cases, for it is not uncommon and may be given in good faith.
Now what if synovial effusion of chronic or recurring form be the striking objective feature of the case under review? In this event always recollect that of all the causes of monarticular disorder injury is far and away the most frequent. Not a few cases of monarticular joint disease come annually to the Royal Mineral Water Hospital, Bath, under the diagnosis of “gout” and “rheumatism.” But in all too many the symptoms are referable in truth to ligamentary strain, displaced cartilage, or foreign bodies, lesions always to be sought for and excluded in monarticular joint affection. Duckworth has it that hydrarthrosis is met with in chronic articular gout, in his deforming variety. He states that “hydrarthrosis is less commonly due to gout than to rheumatism,” but, we would remark, apart from traumatic lesions, more commonly due to gonorrhœa or syphilis than to either of them.
But the reader may say, this dissertation notwithstanding, Where does gout come in? Precisely so, and if his experience tallies with mine, he will find that chronic articular gout localised in one of the larger joints, and one only, is exceptionally rare. Personally, I should never feel justified in making the diagnosis unless I had elicited a history of (1) recurring classic outbreaks in the great toe with (2) an absence of traumatic infective and nerve arthropathies and, on the other hand, (3) demonstrable existence of uratic deposits in situ in the peri-articular tissues, the cartilage or bones as revealed by skiagraphy, or in the related bursæ.
In conclusion, if all these various pitfalls have been avoided, it will almost without exception be found that the final differentiation in doubtful cases will rest between gout and osteoarthritis; and in the vast majority, I had almost said all, it is the latter morbid process that will be found responsible.
This all too lengthy disquisition will not have been in vain if it instil caution. For it is in the monarticular types of joint affection that errors of catastrophic proportion occur more commonly than in any other form of joint disorder.
CHRONIC GOUT OF OLIGO-ARTICULAR DISTRIBUTION
The course of chronic articular gout, as has been observed, may be chequered by acute outbreaks involving three, four, or more of the larger joints. But, apart from this, there are those so-called asthenic and afebrile types of gout in which two or more joints may be the seat of a chronic gouty arthritis. In my experience it is the knees that are most frequently attacked. The joints are enlarged, the seat of more or less effusion, but the distinctive feature is the presence of deformity due to the irregularly rounded or ovoid swellings produced by uratic deposits. Enlargement of the patellæ is also present, and they lose their sharp edges, and sometimes they as well as the neighbouring articular ends are studded with small bony outgrowths, but of minimal size compared with those met with in osteoarthritis. The related bursæ, too, are often the seat of deposits, a valuable clue to diagnosis. Needless to say, such marked cases are nearly always the outcome of oft-repeated attacks, the ultimate deformity being the result of successive accretions of urate of soda laid down in the trail of the exacerbations.
ITS CONFUSION WITH CHRONIC VILLOUS SYNOVITIS
The frequency with which this misconception occurs is very noticeable. If a middle-aged woman of florid complexion and corpulent habit begins to complain of pain and stiffness in her knees with more or less swelling thereof, there is a very prevalent tendency to attribute not only her joint disorder to gout, but any gastric or nervous symptoms that she may simultaneously complain of are translated as being confirmatory of the assumption. It gathers weight too from the traditional and widespread belief that “the change of life” is the period par excellence at which women develop the morbid vagaries associated with “irregular gout.”
Now, as Bassett Jones and I have pointed out in a previous work, this condition, symmetrical villous synovitis of the knees, is a very common joint disorder in women at or near the menopause. Frequently they give a history of numerous pregnancies, or of rapidly increasing obesity, while with or without this latter they display a faulty postural attitude, indicative of lowered muscular and ligamentary tone. Following in the wake of these, the subject develops a symmetrical flatfoot, which, according to the stage at which it is seen, may be of flexible or rigid type.
Now, such is the mutual static interdependence of the component parts of the lower limb that this condition of flatfoot promotes or favours the incidence of villous overgrowths in the proximal joints, the knees. As to the modus operandi we have put forward the following explanation: “The everted foot, with its sunken arch, as before stated, determines an alteration in the normal coaptation of the articular surfaces in the knee, and this incongruence is revealed in skiagraphs by the marked prominence laterally of the external tibial tuberosity beneath the external femoral condyle. Coincidently, and for the same reason, additional strain is thrown upon the internal lateral ligament. This in turn favours a state of passive congestion or hyperæmia of the synovial membrane, which becomes relaxed and thrown into folds, especially at its reflexions near the edges of the cartilages. If, as often happens, the individual is the subject of varicose veins or suffers from a general lack of tone in her muscular or ligamentary structures, this tendency to venous engorgement of the knees is much enhanced.”
“Under the influence of these mechanical factors and their associated circulatory disturbances, thickening and enlargement of the synovial fringes ensue. The inflammatory condition thus produced tends to increase automatically, as, owing to the articular incongruence, the enlarged fringes are very prone to become caught between the joint surfaces; in other words, a vicious circle is produced, as with the increasing villous hypertrophy the liability to internal traumatisms increases pari passu.”
VILLOUS SYNOVITIS STATIC AND NON-GOUTY IN ORIGIN
In short, the joint disorder is fundamentally of static or mechanical origin, and, this being so, the results of anti-gouty treatment are open to a further misinterpretation. The victims, as we have said, exhibit very generally a tendency to obesity. Now, Ebstein and many others hold the view that obesity and gout have affinities. Ebstein, moreover, believes that treatment directed to the reduction of body weight will check the appearance of gouty arthritis or ameliorate the same when avowed. What happens is this: these corpulent subjects are placed on a special dietary. Hydrocarbon foodstuffs are limited, bread, amylaceous food and liquids being also restricted. Naturally, pari passu with reduction in their body weight, their overburdened joints become more equal to their office. But those who assume that the chronic arthritis is of gouty origin attribute, and, we think, wrongly, the beneficial results attained to correction of the underlying “gouty” habit.
We prefer to subscribe to the simpler or mechanical theory, and in view of the widespread and, as we believe, erroneous belief in the gouty nature of this arthritis, we take the liberty of appending the salient features of these cases, while adding further a few remarks on the differential diagnosis of other symmetrical affections of the knees which may also be wrongly attributed to gout.
CLINICAL SYMPTOMS OF VILLOUS SYNOVITIS
The onset is gradual and insidious. Stiffness is the salient symptom, but sometimes the subject is more distressed by a sense of weakness, distension and unreliability. Pain is slight or absent, save when during walking pseudo-locking occurs. The mobility of the joints is usually unimpaired, and if any limitation exist it is the power of full extension that is usually restricted.
Objectively the joint shows either general enlargement or swelling localised to the supra- or infra-patellar regions. Intra-articular effusion which comes and goes is a very characteristic feature. On palpation a peculiar soft silken crepitus will be heard and felt as the patient alternately flexes and extends the limb. The enlarged fringes are also easily to be felt as knots or nodules which can be moved up or down on the underlying bone. The ease with which they can be appreciated depends upon the degree of effusion present at the time. Judging from their symptomatology, it seems probable that some of the cases included in Sir Dyce Duckworth’s category, chronic deforming gout, are of this description.
The diagnosis of villous synovitis should not be considered complete without skiagraphy being undertaken to reveal or exclude osteophytic outgrowths. For the subjective symptoms and signs of early osteoarthritis are practically identical with those of villous arthritis, and although the presence of osteoarthritic lesions elsewhere would be suggestive, skiagraphy alone will enable us to effect a differentiation with certainty. Indeed, Bassett Jones and myself are strongly of the opinion that the life history of osteoarthritis involves two stages: (1) a primary or pre-osteophytic phase, often of prolonged duration, whose clinical characteristics are those of villous hypertrophy; (2) a secondary or terminal stage, in which bony and cartilaginous outgrowths make their appearance.
Other symmetrical disorders of the knees that may be wrongly ascribed to gout are hydrarthrosis and gummatous synovitis.
Bilateral Hydrarthrosis.—Given effusion into both knees which is passive, copious, and persistent rather than recurrent, then its possible infective origin must be carefully canvassed. The common sources are gonorrhœa, syphilis, and tubercle. The history or presence of an urethral discharge and detection of the gonococcus will identify the first named. In syphilis the existence of other lesions, the response to Wassermann’s test and specific treatment are the points on which to rely, and in tubercle, the detection of visceral foci and the sero-reaction will give the clue.
As to the intermittent type of hydrarthrosis, the remarkable periodicity in incidence of the effusion will suffice to obviate any possibility of confusion.
Peri-synovial and Peri-bursal Gummata.—Affecting as they do commonly the knee joints of adults, these may, in the absence of a history of infection, be a source of error. The uneven and nodular swelling may quite easily be confounded with uratic deposits. Pain is slight and mobility but little impaired. The presence of neighbouring scars, a positive Wassermann reaction, and a favourable response to anti-syphilitic therapy will clear up the diagnosis.
CHRONIC GOUT OF POLYARTICULAR DISTRIBUTION
The clinical portrait of tophaceous gout when of widespread distribution is one of the most striking to be met with in the whole domain of medicine, but for the broad outlines of the picture presented we would refer the reader to the chapter dealing with the clinical description of chronic articular gout.
In these polyarticular forms the most distinctive joint deformities are those met with in the hands or feet, more particularly the former. The excrescences produced are the outcome of successive uratic deposits. These latter when massive can scarcely be confused with any other disorder, for the superjacent skin, distended by the ever-increasing underlying uratic deposits, becomes thinned and purplish red in hue, and occasionally ulcerates. I have at present in my wards a case of this nature, and the subject hoards up the exuding “chalk” in a small bottle.
Fortunately such marked examples are relatively rare, though easily recognised; but it is the less marked types that occasion difficulty in diagnosis. The point at issue of course is the differentiation of moderate-sized or small tophaceous swellings from bony outgrowths. Frequently the task is impossible of achievement without resorting to puncture, when, if anything can be withdrawn, microscopic examination may reveal the presence of biurate crystals.
For the rest, attention to the following points will prove helpful in enabling us to differentiate clinically between gouty arthritis and other chronic joint disorders attended by deformities:—
(1) Tophi when of recent incidence are soft, and when of long standing are never so dense or so hard as bony outgrowths.
(2) The overlying skin is thin, and through its substance the subjacent white concretions may sometimes be discerned. It may be adherent, or the seat of ulcers.
(3) Uratic deposits are not located exactly at the level of the articulation. They do not adapt themselves to the contour or shape of the bone-ends.
(4) Unlike osseous growths, they may be slightly movable in lateral directions.
(5) Tophi may soften or disappear after exacerbations of arthritis.
DIFFERENTIAL DIAGNOSIS
The conditions likely to be confused with chronic polyarticular gout are osteoarthritis, rheumatoid arthritis, and the multiple arthropathies met with in affections of the central nervous system.
OSTEOARTHRITIS
Its chief characteristics may be summarised as follows:—It is a disease rarely met with under forty years of age. The mode of onset is generally insidious, never really acute. In this respect it contrasts with gout, the initial outbreak of which is invariably acute. Osteoarthritis attacks both sexes equally. Although it may be polyarticular, its specific tendency is towards a mono- or, more accurately speaking, oligo-articular distribution, with no marked leaning to symmetry. It has a pronounced predilection for attacking the hip, the shoulder, and the spine—sites rarely, if ever, attacked by gout.
Unlike gout, constitutional symptoms, pyrexia and so forth, are generally absent; muscular atrophy is slight, hardly ever pronounced, likewise muscular spasm and contracture.
LOCAL CHARACTERS OF JOINT SWELLINGS
These are best appreciated in the small joints of the hand. Osteoarthritis has an affinity for terminal joints—the so-called Heberden’s nodes. Another favourite site is the carpo-metacarpal joint of the thumb, while the preference of gout is for the metacarpo-phalangeal joint thereof and for the same articulation in the other digits.
The overlying skin, as a rule, is unchanged, and never assumes, as in gout, a dusky red or purplish hue. The margin of the articular surfaces, instead of being smooth and rounded, is broken and irregular, its nodular contour being due to osseous outgrowths studding the line of junction of the bones entering the articulation.[42]
In this respect they contrast with tophi, which are located near to, but not at, the level of the joint fissure. Again, unlike tophi, bony outgrowths are fixed, immutable, undergoing no change save in the direction of progressive enlargement. While the tendency of an osteoarthritic joint is to expand and increase, still the enlarged and gnarled joints never attain the colossal bulbous appearance presented by inveterate examples of tophaceous gout.
RHEUMATOID ARTHRITIS
This affection differs from the foregoing disorder as well as gout in that it is most commonly met with in persons under forty years of age. Moreover, it attacks women much more frequently than men. Of polyarticular distribution, it evinces a marked tendency to symmetrical invasion. Like gout, it has a pronounced preference for the smaller joints, while, similarly, it avoids the hip and shoulder.
Constitutional symptoms are conspicuous: pulse quickened, temperature raised, extreme wasting not uncommon. Intense and widespread muscular atrophy with contracture is a prominent feature, also trophic disturbances of varied nature and degree.
LOCAL CHARACTERS OF JOINT SWELLINGS
In early stages the skin over the joint is waxy white or semi-asphyxial in tint, outline of joint smooth, rounded, and spindle in shape, with, as a rule, no irregular bony projection at the level of the articulation. If seen at a later stage, the swollen joint will be found shrunken from atrophy of all the articular structures as well as the skin. Ultimately it becomes reduced even below its normal size, the small “end-joint” of atrophic or rheumatoid arthritis. The deformities due to muscular spasm are usually in the direction of luxation and hyperextension, and differ from those of gout and osteoarthritis, in which there is more generally lateral displacement.
NERVE ARTHROPATHIES
The joint disorders incidental to tabes and syringomyelia do occasionally find their way to spas for treatment under the mistaken conception that they are instances of “gout,” “rheumatism,” or “rheumatic gout.” In the case of tabes the mistake is often referable to the confounding of its lightning pains with “gout” or “rheumatism,” with subsequent relegation of the swollen joints, whether single or multiple, to one or other of these categories. In the syringomyelic it is, I think, the close resemblance that obtains between the joint lesions and those of osteoarthritis or so-called “rheumatic gout” that accounts for their uncalled-for and utterly useless transference to spas. I have known a case of syringomyelia with multiple arthropathies in the hands sent to Bath under the mistaken idea that they were of “gouty” origin.
These remarkable joint affections will be distinguished by their fulminant onset with marked effusion and absence of pain, tenderness, and heat. In addition, associated phenomena will be present, viz., ataxic pupillary changes and lost knee-jerks in tabes, while syringomyelia is characterised by dissociated anæsthesia, trophic disturbances of bones, progressive muscular atrophy with paralysis.
HÆMOPHILIC ARTHRITIS
It will be recalled that Rieken held the view that so-called “bleeders” were prone to attacks of gout, and that sometimes these alternated with intra-articular hæmorrhages. Nor was he devoid of supporters, for Sir Dyce Duckworth maintained that a definite hereditary relationship obtained between gout and hæmophilia, while that astute observer Jonathan Hutchinson also contended that the vascular weakness was the outcome of gout and aggravated by serial hereditary transmission. Wickham Legg, however, in his masterly contribution questioned the correctness of Rieken’s proposition.
Personally, I cannot out of my own experience confirm or rebut the view that “bleeders” come of gouty stock, nor have I ever met an avowed gouty subject who was likewise the victim of hæmophilia. Quâ its joint complications, hæmophilia to our mind would appear to display closer affinities with peliosis rheumatica than with gout; but, in view of Duckworth and Hutchinson’s claims, it were wiser on our part to withhold judgment, while paying them the deference of being alive to the possibility of there being some obscure connection, though not proven, between the two disorders. Again, as emphasising the necessity for discrimination, we would draw attention to the fact that Konig recognised three stages in hæmophilic arthritis: (1) hæmarthrosis; (2) an inflammatory process, with pyrexia and spindle-shaped swellings apt to be confused with tuberculosis; (3) extensive arthritic changes reminiscent of arthritis deformans. Confusion with gouty arthritis clearly is only likely in the second or third stages, and in the matter of diagnosis the personal and family tendency to hæmorrhages is the most important clue.
XXIII. CLINICAL DIAGNOSIS (continued)
SKIAGRAPHY
As an aid to the differentiation of gouty from non-gouty forms of arthritis skiagraphy has scarcely fulfilled the somewhat optimistic claims at one time made on its behalf. As to acute gout, radiography reveals nothing abnormal in the bones, though Tousey holds that this of itself at once enables us to exclude osteomyelitis, which, he says, “these cases sometimes resemble.”
Turning now to chronic articular gout, Huber in 1896 drew attention to certain focal areas of rarefaction, or diminished density, in the distal extremities of the phalanges. These localised transparent areas in the bone-ends are discrete, circular, or oval in shape. When located near the edges of the bones, they are of segmental contour, and, viewed in profile, give the appearance of small punched-out holes, simulating syphilitic dactylitis. Despite their proximity to the diseased joints, they apparently do not communicate with the articular cavities.
These bony changes Huber held distinctive of gout, and Koehler, Drinberg, and Jacobsohn and other subsequent writers confirmed Huber’s findings, and, like him, held these areas of rarefaction to be the result of uratic deposits at their sites. Strangeways has dissected bones in which these transparent areas were demonstrated by X-rays. The examination revealed that the bone was definitely excavated, filled with a gelatinous-looking substance, and in advanced cases of gout, moreover, a characteristic deposit of urates clung, as it were, to the margins of the cavities.
Similar focal areas of decreased density were noted by Strangeways in certain cases of rheumatoid arthritis, and both he and Burt found it impossible on the X-ray findings to differentiate between these and gout, i.e., without invoking the aid of clinical data.
Apart from these transparent areas, Wynne many years ago pointed out that small nodes or bony deposits are sometimes met with flanking the sides of the phalanges. More recently Ironside Bruce by radiography has again drawn attention to these bony outgrowths near the extremities of the phalanges (Bruce’s nodes). At first these were thought by Bruce to be composed of urates, but Strangeways from a study of macerated specimens has demonstrated their true bony nature, and also that uratic deposits are not opaque to X-rays, as was formerly thought.
In skiagrams of chronic gout all stages of ankylosis may be seen in the interphalangeal joints. In some it is merely fibrous, in others merging therefrom into bony, and not infrequently true synostosis is observed. Deflections or subluxations are frequent features, due either to the thrust of tophi or small bony outgrowths or to peri-articular contractures.
So much for the skiagraphic findings in chronic gout, and now to discuss their valency as aids to diagnosis of this arthritic disorder. The chief controversy centres around the significance of the focal areas of rarefaction which have been found in the bones of the wrists, hands, ankles, and feet of gouty subjects. Here we may comment on one grave handicap, viz., the lack of certainty as to whether the cases radiographed by different observers were true instances of gouty arthritis.
To justify our expression of doubt we may take, for example, the series reported by Drinberg and Jacobsohn. The said “transparent areas” were present in all the eighteen cases, but the presence of tophi was only established in three. Now, as McClure and McCarty rightly contend, “since the tophus is the only universally accepted pathognomonic sign of gout, for studies of that disease only those patients should be chosen in whom tophi are found, and sodium urate crystals from them microscopically demonstrated.” No one can, I think, gainsay the legitimacy of this stipulation.
In accordance with their contention, McClure and McCarty record their radiographic findings in a series of cases all of which exhibited tophi, and from which sodium urate crystals were isolated. Now, in all these cases the focal areas of diminished density, generally held to be peculiar to gout, were present; but they add that “similar changes were present in two other cases which were clinically gout, but in which no tophi were demonstrated.” Also “in another case without tophi, but which was clinically gout, the focal areas of decreased bony density were not found.”
In addition, they examined the skiagrams of 100 cases of chronic arthritis which “had not been diagnosed clinically as gout.” In thirteen of the examples “the focal areas of decreased density, the so-called gouty bony changes, were found, and were fully as well defined as in the cases of true gout.”
Judging from the skiagraphic appearances, there seemed no reason to suppose that the factors responsible for the production of these rarefied areas were in any way different from those at work in true gout. Now, most authorities have claimed that the bony changes were due to uratic deposits in the bones; but it is at least possible that their origin may be otherwise explained.
Thus Nichols and Richardson have shown that, given focal absorption of lime salts, changes apparently identical with those currently attributed to the presence of tophi may result. These same, though they may not be demonstrable either macroscopically or microscopically, are detectable by X-rays.
Such foci of absorption, viz., areas of decreased density, frequently are located in regions subjected to pressure. Thus they may occur at the inner surfaces of the heads of the first metatarsal bones, or they may form underneath large tophaceous deposits in the soft tissues.
Now, Strangeways has shown that it is impossible by radiography to detect tophi in bones. Accordingly we have at present no means of deciding in any given case whether the localised transparent areas in the bones are due to tophi or to focal absorption of lime salts. If we are to cling to the conception that they are due to tophi, then it is clear that tophi in the bones are more common than is currently suspected, and that, ergo, the frequency of gouty arthritis is underestimated. For these transparent foci in bones, according to McClure and McCarty, occur in from 10 to 12 per cent. of cases of chronic arthritis “which clinically are not gout.”
Yet these authorities hold that, despite the fact that they occur in cases of non-gouty arthritides, they have some diagnostic significance. For, taking the work of other observers in conjunction with their own observations, they come to the following conclusions:—
(1) The focal areas of decreased density, heretofore considered as peculiar to gout, are rarely absent in that disease.
(2) Their absence would be some evidence against the existence of gout in a given case.
(3) On the other hand, their presence is no more than suggestive of gout, since they are found in from 10 to 12 per cent. of cases which clinically are not gout.
(4) The focal areas of decreased density, usually held due to tophi, are probably very often merely focal areas of absorption of lime salts.
In continuation these authorities have endeavoured to identify the nature of the arthritis that occurs in gout. Like other workers in this sphere, the study of the radiographs obtained of gouty joints reveals that a variety of changes occur in the bones and joints of the hands and feet in gouty subjects. These, they consider, may be classified conveniently as follows:—
(1) Cases marked by focal areas of rarefaction, without any other perceptible change;
(2) Cases presenting, in addition to these translucent areas, minor degrees of lipping at the articular margins;
(3) Cases in which the changes in (1) and (2) are conjoined with either localised atrophy of the bones entering into an affected joint, or with generalised atrophy of all the bones in the affected limb;
(4) In addition to all the above changes, narrowing of certain joint spaces with marked proliferative and atrophic changes occurs.
In reviewing these findings of McCarty and McClure, it is important to recollect that they were found in a series of cases all of which exhibited tophi. Moreover, it will be seen that the radiographic changes in some are reminiscent of atrophic or rheumatoid arthritis, in others of hypertrophic arthritis or osteoarthritis, while, lastly, the appearances typical of infective arthritis are also represented. In addition, if we recall that focal areas of rarefaction, indistinguishable from those met with in gout, also occur in all types of non-gouty arthritis, we at once see how impossible it is to detect anything in the radiographic findings distinctive of gouty as opposed to non-gouty arthritides.
McClure and McCarty, comparing the radiographic changes in gouty as opposed to non-gouty arthritis, observe that, though rarefactive foci occur in all varieties of non-gouty arthritis, they are conjoined with other bony or joint changes. On the other hand, translucent areas unassociated with any bone or joint alterations have been found only in gout. But whether this can be claimed as distinctive of gouty arthritis is, they think, uncertain, since relatively few opportunities for X-ray examination of non-gouty arthritis in its early stages have been forthcoming.
Continuing, of their four radiographic types of gouty arthritis the second resembles osteoarthritis; but the third and especially the fourth group, they consider, “fall into a peculiar class,” this inasmuch as their characters resemble the infective type of non-gouty arthritis. They claim, however, that a differentiation, radiographically speaking, can be effected, this because of the “sharply localised” extreme degree of bony atrophy which occurs in the infective type of non-gouty arthritis. However, as they admit that radiographs of the latter (infective non-gouty arthritis) have been noted which “closely resemble” the “atrophic and proliferative changes occurring in gout,” their final conclusion is that in the skiagrams even of typical gouty arthritis there is nothing in the bony or arthritic changes that is diagnostic of gout.
For myself, I must admit that I have come to the same conclusion as McClure and McCarty, viz., that the skiagraphic findings in gouty and non-gouty arthritis trench so much the one upon the characters of the other that I should be loth indeed to base a diagnosis of gout simply on the revelations of skiagraphy. The chief interest to my mind, as I have previously observed, centres round those examples in which peri-articular tophi are associated with underlying bony and arthritic changes (as revealed by X-rays) indistinguishable from those typical of infective arthritis of non-gouty type.
We have seen also that local foci of rarefaction may be met with in infective arthritis of non-gouty type. Moreover, the proliferative and marked atrophic bony changes found in some instances of gouty arthritis are quite compatible with their infective origin. Witness how impossible it is to differentiate skiagraphically between atrophic arthritis and gouty arthritis, and at the same time let it not be forgotten, on the other hand, that the dividing line between the infective arthritides and the more acute forms of atrophic or rheumatoid arthritis is by no means sharply defined. Review this also in light of the fact of the close resemblance that obtains between acute articular gout, especially the polyarthritic variety, and types of arthritis of avowedly infective origin, and we see at once how close is the clinical similitude. We turn to radiography, and here again we are met with the same family resemblance, suggestive of a probable community of origin. How clear then the inference that it is on tophi, and tophi alone, that we must base an absolute diagnosis of gouty arthritis. Moreover, since tophi are not detectable by skiagraphy, our mainstay must be physical examination directed to their detection. As for those cases of so-called “clinical gout,” viz., unattested by tophi, it is probable that their absolute identification, as such, will never be attainable on purely clinical, but on bacteriological, data, which, it is to be hoped, will before long be forthcoming.
DIFFERENTIAL DIAGNOSIS
Infective Arthritis.—According to Goldthwait, of Boston, no changes can be detected by skiagraphy in bone or cartilage in infective arthritis. The density of the former is in no way diminished, while the cartilage retains its normal thickness. If, however, the infective arthritis is of destructive character, new bone may be thrown out in the process of repair. If then in such cases sole reliance be placed on the X-ray appearances without any reference to the clinical history and course of the disorder, then, as Goldthwait says, this irregular formation of bone is likely to be confused with the X-ray findings in osteoarthritis. It is, however, possible, according to him, to distinguish the nature of the case by careful scrutiny of the skiagraphs.
The new formation of bone in these destructive forms of arthritis conforms in every way to that seen as a result of septic osteitis or periostitis. In other words, the osteophytic outgrowths take origin at the focus of infection, wherever that may be, and not, as in gout and osteoarthritis, at the margin of the cartilage. Still one must recollect that in gout exostoses (Bruce’s nodes) develop sometimes at the sides of the phalanges. These outgrowths are not peculiar to gout, but may be met with in infective forms of arthritis. I am inclined therefore to refer their origin to a local osteitis or periostitis of infective source. That Bruce’s nodes, though not diagnostic of gout, are frequently met with therein, is, I submit, but further evidence of the intrusion of an infective element in the genesis of gouty arthritis.
Hypertrophic or Osteo-arthritis.—This is marked by proliferative changes at the margins of the articular ends of the bones. With the advance of the disease the shafts of the related bones become increasingly dense. In chronic gout, too, the margins of the cartilages may be studded with little nodules. Radiographically speaking, they cannot be distinguished from those met with in osteoarthritis, save only that they never attain the massive size met with in the latter disorder. The diagnosis in doubtful cases will practically always rest on the clinical history, and more pertinently on the presence of tophi.
Rheumatoid or Atrophic Arthritis.—If the changes in the cartilage and bone in osteoarthritis are active and proliferative, these same in rheumatoid arthritis are retrograde and passive in character. In short, hypertrophy of these structures in the former, atrophy in the latter, constitute the distinguishing features.
The morbid process in the articular ends in rheumatoid arthritis is one of rarefaction and softening. The cartilage may undergo total or partial absorption, a change to be detected in the very early stages. The bones participate in the pathological change, the first evidence of which is an abnormal translucency to the rays, usually, but not always, confined to that portion of the shaft entering into the joint. Eventually the articular ends of the phalangeal and metacarpal bones may undergo erosion, in some cases to a very marked degree, the bones more or less telescoping into each other.
Now, owing to the fact that in gout also considerable disintegration of the bone may result, the appearances in some instances may resemble those found in the skiagraphs of rheumatoid joints. Stress has been laid on this similarity by Strangeways, and it was also previously remarked by Goldthwait. The latter, however, claims that while in atrophic or rheumatoid arthritis the bone, though thin, maintains its outline, on the other hand in gout the outline of the bone is not distinguishable owing to its more complete destruction by the morbid process. Goldthwait holds that the resemblance of chronic articular gout to rheumatoid arthritis is most noticeable when the articular ends of the bone in both instances are the seat of the disease. In other examples, however, the shafts of the bones being affected by the gouty disorder, they may show punched-out areas. These latter, however, are but focal areas of rarefaction seen in profile, and inasmuch as they may be met with in infective arthritides of non-gouty type, too much reliance cannot be placed on their presence as distinctive of gout, much less as a criterion of differentiation from other arthritides.
We have to remember, too, that marginal proliferative changes may occur in rheumatoid arthritis. They are, like those met with in gout, miniature replicas of the bony outgrowths of osteoarthritis.
In conclusion, the resemblance between the skiagrams of chronic gout and rheumatoid arthritis is so close as absolutely to forbid our sole reliance on skiagraphy to effect a differential diagnosis. In short, skiagraphy, though of great and probably increasing value, cannot for one moment be allowed to usurp the place of careful clinical observation, to which it must be held always subsidiary. Last, but not least, pending fresh radiographic revelations, our diagnosis of chronic articular gout and alike its differentiation from rheumatoid arthritis and other arthritides must rest on the one unimpugnable criterion, the presence of tophi.
XXIV. IRREGULAR GOUT
“It is not a sacred disease. There will therefore be no profaneness in handling it freely,” affirmed Benjamin Rush of gout some hundred years since.
Nevertheless one approaches with diffidence this debatable ground, so hedged in by high sanction and tradition. Albeit reverence for authority must, in the interests of progress, be tempered by that spirit of inquiring scepticism which would sift the chaff from the grain, this the more emphatically in that of all morbid conditions “irregular” gout, by the very vagueness of its clinical content, lends itself the more easily to unbridled inference, hazardous conjecture, and fanciful surmise.
As for the unlicensed freedom too often exercised in relegating disorders to this category, Rush would appear to have out-heroded Herod, pace the following rhetorical reflections, for they could scarcely rank as clinical observations. “The great toe and the joints of the hands and feet are no more its exclusive seats,” said Rush, “than the stomach is the throne of yellow fever. In short, gout may be compared to a monarch whose empire is unlimited. The whole body crouches before it.... The gout affects the glands and lymphatics. It produced a salivation of a profuse nature in Major Pearce Buller, which continued for two days. It produced a bubo in the groin in a citizen of Philadelphia. He had never been infected with the venereal disease. Of course no suspicion was entertained by me of its being derived from that cause.... Scrofula and all the forms of dropsy are the effects in many cases of a disposition of the gout to attack the lymphatic system.... A distressing collection of air in the rectum, which renders frequent retirement from company necessary to discharge it, is likewise a symptom of gout.”
It is difficult to conceive that any such pronouncement could have emanated from a physician of Rush’s standing and repute, a contemporary, be it noted, of Heberden, to whose masterly commentaries on the history and cure of gout all posterity is indebted. Nevertheless as recently as 1854 Sir Spencer Wells claimed that “any attempt to describe the nervous diseases of females caused by gout would lead to an enumeration of almost all forms of their diseases, especially those usually considered as hysteric. The intestinal derangements with tympanitis, neuralgia, or colic, the hysteric pain in the right epigastrium, the cardialgia and gastrodynia, the hysteric vomiting and epigastric spasms, the morbid sensibility of the pharynx and fauces, hysterical palpitation, asthma or bronchitis, loss or alteration of the voice, some forms of hysteric paraplegia or hemiplegia more or less complete, chorea or tetanus, some of the curious paroxysmal affections observed in hysteria, and all the varieties of neuralgia and simulated inflammation, commonly called hysteric, frequently arise from the presence in the blood of the impurities which are the true characteristics of gout.”[43]
Truly, in light of this heavy indictment, one scarcely wonders that Rush classed the domain of gout as limitless. But one must recollect that, nosologically speaking, our forefathers were sadly hampered. Anomalous symptoms and disorders had to be referred to one or other of the available titles of disease, and what term more elastic than the timeworn “gout,” so easy to saddle with vicarious responsibilities?
But pari passu with advancing knowledge of the pathology of the nervous system and the rise of hysteria to the status of a clinical entity gout was shorn of the excrescences heaped on it by Laycock, Wells, and others.
But nevertheless the emancipation of gout from nervous and other alien disorders was slow of achievement, and largely, I think, through the wide acceptation of Murchison’s theory of a pathological state allied to gout and termed by him “lithæmia,” or the “uric acid diathesis.”
According to this authority, the deposit of lithates in the urine is a “manifestation of a morbid condition of the blood and of the entire system,” the outcome of a functional derangement of the liver. Such hepatic disturbance might endure for years without manifesting any other symptom than a frequent deposition of urates and occasionally uric acid in the urine. But, added Murchison, the same if neglected “may ultimately be the means of developing gout.”
Clinically it manifested itself by a variety of symptoms—depression of spirits, irritability, lethargy, headache, pains and aches in the limbs, vertigo, insomnia, dyspepsia, palpitation, raised blood pressure. Such were the motley group of disorders affiliated by Murchison to lithæmia. But his disciples, more ardent, set no limit to the manifestations of uric-acidæmia.
Not only gout, but rheumatism and allied disorders, were amongst its progeny, and Osler tells us that one writer enumerates not fewer than thirty-nine separate morbid conditions associated with lithæmia. But leaving aside the extravagant claims of Haig and his followers, the impression even now is but too prevalent that gout and lithæmia are convertible terms. There is little or nothing to justify the assumption that an increased output of uric acid in the urine or deposition of urates therein is diagnostic of gout. Such, moreover, presupposes the further assumption that uric acid is the cause of gout.
We may affirm that certain symptoms betoken malassimilation of food or defective tissue metabolism. But it is by no means certain, as Murchison held, that a functional disorder of the liver is the fons et origo mali, much less that uric acid is the sole noxious substance. Yet in a masterly discussion of the subject Pratt, of Boston, tells us that as recently as 1895 a “leading clinical teacher” affirmed that “headache, migraine, depression of spirits, shooting pains, cramps, palpitation, vertigo, are a part of the symptomatology of lithæmia.”
Surely, if we are to make any pretence of reducing the phenomena of lithæmia or irregular gout to a scientific precision worthy of the present status of medicine, we should fight shy of such sweeping assertions. The caveat, we fear, is not superfluous. For as that judicial physician, Austin Flint, once satirically observed, “the designation ‘uric acid diathesis’ is used by some physicians in a rather indefinite way to describe various morbid states which may not at any time be accompanied by deposits of urates, and in which there is no proof of an excess of uric acid in the blood.”
Caustic as was this stricture, it was no less prophetic than apposite. For recent blood analyses have, as Pratt states, demonstrated that there is no increase of uric acid in the blood in that medley of disorders attributed by Murchison and his followers to “lithæmia,” or “the uric acid diathesis.” Here we would inveigh strongly against the too prevalent habit of stigmatising as “gouty” such symptoms as headache, vertigo, palpitation, etc., not only without any evidence of their being of this nature, but frequently when no attempt has been made to eliminate “errors of refraction,” aural disorder, etc. Moreover, granted that such possible sources have been excluded, we have no justification in invoking “gout.” For, as noted, all modern observations fail to demonstrate the presence of uricæmia. Under such circumstances, given that the anomalous symptoms are inexplicable, would it not be wiser to content ourselves with the assumption that their presence postulates, not lithæmia, but a toxic condition of the blood plasma? This at least carries with it the inference that a search should be made for the focus of toxic absorption, whereas for but too many the term lithæmia, even when undemonstrated, is held to be self-explanatory and final.
Turning to another aspect of this subject, we are reminded by Duckworth that Hutchinson “directed attention to various maladies affiliated with what he terms rheumatic gout and gout, but differing somewhat from both, and these include various eye troubles, such as iritis, hæmorrhagic retinitis, and some forms of glaucoma, lumbago, sciatica, chronic rheumatoid arthritis, Heberden’s nodes, and possibly hæmophilia.”
As to the so-called “gouty” origin of the various eye troubles, these will be dealt with separately by Mr. Beaumont in his section. For the rest, hæmophilia may, we think, be safely discarded, Heberden’s nodes relegated to osteoarthritis, while rheumatoid arthritis has long since vindicated its claim to clinical individuality.
But as to lumbago and sciatica, these cannot be so easily disposed of, as a reflection of Heberden’s brings home to us. “It must be owned,” says he, “that there are cases in which the criteria of both are so blended together that it is not easy to determine whether the pain be gout or rheumatism.” Our own attitude towards this vexed point was precisely defined in a previous chapter in which we dealt with the affinities between gout and other diseases.
Having dealt with the broader and more extravagant claims made on behalf of the clinical content of irregular gout, we now restrict our purview to those disorders, chiefly visceral in site, which even to-day are referred by some to this category. We shall in the first instance deal with that variety known as retrocedent gout, and shall subsequently proceed to discuss other so-called irregular manifestations of the disorder.
RETROCEDENT GOUT
The term retrocedent or suppressed gout still lingers in medical nomenclature, largely, we think, as a tribute to tradition, for rarely indeed is it invoked in current literature. Known since the days of Galen and Aretæus, it originally signified a condition in which sudden inhibition of the acute joint affection is followed by or coincides with the development of serious internal symptoms referable either to the gastro-intestinal, cardio-vascular, or nervous system. Thus, there may be, e.g., vomiting, diarrhœa, dyspnœa, cardiac arrhythmia, cerebral hæmorrhage, delirium or coma.
Naturally for our forefathers the abrupt subsidence of the joint disorder with the incidence, as fulminant, of severe and alarming visceral symptoms appeared to be an example of true metastasis. That death, tragically sudden, so often ensued, but rendered more imperious the necessity for explanation; and, in the then state of knowledge, the proffered assumption could hardly be regarded as anything other than a perfectly legitimate and useful hypothesis.
The retrocession of the articular affection in acute examples of gout ensues abruptly, but in chronic types it usually transpires more gradually. Often no cause is assignable, but frequently the so-called metastasis has followed exposure, chill, or the imprudent application of cold to the inflamed joints. The late Dr. Parry, of Bath, in one winter saw two instances of apoplexy follow “the removing of gout in the extremities by immersing the feet affected in cold water.” In some, following the same revulsive procedures, severe cardiac pain has ensued with syncopal attacks, sometimes fatal, while in others gastro-enteric symptoms of like gravity have developed.
It is the asthenic types of gout that, according to Duckworth, are most prone to metastasis. When the phenomena occur rapidly, flitting from place to place, they have been designated “flying gout.” Nevertheless, as before said, the most dramatic examples arise in acute sthenic gout, though in their instance less likely to occur spontaneously than in sequence to depressing external agents, e.g., cold lotions, etc.
Reviewing the recorded examples of retrocedent gout in the light of latter day experience, it is, we think, most significant that no such dramatic examples apparently occur nowadays, at least none to which the term “retrocedent gout” appears applicable. The designation, indeed, bids fair to become obsolete. What then is the explanation? That even to-day cases of acute articular gout yield to, or are replaced by, functional visceral disturbances, of varying degrees of gravity, is certainly true. But, partly through increase of knowledge and partly through the growth of a more critical attitude, we seldom, if ever, feel justified in ascribing them to gouty metastasis.
Take “gout in the stomach,” to which organ, in the days of the Regency, it appeared to fly on the slightest pretext, a “vulgar belly-ache taking rank by courtesy” as such, before Sir Thomas Watson pricked the bubble of these pretentious ailments by his suggestion that “gout” (so called) in the stomach sometimes turned out, under the test of an emetic, to be nothing more than pork in the stomach. A caustic stricture, but doubtless well merited. For the symptoms held typical of “gout in the stomach” are but those of gastric irritation, with nothing to suggest that they are of “gouty” origin.
Again, as Brinton in his classic exposure of this clinical myth observes, some of the recorded instances doubtless derive their melodramatic aspects from unrecognised biliary colic. As he rightly says, some of the cases instanced by Scudamore were jaundiced usque ad unguem. Gallstones, too, are among the many derivatives of the so-called “gouty” habit. The age incidence of both disorders is identical, whence doubtless the conception of the relationship. But what of the abdominal catastrophes attached to gallstones, all wholly unguessed at in those days? What, too, of the unrecognised and doubtless frequently coincident renal disease, with its menace of uræmia—pain, vomiting and prostration, not to mention Buzzard’s reflection that some cases of gout in the stomach were probably referable to gastric “crises,” i.e., tabes dorsalis?
If we recall that none of these sources of fallacy—and we have named but the more common—were eliminated, and also the absence of any anatomical proof post mortem of gastric lesions, one may well ask with Brinton, “Is there any ‘gout in the stomach’ left after the subtraction of these various affections?” Personally, I can say with Brinton that “I know of no such case; have never seen one; have never been able to get trustworthy evidence of one from some of the most accomplished physicians living, or from the best records.”
Reverting to the cardiac and cerebral phenomena that have sometimes followed the retrocession of acute gout, the same difficulties confront us. The conclusion that they are examples of retrocedent gout is drawn from premises which really do not support it. Strictly speaking, there is nought but the time relation to go upon, and the laconic comment “Non sequitur” is obvious.
To continue, the more we know of the causes and effects of disease, the less relevant becomes the time relation, and the nearer do our conceptions of cause and effect approximate to the more truly valid conception of ground and consequence. But what grounds have we for assuming that the anginal, the syncopal attack, or the apoplexy is the consequence of gout, that it is exclusively due to the materies morbi of gout?
The very disparity between the local lesions seems to exclude the possibility of their being due to one and the same cause: in the joint, acute inflammation; in the heart and brain, degenerative changes. Where then the nexus? Surely it is but a time relation, a coincidence, the outcome of, concurrent though unrelated cardiac and vascular lesions. In short, the cases of so-called retrocedent “cardiac” and “cerebral” gout usually resolve themselves into cardio-mural degeneration, arterio-sclerosis, or renal disease.
OTHER IRREGULAR MANIFESTATIONS
The more dramatic examples of retrocedent gout, as before stated, occur mainly in the acute varieties of the disorder. But the same visceral metastases are occasionally linked up with the less severe articular manifestations, or with that vague clinical entity known as “goutiness,” the same being frequently known as “wandering” or “flying” gout. Most of the examples met with in the present day belong to the last category. This may possibly find its explanation in the growing infrequency of the more acute or sthenic types of gout.
Both of the mild and of the severe forms of metastasis the same pathological interpretation is hazarded. The gout is described as “suppressed” or “retrocedent.” According to the former conception, the gouty process itself suffers inhibition, while the latter term signifies deflection of the materia peccans of gout from the joint into the viscera. Of the twain the former hypothesis seems to me the more plausible. Thus, given an acute gout at its inflammatory zenith, it is conceivable that, if abruptly checked, the same might reflexly precipitate the occurrence of internal lesions in structures undermined by insidious and pre-existing degenerative changes. In other words, the aborted attack is not the cause, but the occasion, of the cardiac failure, the apoplectic stroke, the uræmia, etc.
On the other hand, given that such were due to actual transference of the gouty poison, one would expect that it would induce the same inflammatory phenomena in the viscera as in the joint. But there is no anatomical proof that such occurs, no evidence of an actual invasion of the impeached viscus by the gouty inflammation. Uratic deposits have, it is true, been found post mortem at the site of visceral lesions, but, be it noted, generally in degenerating tissue altered by other morbid processes. Some, however, affirm that in such the gouty process has quâ the uratic deposits left, so to speak, its attestation behind it.
But any degenerative focus may in a gouty subject become the seat of such a deposition. Yet it would be presumptuous to infer its gouty origin from this fact alone. Such are common in chronic nephritis, and this apart from gout. What need for wonder then that the same should occur in gouty subjects, with their blood surcharged with uric acid?
Were such uratic deposits located at the site of inflammatory as opposed to degenerative visceral foci, it would to our mind give more colour to the assumption that they were the outcome of a true gouty process; in other words, that, as in the joints, they were the sequel or concomitant of acute gouty inflammation. But it is not so.
As for the structural or organic degenerations met with in gouty subjects, very many, if not all, as Longstreth rightly says, “belong to some one of the great general classes of tissue changes, some of which are due to special causes, but the most of them own many causes. One of these many causes can be under certain circumstances gout, but there is really nothing special in the appearances by which we can unequivocally pronounce them of gouty origin.” With this view few would join issue, save only the reservation that the scleroses so commonly met with in gout, if due thereto, must owe their origin to some more vital agent than uric acid, a few milligrammes more or less in the blood content thereof.
It will be seen then that the anatomical evidence that gout can affect the internal organs is wholly lacking. The criteria then upon which the assumption is based that this or that functional disturbance is a manifestation of irregular or visceral gout are wholly clinical.
Doubtless the conception of irregular gout was derived from “the unaided operation of custom.” Thus, when one clinical event, A, was noticed frequently to precede another, B, the idea of an association between A and B was generated, and by virtue of this association A was said to be the cause of B. But obviously the fact that B has followed A does not establish any necessary connection between the two clinical events. In other words, the idea of a causal relation is in a sense a purely intellectual feat, a clinical inference presumptive and retrospective.
The evidence that a relationship exists between irregular and regular manifestations of gout rests upon the following sequences and alternations of clinical events:—
(1) The subsidence or disappearance of functional visceral derangements following the development of articular gout;
(2) Their occurrence directly after an articular paroxysm has been apparently suppressed;
(3) Their recurrence and alternation with arthritic outbreaks, this in some instances repeatedly;
(4) Lack of any appreciable cause for the functional derangements and their indefinite anomalous character;
(5) Their favourable response to specific gouty therapy.
As before noted, digestive troubles frequently precede the initial outbreak of articular gout. The same likewise are frequent in chronic cases between the intervals of arthritic seizures.
Now it has been customary to regard the alimentary or other disturbances that precede an initial articular attack as “gouty,” and likewise those that intervene between the gouty paroxysms in long-standing cases. In other words, in light of the subsequent articular outburst, what was mysterious ceases to be a mystery. All the vague “acidities, flatulencies, megrims, and biliousnesses, of whatever occult kind,” are forthwith hailed as “gouty,” this merely upon the ground of the sequence of clinical events, because the symptoms have disappeared from, e.g., the stomach to reveal themselves in the joint or joints, or vice versâ.
Now my own view is that the antecedent hepatic or digestive disturbances that so frequently precede initial attacks of gout are in all probability, nay assuredly, not gout. They should rather be regarded as the cause, the foundation, of the malady than its effect, a cause inoperative save in the presence of individuals victimised by inherent morbid tissue potentialities. For similar symptoms are but too common in the non-gouty. They are very common antecedents of, e.g., rheumatoid or atrophic arthritis. Nevertheless we do not when the arthritic disorder subsequently manifests itself talk of the preceding digestive disturbances as “rheumatoid” dyspepsia. Then why this presumptive and retrospective diagnosis of similar prodromal phenomena as “gouty” dyspepsia? For there is pending the articular outbreak nothing distinctive in the digestive derangements, nothing that would enable us to diagnose them as “gouty.” They might, for aught we know, be significant of oncoming rheumatoid arthritis.
Now in the case of the latter we regard the prodromal digestive phenomena as probably indicative of some infection located somewhere in the alimentary tract. It would be wiser, I think, to adopt the same attitude in regard to our “gouty” examples. Moreover, as we know, such dyspeptic symptoms recur from time to time throughout the life history of both rheumatoid and gouty arthritis. In the former disorder we regard them as indicative of recurring infection, followed as they so uniformly are by exacerbations of the joint trouble. Is it not time we adopted the same attitude towards the gastric or hepatic functional disorders that punctuate the course of chronic gout with a periodicity that rivals that of the articular paroxysms?
Unquestionably to my mind when we have regard to the extreme frequency with which local foci of infection, e.g., oral sepsis, etc., are found in gouty subjects, this would be the more rational attitude, the one more in conformity with modern medical thought.
But if we would condemn those who, in the presence of unequivocal tokens of gout, label antecedent or intercurrent dyspepsias, etc., as “gouty,” what are we to say of those that even in patients who have never had regular gout or exhibited tophi yet presume to classify their associated digestive troubles as “gouty”? This, I contend, is wholly unjustifiable. I would say more, that such conjectures are hazardous in the extreme, this both in the overtly gouty as well as in the non-gouty. I recall the instance of an individual who suffered from classical articular gout which palpably alternated with attacks of abdominal pain, but the clue to the true nature of the latter symptoms, as revealed at operation, was a chronically inflamed appendix. If so in this case, how many so-called “gouty” acidities have resolved themselves into appendicular or gall-bladder dyspepsia!
My conclusion then is that the gastro-intestinal disorders attributed to gout cannot legitimately be regarded as examples of irregular gout. They should not be held “symptomatic” of, but etiologically related to, gout, a view more calculated to lead to exact diagnosis and rational therapy, and incidentally to elucidate the true nature of gout.
In respect of other organs and the symptoms connected with them in “gouty” persons the case is very much the same. Always and ever are we confronted with the same difficulty, inability to determine whether antecedent, co-existing, or consecutive affections in certain examples of gout, are not associated merely by coincidence.
Disturbed cardiac action is not uncommon in gouty subjects, palpitation and arrhythmia and syncopal threatenings, and frequently symptoms difficult of differentiation from true angina pectoris.
I am reminded of an old physician whom I saw in consultation some years ago, who suffered from alarming attacks of precordial anxiety. He was well on in the sixties, and very obese. He was convinced that his cardiac irregularities, etc., were of gouty origin, and often exclaimed regretfully: “If I only dared to take two bottles of port, and got it in my toe, all would be well.” He had never had an articular outbreak, and based the diagnosis of his case on the fact that from time to time his urine for long since contained excess of urates. Having suffered much of many physicians, he at last grew restive, took the bit between his teeth, rushed to a spa, and forthwith embarked on a very strenuous course of “waters and baths.” At once he got a severe attack of acute polyarthritic gout, and mirabile dictu, all his cardiac troubles straightway ceased.
Retrospectively viewed, many would regard the preceding cardiac condition as of “gouty” source. That the old gentleman, of florid countenance, plethoric build, and lethargic habit, was potentially “gouty,” there is no doubt. But he was also abnormally fond, not of alcohol, but, curiously enough, of sweetmeats and cakes of all sorts, hence “dyspeptic.” He had a feebly acting heart, but no detectable valvular lesion, though mural degeneration seemed likely. My own diagnosis was flatulent dyspepsia with secondary cardiac disturbance, and finally acute gout, the exciting cause of which, as I have so frequently seen, was a course of hydrotherapy. The patient never regretted his venture, and, I am glad to say, lived for some years.
Such cardiac paroxysms are not uncommon in the “gouty,” and, alarming though they are, I question if purely functional disturbances of this nature ever prove fatal. As to the valvular lesions and mural degenerations observed in the “gouty,” there is little or no evidence that they are dependent on gout. Indeed, the lack of a tendency to endocarditis is one of the criteria distinguishing gout from acute rheumatism. I note that in one textbook pericarditis is classed among the cardiac manifestations of irregular gout. But it must not be forgotten that renal disease, a frequent concomitant of gout, predisposes to pericarditis, which, indeed, occurs in granular kidney even when unassociated with gout.
As to the respiratory organs, such chronic maladies as bronchitis and asthma are very frequent in the “gouty,” but I question if they are more so than in non-gouty subjects. In any case their symptomatology and course are the same whether gout be present or not. Much, too, has been made of the fact that asthmatic and arthritic manifestations may alternate. But we must recollect that asthma per se has a paroxysmal tendency; it has a tendency to periodicity and a liability to be excited or aggravated by much the same factors as favour outbreaks of gout. It is said, too, that there is a “gouty” pneumonia, and that the same has been replaced by an acute articular paroxysm. But, in respect of all these alleged “gouty” respiratory disorders, would it not be more scientific to cease talking of them as “gouty” and instead to speak of them as bronchitis and asthma occurring in “gouty” subjects? This, I may remark, is not to say that we should take no count of the reigning diathesis in our treatment of all associated affections.
Of the nervous phenomena relegated to gout we hear nowadays less and less. “Gouty” headaches are almost a thing of the past. The acute “gouty” delirium of older writers in many cases was but an euphemism for alcoholism, and likewise the spinal paralyses; while the convulsions and comas were certainly almost always attributable to uræmia. It would be held rash to-day to speak, like our forefathers, of “gouty” cystitis, urethritis, or orchitis, for there is no evidence of any pathological connection between them; and the same stricture is also applicable to the many cutaneous affections affiliated without sound pretext to the materies morbi of gout.
In the early part of the nineteenth century the French school were most insistent on the prevalence and variety of the cutaneous manifestations of l’arthritisme; but even by them the all-pervading influence of gout in the etiology of skin disorders is no longer held even as a working hypothesis.
Conclusions.—The sum of my experience and reflections on so-called “irregular” gout leads me to regard it as an “abstraction” rather than as a proven clinical fact. Moreover, if I may judge by the “admission certificates” to the Royal Mineral Water Hospital, Bath—a fair test, as I maintain—many are of the same mind as myself, for during the past ten years I do not recall a single instance in which a patient sought admission thereto as suffering from “irregular” gout.
But some writers on gout—indeed, I think I may say all—whatever doubts they entertain as to the propriety of retaining the term, yet qualify their pronouncement in favour of some particular variety of anomalous gout, visceral, cutaneous, or other. Still, in justification of my own uncompromising attitude, I must say that dispassionate analysis of their eclectic claims, in light of present day knowledge, to my mind fails to show any adequate reason for the faith that is in them. Of some of them I feel sure that sub-consciously they have been influenced by a respect for tradition, forgetful of Pliny’s sentiment,—
“Quamvis enim cedere auctoritati debeam, rectius tamen arbitror, in tanta re, ratione quam auctoritate superari.”—Lib. i., Ep. 20.
But, to resume, this much at any rate may be affirmed, viz., that there is no proof that visceral disturbances or cutaneous disorders are due to uric acid. On the other hand, in view of my contention that the inherent morbid potentialities of the “gouty” demand for their fruition the intervention of an infection, the reader may rightly ask whether the same agent may not be capable of evoking the visceral or cutaneous, as opposed to the arthritic, manifestations of gout.
Trousseau, a whole-hearted advocate of irregular gout, drew an analogy between gout and syphilis. Somewhat contemptuously he observes: “To those physicians in whose eyes localisation constitutes the particular disease the differences in appearances are so many different diseases, while to those who consider that the disease consists much more in the aggregate of the general phenomena, in their evolution, in their progress (and that, thank Heaven! is the direction in which sound observation leads), these affections, differing in appearance, are only multiplied expressions of the same species of morbid action. To the real physician exostosis, alopecia, psoriasis, roseola, bubo, and chancre are always syphilis—syphilis in different garbs.” In the same way he held that the infinitely varied manifestations of irregular gout were all affiliable to one and the same morbid agent. He claimed, too, that visceral gout was “the result of a sort of imperfect inflammation analogous to that which manifests itself in the joints.”
Unfortunately for the cogency of the argument, there is no proof that such visceral inflammations as do occur in the “gouty” are of gouty origin. Unfortunately, too, the microbic agent that we postulate as responsible for “gouty” arthritis is as yet unisolated. If this disability be removed, it might be found that the said organism was capable of originating, not only the arthritic, but the alleged visceral, forms of gout. But pending such discovery I am of opinion that the term “visceral” gout should be abandoned, in other words that we should cease to talk of, e.g., bronchitis, dyspepsia, etc., as “gouty,” and should talk of them as bronchitis or dyspepsia occurring in the gouty. In this way we may escape, or, better, render uncalled for, the scathing criticism of Pye Smith:—“It has become common to ascribe bronchitis, dyspepsia, gastralgia, iritis, gravel, cystitis, and even psoriasis to the ‘gouty’ diathesis; but the evidence is very slight, and the ‘gout’ to which such evidence as there is applies is the distillation of morbid humours which belong to a bygone pathology.... There is no reason to believe that gout ever flies to the stomach, but over-indulgence at the table may produce acute dyspepsia as well as inflammation of the great toe. Elderly people are liable to gravel, gout and cough; and while lead and drink may lead to gout and chronic Bright’s disease, cirrhotic kidneys favour an attack of gout.”
INFANTILE GOUT
While subjects of gout have told me that they had had an attack in their teens, I have never myself seen an instance. Still less can I claim to have seen what I felt justified in calling “gout” in children. On the other hand, if, as one authority states, “tonsillitis (quinsy), enlarged tonsils, granular states of the pharynx, and catarrhal conditions of the throat and respiratory mucous membranes are not infrequent expressions of gouty inheritance in children,” then, of course, all of us must be quite familiar with “infantile gout.”
But even this formidable list of legacies from gouty parents is eclipsed by a more recent writer, J. Comby (1902), who, discussing “infantile arthritism,” divides children coming of gouty stock into two types: the “lymphatic” and “nervous.” The children of the former class suffer from fleeting swelling of the lymphatic glands, rhino-pharyngitis, tonsillitis, and, if they be girls, from chlorosis. Also they are given markedly to tachycardia, bradycardia, and vasomotor ataxia. They are also especially liable to asthma and the crises of dyspnœa, and pulmonary congestion may alternate with urticarial and eczematous eruptions. Truly, their lot is hard, for they fall a ready prey to colic, constipation, all varieties of dyspepsia, not to mention nocturnal and diurnal enuresis!
Comby also claims that these gouty children are especially liable to recurrent or cyclical vomiting. In this matter he is confirmed by J. Thomson, who noted that these children not infrequently give a history of having had asthma, urticaria, eczema, stammering, and other nervous complaints, also that in many instances uric acid crystals or a copious deposit of urates have been noted in their urine.
As to the “nervous” type, they labour with insomnia, night terrors, convulsions, and when older with migraine. To these liabilities must be added undue proneness to acne, seborrhœa, psoriasis, chilblains, angio-neurotic œdema, urticaria, etc., not to mention muscular and joint aches and pains.
Whether this medley of distempers can with any pretensions to scientific reason be affiliated to a gouty heritage, or whether they can be regarded as expressions of a budding “gouty diathesis,” is, I submit, of the nature of pure speculation. That the child who suffers with cyclical vomiting may show uric acid crystals or urates in his urine is certainly no proof that he has inherited gout, much less that he is actually “gouty.” In uro-lithiasis the uric acid is precipitated in the urinary passages, viz., strictly speaking, outside the body, whereas in gout the pathological error originates within the organism. More apposite is Uffenheimer’s observation, previously noted, that children of this type suffer the same disturbances of purin metabolism as are met with in adult gouty subjects.
If the fact is confirmed that the output of exogenous purin in such children is diminished or retarded, it would certainly be a most interesting finding, possibly with a now unguessed-at significance. But we should recall that even in the subjects of regular gout such is not invariable, and, moreover, occurs in diseases other than gout. Pending further exact investigations I think it would be wiser not to indulge in such vast generalisations, mindful of the sentiments expressed by the illustrious Sydenham in his letter to Dr. Gould:—
“I have bin very careful to write nothing but what was the product of careful observation. So when the scandall of my person shall be layd aside in my grave it will appear that I neither suffered myselfe to be deceived by indulging in idle speculations nor have deceived others by obtruding anything to them but downright matter of fact.”