Acute Generalised Gout

While gout may throughout its life history confine its ravages to the foot, if not solely to the toe joints, it may, even in the initial attack, involve many articulations. Such cases usually, if not always, occur in persons of marked gouty heredity. In its simplest forms the orthodox monarticular seizure is simply exchanged for a sequential implication of each big toe joint. If so, as Trousseau pointed out, the joint that is the last to be involved is least affected, and the soonest to get well again, while the accompanying œdema is of shorter duration. But in more severe cases not only the big toe, but the tarsal joints, the knee and the hand, may be invaded in the first attack. Occasionally, too, the disorder displays concomitantly its tendency to involve other structures, tendons and aponeuroses, e.g., the tendo Achillis, plantar fascia. Such widespread initial involvement is usually preceded by prodromal phenomena of unusual severity and prolonged duration. These initial attacks of polyarticular distribution are extremely rare.

Far more commonly acute gouty polyarthritis supervenes after several attacks of classic location have been suffered. The gouty inflammation in these cases invades the joints after a serial fashion. But each joint as it becomes involved goes through the same painful cycle. Thus, for five or six days the pain goes on increasing, then abates, and finally the wished-for crisis comes. So it happens that the gout may be raging simultaneously in several articulations, though in each at different stages of evolution. Consequently the symptoms do not pursue an even tenor, but are made up rather of a series of little attacks—series et catena paroxysmulorum, to invoke Sydenham’s expression.

Frequently periods of apparent recovery take place. The temperature remains normal for some days, and welcome convalescence seems established, when, to the victim’s despair, the temperature again rises, and the same weary cycle, though perhaps shorter, is yet to be endured. Running this chequered career, the disorder may last for six weeks or two or three months.

In such attacks not only the feet, knees, hands, and elbows, may be promiscuously involved, but often also the ligaments, bursæ, tendon sheaths, and aponeuroses. The suddenness with which the disorder shifts its seat from one joint to another, or from joints to bursæ or muscles, often leads to its confusion with acute rheumatism. In other words, that fixity distinctive of gout in its monarticular forms is here exchanged for mobility, that specific quality of acute rheumatism.

Naturally, the implication of so many varied structures casts its impress on the clinical picture, inasmuch as the physical characters vary with the different textures involved, their capacity for inflammatory distension, etc. On the dorsum of the hand and foot redness and œdema will be prominent, and Scudamore noted that the flush might be widely diffused, simulating erysipelas, with here and there small ecchymoses.

When structures more deeply placed, i.e., tendon sheaths at ankle, knee, and wrist, are singled out for attack, swelling is less marked and redness of the skin more patchy in distribution. The bursæ at the elbow or back of the knee may swell with extraordinary rapidity. The parts become exquisitely tender and painful, while the overlying skin takes on an angry blush. They may subside, but more often continue permanently enlarged, defiant of reduction.

Involvement of the olecranon bursa is very typical of gout. Pratt, of Boston (1916), tells of a case in which the subject had during twenty-seven years suffered from recurring attacks of acute gouty polyarthritis. The eight or ten physicians who had treated him had all regarded the disease as rheumatic fever. Pratt himself observes: “I did not feel sure of the diagnosis until I saw the swelling on his elbow, which presented the typical picture of a chronic gouty olecranon bursitis.”[34] Occasionally the bursæ when filled with uratic deposit undergo suppuration following injuries. The bursa in connection with the great toe frequently becomes acutely inflamed, and Scudamore in a gouty hand saw an old ganglion take on the same inflammatory reaction.

The tendon sheaths when involved lead to great disablement, as even the most tentative attempts at movement give rise to sudden and agonising cramp. The tendo Achillis is a favourite site, or the tendons of the wrist, or the ligament of the patella. The same is true of the aponeuroses, the predilection being for the lumbar or gluteal fascia, in which instance it may extend to the sheath of the sciatic nerve. These extensions of gout to tendon and nerve sheaths frequently outlast the articular lesions, and may become the dominant element in the clinical picture.

Naturally, when not only joints, but bursæ and other structures, are involved and implicate both upper and lower limbs, the victim presents a pitiful spectacle, one of almost complete helplessness. Œdema and general venous turgescence may be very pronounced in one or more members, giving a subjective sensation of almost overwhelming weight in the limb.

Reverting to the constitutional symptoms, the outstanding feature is that, notwithstanding the widespread involvement of joints with manifest local inflammatory reaction, the pyrexia is of moderate grade, and so frequently, indeed, is it afebrile that this peculiarity is of diagnostic significance.

Changes in the Blood.—The findings are extremely interesting in view of the high grades of leucocytosis to be met with both in pyrexial and apyrexial examples.

In a case of acute gouty polyarthritis under my care the blood picture was a very striking one. The patient had suffered from gout for some eleven years, with recurrent acute exacerbations. There was widespread involvement of the joints both in upper and lower limbs. On the dorsum of the mid-phalangeal joints small semi-solid swellings were present, the exact nature of which was somewhat puzzling. But inasmuch as the pinna in both ears was studded with tophi, this seemed to provide a clue. The auricular tophi were verified microscopically. The extra-articular phalangeal swellings were then aspirated with a hypodermic syringe. A turbid straw-coloured fluid issued, which microscopically was found to contain biurate crystals. His temperature rose nightly from 101° up to 102° F., with morning remissions. The left knee and wrist were the seat of effusion, and some of the small finger joints were inflamed.

Blood Count.

Differential Count.

The left knee joint was aspirated by Dr. Munro. A clear fluid of straw yellow tint was withdrawn, which yielded some fibrin on standing. The cytological examination gave the following results:—

Total Count.

Differential Count.

Attempts at culture on broth and agar proved sterile. In addition three separate blood cultures, taken at intervals of a few days, on agar slopes and broth, all gave negative results.

In another instance of polyarticular distribution the subject was seen during the inter-paroxysmal period. He displayed auricular tophi, the crystalline content of which was verified microscopically.

Blood Count.

Differential Count.

Chalmers Watson some years previously investigated the blood in cases of acute gouty polyarthritis both during an exacerbation and in the inter-paroxysmal period. His findings were as follows:—

During the attack the films showed very marked leucocytosis. Also there was present a large number of peculiar myelocyte-like cells, these more than half as numerous as the ordinary finely granular oxyphil leucocytes.

Shortly after Chalmers Watson, Bain published his results of blood examination in acute gouty polyarthritis. He also noted the presence of a distinct leucocytosis. A differential count disclosed a marked increase of the eosinophil cells, and he adds: “There was present a moderate number of the peculiar myelocyte-like cells originally described by Chalmers Watson.”

Dr. Munro, though he carefully examined the gouty blood films to this end, was unable to identify the myelocyte-like cells noted by these observers.

Recently, through the kindness of my colleague Dr. Waterhouse, Dr. Munro and I had again an opportunity of examining the blood in a case of this kind during the inter-paroxysmal period. The subject, a male, had had repeated attacks at the classic site, with subsequent extension to other joints. Multiple tophi were present in both ears, and the crystals of uric acid were demonstrated microscopically.

Blood Count.

Differential Count.

The blood picture, it will be seen, is one of erythræmia—a marked leucocytosis, a normal differential percentage count, pronounced secondary anæmia.

Da Costa also notes, in a case of gout, erythræmia (7,125,000) with a leucocyte count of 14,000. Ewing, too, records an instance of chronic gout with huge tophi, seen in an acute exacerbation, in which the blood gave a leucocyte count of 21,000 with 70 per cent. hæmoglobin. In another severe instance of subacute type the same observer again met with leucocytosis (15,000).

In regard to these interesting blood findings, it is to be cordially hoped that as the somewhat rare opportunities occur they will be taken full advantage of.

As to the other general clinical features the nervous system, as might be expected, is often greatly perturbed, and the mental distress and anxiety in some instances appear to cause even more irritation than the bodily pain. Febrile movement when present accords with that observed in monarticular sites, save only in the tendency to relapses. Sweating is not a common feature, as in acute rheumatism. Neither does acute endocarditis occur in gout. On the other hand, as this acute polyarticular form may recur throughout years, it may in its later stages be complicated by nephritis.

Furthermore, in its differentiation from acute rheumatism the more advanced age of the sufferer, always over thirty-five and more often nearer fifty or over, will be of help. The presence of an hereditary taint, the nature of the occupation and personal habits, and more pertinently the history of a classical attack in the great toe, may give a clue.

But in this, as in all other varieties of gouty arthritis, the one and only unequivocal objective proof of the nature of the disorder is the presence of tophi. Lamentable indeed is the frequency with which this fact is forgotten, to our confounding and the patient’s detriment. As Hilton Fagge, discussing the diagnosis of gout, long since observed: “All those parts which are apt to be the seat of tophi should be examined. If a single deposit of urate of soda can be found it settles the question.”

In conclusion, before passing to consideration of chronic articular gout, it will be convenient here to discuss certain concomitant phenomena of the acute types. We refer to the muscular and nerve forms of fibrositis, which, we hasten to add, are of common occurrence also in the chronic types of articular gout.

Collateral Phenomena of Gout

The liability of acute articular gout to be complicated by muscular and nerve disorders has already been briefly alluded to. Also it was pointed out that in respect of this tendency gout displayed an analogy with the specific infections, viz., in that these latter too are prone not only to arthritic, but to muscular and nerve, lesions also.

Our forefathers, greatly exercised by this apparent overlapping of “gout” and “rheumatism,” in their efforts at discrimination drew fanciful contrasts between the subjective sensations produced by gout and rheumatism, but all to no end, for said Heberden, “It must be owned 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.”

Gradually, however, a change in attitude made itself felt. It became no longer customary to regard such examples as blends of gout and “rheumatism,” but to hold the muscular and nerve disorders as also attributable to the underlying gout. Thus, so impressed was Garrod with the frequency of the incidence of lumbago and sciatica in gouty subjects that he was doubtful as to whether they ought to have been classed by him as among the “diseases to which gouty persons are particularly liable.” He thought “they might perhaps have been properly classed among the forms of irregular gout.”

Duckworth, again, felt sure “that much so-called ‘muscular’ rheumatism is really gouty,” and forthwith ranked its manifestations among the irregular forms of gout. Hilton Fagge was likewise convinced that the muscular types of fibrositis are frequently and obviously related to gout; while Sir William Gowers, discussing this same muscular fibrositis, is even more explicit: “It is currently associated with gout, and the truth of the belief is soon impressed upon the practitioner. But it is gout with a difference: it may occur in those who are gouty in the common sense of the word, but some of the most severe cases I have seen, especially the brachial form, have been in those who have inherited a tendency to gout, but have not merited its development.”

Turning to the nerve manifestations, Charcot long since pointed out that gout and sciatica might co-exist, while Gowers is insistent that “underlying most cases of sciatica is either the state of definite gout, or that ‘rheumatic diathesis’ in which the fibrous tissues suffer, especially those that are connected with the muscles, a form closely connected with common gout by co-existence or descent.”

As to my own opinion, I have, in collaboration with Bassett Jones, discussed in detail this relationship of gout to fibrositis in our monograph on the latter disorder, and I shall largely transcribe our remarks therein on this vexed point.

Of all the conditions reputed to be etiologically related to fibrositis, in none of them is the connection more obvious or more easily traceable than between this affection and gout. Whether or no the hyperplasia of the connective tissues be directly due to the gouty toxin must perforce for the present remain uncertain. But there is no doubt as to the relatively frequent incidence of fibrositis in “gouty” subjects. It is as true to-day as when Scudamore wrote it that occasionally “a patient when he has gout in the regular situations suffers, in consequence of some partial exposure to cold, a rheumatism in other parts, as in the muscles of the neck, or in the shoulder joints; and a seizure of lumbago at the time of the invasion of the gout is also not uncommon.”

Apart from the simultaneous incidence of gout and fibrositis in the same subject, it is equally certain that the victims of a “gouty” heritage are unusually prone to develop fibrositis.

Thus, in a series of 1,000 cases hereditary or acquired gout was present in no less than 281—viz., a percentage incidence of 28·1. While this taint was more in evidence in fibrositis of the joints, it obtained appreciably in regard to all muscular types of the affection, more especially lumbago, its influence also being very obvious in the case of sciatica and other types of nerve sheath involvement.

In light of this, we must admit being somewhat nonplussed by those who confidently affirm that “gout” plays little or no part in the production of “fibrositis.” Speaking from an extensive experience, we confidently believe the reverse is the case, and that the gouty element is but too frequently overlooked in examples of this affection.

Approaching another aspect of this vexed question of the relationship of gout, what of the ambiguous attitude of those who, while denying it any share in the causation of lumbago and other types of muscular fibrositis, yet at the same time attribute to gout an important etiological rôle in the allied conditions sciatica and brachialgia?

Thus, they maintain that the fleeting attacks of lumbar fibrositis or lumbago which ensue after dietetic indiscretions have no relation to gout, but are simply indicative of some digestive disability on the part of the individual for certain articles of diet. Hardly to our mind a satisfactory mode of differentiation; much less can it be held to put out of court the influence of gout. For are not the gouty precisely the very persons who display this inability to cope satisfactorily with unusual or excessive meals? Hence the frequency with which in their instance attacks of lumbar fibrositis, often transient, almost invariably ensue when any unwonted excess of purin-containing food has to be disposed of, and especially when at the same time katabolic changes have been stimulated in the body by the ingestion of alcohol, not necessarily excessive in amount.

That the lumbar regions should have been singled out is the more remarkable, for, if there be one form of fibrositis more than another prone to be associated with gout, it is precisely lumbago.

Our difficulty, moreover, in appreciating the cogency of this plea for excluding the influence of gout in muscular fibrositis is the more accentuated in that those who advocate it claim that this very gout is the salient etiological factor in sciatica and brachialgia.

This position is untenable, and for the following reasons: the pathological lesion in both instances is the same—viz., fibrositis; in lumbago and deltoid rheumatism it implicates the sheaths and interstitial tissues of the muscles, in sciatica and brachialgia the similar investments of the nerves.

Strictly speaking, therefore, any differentiation that we can effect between muscular and neuralgic types of fibrositis is perforce merely topographical. To draw etiological distinctions is well-nigh impossible, for the very continuity of the fibrous tissues favours the passage of one type into the other. Hence clinically we find that the bulk of our cases of sciatica are preceded by lumbago, and similarly many cases of brachial neuralgia or neuritis develop by extension out of a pre-existing deltoid fibrositis.

In light of such transitions of muscular into neuralgic types of fibrositis, it seems inconsistent to postulate a gouty origin for the latter and at the same time to deny it any share in the production of the former. For ourselves, we fully recognise gout as the most potent predisposing factor in sciatica and brachialgia, and ergo in the closely associated and often antecedent muscular types of fibrositis.

While insisting on the importance of gout as a predisposing factor in fibrositis, we feel called upon to emphasise the fact that we are not sheltering ourselves under that nebulous term “latent” gout, for our contention is based on the ground that in the vast majority of the cases for which we claim a gouty origin unequivocal proofs of gout, such as tophi, etc., were present.

Incidence of Gouty Stigmata in Various Types of Fibrositis

Out of 343 instances of fibrositis of the joints such stigmata of gout were present in 118 males and nine females. Of muscular types, taking as our example lumbago, we find that out of twenty-seven examples no less than ten displayed definite evidences of a gouty taint. Similarly, out of thirty-eight cases of lumbago complicated by other manifestations of fibrositis eleven males and one female were of gouty habit. Also in twenty-three cases of lumbago associated with arthritic fibrositis six males, but no females, displayed the same proclivity. Lastly, out of thirty-eight cases of lumbago complicated by right or left sciatica ten were of the same diathesis.

Passing in turn to consider this same factor in relation to sciatica, we note that out of 142 examples twenty-four men and three women were gouty. Occasionally, too, apart from glycosuria, it appears to be responsible for bilateral sciatic pains, for in three examples of this nature gout was present.

James Taylor is also very definite on this point, that, glycosuria aside, affections of individual peripheral nerves occur frequently in the gouty. There is little doubt, he says, that sciatica is “frequently present in the gouty and is sometimes directly due to that state.” While admitting that in many, if not most, cases of sciatica there are associated arthritic changes in the hip joint, he yet affirms his belief that “there are some in which the neuritis is a primary condition.”

With this statement my own experience accords, but with a reservation, viz., that the sciatic neuritis is apparently secondary to a lumbar or gluteal fibrositis, with sequential involvement of the sciatic nerve sheath and extension to the nerve trunk.

Taylor holds also that anterior crural and brachial neuritis may be directly due to gout. As to brachial neuritis, he says: “I have known it occur apart from any recognisable arthritic change in a patient who was the subject of gout.”

Having regard to the flippant manner in which the term “neuritis” is but too frequently bandied about, it is refreshing to note that in all Dr. Taylor’s cases “the existence of the neuritis” was shown “by the tenderness of the nerve trunks, the spontaneous, often severe, pain, and atrophic changes both in the skin and the muscles—the glossy skin and atrophied muscles.”

As for the involvement of other nerves, trigeminal neuralgia is held to be the most common; but, for myself, I have never felt justified in claiming any such example as gouty. Nor am I satisfied that persons of gouty habit are more prone than others to attacks of migraine.

Lastly, I cannot confirm out of my own experience Duckworth’s statement that “herpetic attacks in all varieties of ‘gout’ are common.” Nor have I seen shingles co-exist with acute gout, neither have I come across any examples of so-called gouty spinal meningitis!

In conclusion, I would submit that:—

In regard of this last postulate, it is well known that gouty persons who contract gonorrhœa are more prone than the non-gouty to develop gonorrhœal rheumatism, in other words, to sustain a widespread infection involving the fibrous tissues, not only of the joints, but of the muscles and even of the nerve sheaths. With this concrete example to hand, is it not reasonable to suppose that such a constitutional taint will favour the incidence also of other infections or sub-infections, and that this may explain the relative frequency of fibrositis, not only in the actually gouty, but in those of gouty heritage, this the more cogently having regard to the fact that so much exact evidence is forthcoming in favour of local infection as the cause of all types of fibrositis?