The Project Gutenberg eBook of Gout, by Llewellyn Jones Llewellyn.

With the passing of Jonathan Hutchinson disappeared the premier British exponent of l’arthritisme, that generic term so attractive to our French confrères. Whether gout and rheumatism are branches of one common stem need not detain us, for it is an abstraction more suitable to the philosophic age of medicine before pathology emerged as an exact science. Be this as it may, there has been in the past, and there still remains in the present, as a bond of union, a universal belief that both are subtle causes of disease of the eye. But the age of hypothesis is giving place to the era of facts, and we find in recent writings a more cautious expression of individual opinion, a less dogmatic positivism regarding the relationship of gout and rheumatism to ocular disease.

In referring to modern text-books we find Parsons[44] describes gout as one of the “alleged causes” of iritis. In rheumatic iritis he states that the patients “are often gouty.” The gouty nature of iritis is indicated by the similarity of onset of some cases of iritis with that of gout. “Iritis in an elderly patient is likely to be gouty, often starting suddenly in the night and sometimes ushering in an attack of gouty arthritis.” In episcleritis “rheumatism and gout are commonly indicated as the chief causes.”

Werner[45] includes gout in a list of disorders of metabolism which produce iritis “by means of toxins of a chemical nature.”

Sim[46] considers that iritis occurs in gout “as the result of some toxic influence”; and in addition he says, “Iritis is to be met with in gout.”

These authors express accurately, I think, the present views with regard to gout as it affects the eye; with each there is a tone of restraint and suggestion rather than of boldness and assertion, and the contrast to Hutchinson’s emphasis is noteworthy: “I believe,” he tells us, “that iritis due to the arthritic diathesis is a common malady.”

Among the many and indiscriminate diseases of the eye which have been considered to be due to gout are included blepharitis, conjunctivitis, episcleritis, scleritis, orbital cellulitis, neuro-retinitis, retro-bulbar neuritis, optic neuritis, optic atrophy, iritis, cyclitis, choroiditis, glaucoma and retinal hæmorrhage. Truly an all-embracing rather than an eclectic list, a medley of diseases without any melody.

Evidence of Gout in the Eye.—When we inquire what is the evidence which justifies the belief that gout causes ocular disease we find little more than a traditional hypothesis inherited in a long line of succession from the Fathers of Medicine. Nevertheless the opinion that there is a connection is widespread, not only in Europe, but also in America.

In considering this relationship we cannot overlook the effects of the diathesis on other viscera. How in these is a diagnosis of gouty origin arrived at? It would appear that the assumption of an irregular form of gout is based upon the following observations:—

(i.) That it sometimes happens that an undoubted attack of articular gout aborts and is followed by symptoms referable to a grave visceral disorder, e.g., gout in the stomach (retrocedent gout);

(ii.) That sometimes the converse occurs, viz., that an attack of visceral disorder may suddenly be replaced by an acute articular manifestation;

(iii.) That such visceral derangements may alternate, not only with articular, but also with other, such as cutaneous, outbreaks;

(iv.) That eye disease has been known to wax and wane in unison with concurrent arthritic gouty manifestations;

(v.) That occasionally in gouty people an attack of iritis of sudden onset in the night has been followed by remission of the symptoms in the day[47];

(vi.) That visceral symptoms in the gouty are anomalous and inexplicable on any other basis;

(vii.) That the treatment usually advocated for gout has a favourable influence.

Deposition of Urates.—Two cases are recorded by Garrod in which there was a deposit of urates in the sclera. These instances do not appear to have been confirmed by other observers, and they may be regarded as exceptional cases, occurring, it should be noted, in the outer envelope of the eye. But though these tophaceous deposits may occur in the sclera and in the eyelid, they have never been known to invade the intrinsic structures, such as the iris or ocular media. The eye, in fact, is on all fours with the sites of urates elsewhere—deposition occurs in parts of relatively low vitality.

Although urates are not found within the eye, there is in other morbid ocular conditions quite frequently a deposition of foreign matter, such as alien crystals, of varied description. For instance:—

In the choroid there may be true bone which forms a cup so extensive that it can be felt by the finger, or, again, there may be calcareous plaques.

The retina may undergo colloidal changes or be the site of carbonate of lime or of cholesterin.

In the iris degenerative calcareous or osseous deposits are occasionally seen.

The cornea may be affected by hyaline degeneration with deposition of lime salts.

In all these cases the foreign particles, whether crystals or otherwise, are usually the retrogressive changes of senescence proclaiming that the forces which make for degeneration are more potent than those which make for regeneration.

But urates are not found in the eye, even though the patient is gouty. On the other hand, both in gouty joints and in other similarly affected parts of the body we find a deposition of urate of soda.

Gouty Diathesis.—From the days of Sydenham—himself a martyr to gout—diathesis has been a name to conjure with, and an all-sufficient diagnosis. In the podagrous patient any intercurrent disorder, any inexplicable ache or pain, was ascribed to gout, and patient and doctor were alike satisfied. “Tempora mutantur,” but still we are prone to call morbid conditions gouty when they occur in gouty people.

If we accept the theory that gout is due to an excess of uric acid in the blood, the view which I have expressed elsewhere[48] that gout does not cause iritis is directly challenged. For if it be granted that a sudden outpouring of so non-toxic an acid causes an acute inflammation—for instance, in the synovia of the great toe—why should not our faith incline us to go further and find in this malevolent, though bland, acid a source of inflammation affecting the fibro-muscular meshwork of the iris?

If, however, we adopt the infective theory, then the association of the uratic deposits no longer dominates our creed—we view them as mere clinkers and by-products erupted from the furnace.

The infective theory of gout also lends plausibility to an association with iritis, for this latter is a disease of infective origin. For the intimate relationship of all forms of asthenic arthritis with iritis is of very frequent occurrence, but is practically never seen in the more sthenic arthritides: rheumatic fever, acute gout and traumatic arthritis.

Nearly fifty years ago Jonathan Hutchinson drew up a “Report on the Forms of Eye Disease which occur in connection with Rheumatism and Gout.”[49]

At the present day it is not easy to differentiate his 117 cases according to modern classification, but he includes gout, rheumatism, rheumatic arthritis, etc. The differential diagnosis between gout and rheumatism was simplified by the creation of a mule—“rheumatic gout”—and upon its back were packed the doubtful cases.

Hutchinson’s views regarding the essential difference between gout and rheumatism are crystallised in his statement that in rheumatism there is an arthritic susceptibility to weather, in gout an arthritic susceptibility to diet.

Osteoarthritis also seems to have been included as one of the gouty diseases, probably because post-mortem examination revealed uratic deposits in the disorganised cartilage. This, however, would appear to be an epi-phenomenon, and must not be allowed to obscure the essential distinction between true gout and osteoarthritis. It is a sign of articular disorganisation of long standing, and is the homologue of the similar deposition of crystals, etc., already referred to as occurring in the eye as the result of chronic disease therein.

The significance of tophi, as the touch-marks of gout, is undoubted, but even if they are detected in the eyelids or elsewhere, we are skating on thin ice if we rashly declare that a coexisting intra-ocular disorder is gouty. Most forms of iritis betray the same clinical facies, although the etiological causes are diverse. But in none do we find any appearances pathognomonic of gout.

The argument that because a patient has tophi therefore the iritis is also gouty does not hold good, for gout does not confer immunity from other diseases, and even though we cannot prove an alibi for the diathesis, we can often in these cases also indict gonorrhœa, pyorrhœa or some other pathogenic agent.

The favourite site for tophi is one in which blood-vessels are sparse; but, although the cornea is void, imbibition of blood from the marginal looped plexus of capillaries and an abundant lymph supply provide amply for nutrition, and tophi are not found in this locality. The sclerotic, however, has a meagre supply of vessels, and for some unexplained reason tophi rarely invade it. In the eyelids, on the other hand, possibly from the cartilage being rich in sodium, tophi are occasionally seen. If we accept the tophus as the one unequivocal criterion of gout, we are not justified in labelling an iritis as gouty in its absence. If we do, our diagnosis is presumptuous and not absolute. Strictly speaking, the diagnosis cannot be made. We may the more readily admit our limitations, inasmuch as they are a blessing in disguise, and suggest a further etiological search.

In Hutchinson’s list of eye diseases which occur in association with rheumatism and gout there is a history of gonorrhœa in twenty-six cases, syphilis in seventeen, of both gonorrhœa and syphilis in six. Herpes occurred in two, pustular acne in one, eczema in one, albuminuria in one, ague in one. Bad teeth are reported in two. In all the total was fifty-seven cases out of 117 (48·7 per cent.) in which there was a possible source of infection. It is probable that this percentage would have been materially increased if at that time it had been recognised how great is the influence of pyorrhœa and other sources of infection in the etiology of irido-cyclitis.

With regard to all infections it is only in the present day that full advantage is taken of bio-chemical and bacteriological methods of differentiation. How frequently the true origin of disease must have been overlooked when the pallid spirochæte was unknown, when the Wassermann test was not applied, and when the complement fixation test for gonorrhœa was not recognised.

With regard to a combined cause it has been maintained that gonorrhœa is always more severe in the gouty than in other people, and it may be that the more intense the gonorrhœa the more likely may it be to produce constitutional symptoms, of which iritis is one. In all such the combination of gout and iritis would indelibly impress upon the mind of the surgeon the intimate association of joint and eye. It was long ago recognised that many forms of joint disorder were associated with iritis, and, as the cause of the arthritis was not always gout, Mackenzie introduced the generalisation “arthritic iritis.” “Not being able,” he tells us,[50] “to determine the diathesis which predisposes to this ophthalmia” (iritis), “I use arthritic as a conventional term, without adopting it in the strict sense of gouty.” The expression is well worthy of retention for the reason that it warns us to be prepared for an attack of iritis in many forms of arthritis and arthralgia.

In the following articular diseases the triad joint, muscle and nerve disorders is not uncommonly linked with iritis:—

Iritis occurring in these last suggests the possibility of error in the diagnosis of the putative parent disease. Especially is the clinical similarity of gonorrhœal (polyarticular) rheumatism to rheumatoid arthritis to be borne in mind.

The Relative Incidence of Iritis.—In the text-books it is often stated that the syphilitic form of iritis is the one most frequently met with, and that gouty iritis, if it is met with at all, is much more rare. But in these comparative statements we have no clue to the frequency of iritis with syphilis, nor of iritis with gout. For a true analogy we do not want the syphilographer to tell us the aggregate number of cases of iritis that he has seen, but what is the percentage of cases of syphilis in which iritis occurs, and we want the gout physician to state his percentage of iritides in gout, or, negatively, what is the percentage of cases in which iritis does not occur.

If gout is a more prevalent disease than syphilis, it does not follow that “gouty” cases of iritis will be more numerous than those due to syphilis. Let us suppose, for the sake of clearness, that 1 per cent. of people suffering from gout get iritis, and that also 1 per cent. of people infected by syphilis get iritis, and that in a certain town there are two hundred people who are gouty and one hundred people who are syphilitic. It is probable that there will be two persons suffering from gouty iritis (always supposing there is such a disease), but only one from syphilitic iritis. The absolute totals will differ, but the relative will be identical. It is clear, then, that infectivity cannot be gauged by the statistical enumeration of the consulting-room. Gout is a rarer disease than our patients would have us believe, but accepting their views, even then we should expect to see more cases of iritis caused by it, if such existed; we should expect to find more definite proof of a causal connection, and less frequently a history of gonorrhœa, of pyorrhœa, and of syphilis.

we can at once exclude all cases of ocular disease as gouty in the absence of either factor. According to Garrod, “true gouty inflammation is always accompanied with a deposit of urate of soda in the inflamed part.” We should therefore expect that uratosis would occur in situ if an iritis were gouty. But it does not: the touch-mark is absent, and there are no chemical, pathological or clinical signs of urates in the iris after the inflammation has subsided. What then is the alternative? Either Garrod’s aphorism is inaccurate or iritis is never gouty. In other words, we must postulate that an iritis may be regarded as gouty without uratic deposits. If this be the case, the so-called gouty iritis may well rank with the occult migraines, flatulencies and acidities which are termed irregular, suppressed or latent gout. Strictly then it would be a latent gouty iritis fit to rank with that last refuge of the uric acid enthusiasts, the “latent nephritis” which they worship as the fons et origo mali of gout.

Metastasis.—The predilection of the gonococcus for synovial membranes is seen not only secondarily to urethral infections, but also in ophthalmia neonatorum, in which the joints of infants are affected sequentially to the eyes.[51]

The gonococcus also has been found in cases of peritonitis, pleurisy, pericarditis, etc., but it is said to have only once been isolated in the eye in iritis.[52]

It is not only the gonococcus which can initiate a metastasis from the eye to the joints, to the peritoneum, or elsewhere. The same process may be started by the bacillus typhosus, by the streptococcus of erysipelas, and by that of puerperal septicæmia.

De Grandmont[53] records the case of a young man recovering from typhoid, complicated with jaundice and nephritis, who was attacked by iritis with posterior synechiæ and hypopyon. Paracentesis was done, and the pus of the anterior chamber was transferred to agar-agar. Two days later a pure culture was obtained presenting all the reactions and characteristics of the bacillus of Eberth. Of this culture a small quantity was injected into the vitreous of a rabbit. A month later the rabbit was killed, when the liver and intestines were found to be infiltrated with the same bacillus of Eberth.

In erysipelas de Grandmont has seen a hyalitis from which a culture was grown on gelatine that presented all the morphological characteristics of erysipelas.

He has also met with a case of hyalitis associated with puerperal septicæmia, and he has no doubt that it was the result of a similar microbic invasion of the vitreous.

Gout does not render patients immune from tuberculous, syphilitic or gonococcal disease, and when in such so-called diathetic stocks an iritis occurs, especially in gonorrhœa, years after the primary disease, it is probable that gout, rather than lues, will be assigned as the cause.

The local appearances of iritis are identical in gonococcal and other infective iritides; they resemble clinically those seen in syphilis and tubercle except that in these there are sometimes condylomata of the iris in the one and tuberculous nodules in the other. To be comparable a gouty iritis should be characterised by iritic tophi.

“Arthritic” Iritis.—Forty-eight is a large percentage in Hutchinson’s cases of ocular disease associated with gout and rheumatism, and it is justifiable to assume that there was something more than coincidence in the triple entente of diathesis, arthritis and iritis. But the fact that the poisons of syphilis and gonorrhœa, etc., are potent causes of iritis is indisputable, and therefore the patients might have suffered from it even if they had never had either gout or “rheumatism.” Consequently these articular diseases are both superabundant and superfluous, and they may have no etiological status. A patient afflicted with arthritis is very susceptible to an associated attack of iritis provided that there is a septic focus anywhere in the body.

A practical point to remember, especially in gonorrhœa, is that the onset of joint trouble should warn us to anticipate the possibility of an associated iritis and should prompt us to instil atropine at an early stage. We should forestall the disease by treating the suspicion. The frequency with which gonorrhœa is followed sooner or later by iritis entitles this ocular phenomenon to be considered a secondary symptom of gonorrhœa, as it is of syphilis.

Before the potency of distant infective foci (for example, in nasal disorders, pyorrhœa, sinusitis, etc.) to produce ocular disease was recognised, there was justification for the inclusion of a so-called idiopathic iritis, but it is seldom now that we have to be satisfied with this negative diagnosis. Nevertheless the assignment of a toxæmic etiology must be based on a definitely ascertained focus of toxic absorption, or failing this, at least on symptoms of general malaise which render such a focus highly probable.

Frequency a Factor in Diagnosis.—It was known a century before the birth of bacteriology that gonorrhœa caused iritis. It was also noted that certain constitutional symptoms occurred in syphilis, and that among them not infrequently iritis was one. Observation and deduction was the process with our forefathers, and it seldom led them astray.

If in any sequence of events cause and effect are to be established when there is no obvious proof of connection, we may have to be content with an empirical diagnosis, and this was the position before the discoveries of bacteriology enabled us to place the etiology of iritis on a firm basis. How then did our ancestors know that syphilis and gonorrhœa caused iritis? Was it not—

(1) That the frequency of the association was the essence of the diagnosis,

(2) That there was absence of any other recognised cause, and

(3) In the former disease the effect of anti-syphilitic therapy?

(1) No marked frequency of association of ocular disease and gout,

(2) That when iritis does occur there is often some other possible source of origin, and

(3) That anti-gout treatment has only a doubtfully beneficial effect.

“Gouty” Iritis is not a Clinical Entity.—Before a symptom or affection can be classed as secondary to a primary disease there must be evidence of a connection stronger than post hoc, ergo propter hoc. For instance, in syphilis an iritis frequently follows which may be of the specific condylomatous type, and a laboratory examination of the inflamed iris may demonstrate the presence of the spirochæte. On the other hand, an iritis occurring in a gouty patient is indistinguishable from that form which results from infections of undifferentiated type. Moreover, iritis so seldom occurs associated with gout, and when it does there are so often present other well-recognised possible causes, such as pyorrhœa or gonorrhœa, that the doubt about the paternal relationship of gout to the iritis is overwhelmingly strong.

Iritis.

	Gout.	Syphilis.	Tubercle.	Toxæmia.
Pathognomonic symptoms.	0	Gumma of iris.	Tubercles of iris.	0

If pathognomonic symptoms were always present the differentiation of the various causes of iritis would be less difficult. But this is not the case, and consequently, whatever the primary cause, the appearances of the iritis, in spite of the pathogenesis, objectively resemble each other in very many instances.[54]

Medical authorities call certain cases (not varieties) of iritis gouty; they are content to rest the diagnosis on the ground that they occur in gouty people. Yet there is not a single ocular symptom which differentiates the disease from a similar one in non-gouty subjects. Before the dogma can be accepted that because a gouty man has iritis it is therefore a gouty iritis and, like the poet’s primrose, nothing more, it must be shown that irido-cyclitis is proportionately more frequent in people who are gouty than in those who are not. Even then it is suggestive, but not conclusive, for it is conceivable that, although gout is not strictly the cause, yet it may so reduce the resisting power of the iris that it becomes a readier prey to some lurking organism.

It is commonly reported that the existence of a gouty diathesis gives to any inflammatory condition of traumatic origin—synovitis, for instance—a special tendency to chronicity, and I would not deny that it may have the same influence in the case of iritis of traumatic endogenous origin.

If then a gouty man is not immune from other possible causes of iritis, one of these, and not gout, may be responsible for it. Especially is a gouty diagnosis doubtful when there is a focus of suppuration in the tonsils, teeth or elsewhere. Also the prolonged hibernation of the gonococcus, for many years after the attack of gonorrhœa, is apt to be overlooked. The presence of excess of uric acid in the blood, which sometimes occurs in these patients, may mislead us into the belief that we have a true gouty iritis to deal with. But even although it is ascertained that a hyperuricæmia of 4-8 mg. of uric acid is present, it is no proof that the co-existing iritis is necessarily gouty. We might have an even higher content of uric acid in the blood in leukæmia, and yet no iritis be present. It may be admitted that on rare occasions iritis occurs in leukæmia, but no one suggests that the leukæmia or the associated iritis is due to uric acid toxæmia. We should be on infinitely surer ground if not uricæmia, but uratosis, were present. We could then, at any rate, confidently assert that, whatever the origin of the iritis, it had supervened in a subject of gouty habit. I do not think that we, as clinical observers of iritis, should go further than to say: “The man is gouty; his iris is inflamed.” Here in Bath, among hecatombs of gouty people, irido-cyclitis is one of the rarer associated diseases requiring treatment. When it does occur it is usually of obviously septic genesis rather than of gouty origin.

Contrasting gonorrhœa with gout, we find in the former when there is systemic infection, as shown by arthritic complications, there may be also iritis, so often, in fact, that it is legitimate to bracket it as a related symptom. It is a toxæmic condition in which we rely on the frequency of the combination to diagnose the cause.

In writing on iritis in 1908,[55] I referred to the rarity of the association of gout and iritis. In an analysis of 17,197 cases of “rheumatism” and rheumatoid arthritis occurring at the Royal Mineral Water Hospital, Bath, in twenty years, there were twenty patients who suffered from acute or subacute iritis. During the same period there were 2,159 gouty patients not one of whom had iritis. In a special hospital it is possible that the diagnosis of gout might be limited by a stricter nosological differentiation than occurs in private practice. It is, moreover, not uncommon for ophthalmic surgeons to see patients who call themselves gouty, or who say that their doctors have told them that they are, and yet on examination no corroboration is found, no clinical outbreak, or, more pertinent, no tophi. They come to us with an attribution of iritis to gout without the filmiest shadow of evidence.

In considering the correlation of cause and effect it not infrequently happens that we find no obvious connection between the one and the other. In syphilis, for instance, alopecia is a usual secondary symptom, and we rely on the frequency of the sequence to satisfy ourselves that it is no mere coincidence. If it could be shown that alopecia did not occur more frequently in syphilitic people than in non-syphilitic we might justly doubt the connection. The same reasoning may be applied to iritis and gout: the association is so rare that it is negligible. To justify a causal connection between diseases the possibility of a fortuitous concurrence must be excluded, for when the double event occurs only very exceptionally, it is difficult to exclude the long arm of coincidence.

A man has iritis and tophi; ergo we say he has gouty iritis. But why? They co-exist, it is true, but where is the link of attachment of cause and effect? How different is our attitude if we know in another case that our tophaceous iritic patient has gonorrhœa. We then say, gonorrhœal iritis in a gouty subject. Would it not also in the first case be more scientific if we frankly confessed that it was an infective iritis of undifferentiated type occurring in a person of gouty diathesis?

In considering the iritides in relation to gout there are two types which demand our attention. With the possible exception of traumatic iritis, this grouping embraces all the etiological varieties of the affection. In the first are those cases which are due to specific infection, such as syphilis, gonorrhœa and tuberculosis. In the second are those infections of undifferentiated type in which the causal germ has not yet been isolated. Now clearly we must read the latter in the light of their analogues, the specific iritides. In them the modes of onset, the clinical course, are duplicated, presenting similar variations, and they are doubtless the reflexes of the varying grades of intensity of the causal organism.

Concussion iritis would fall into line, for it is possible in this case that the iris is rendered a pars minoris resistentiæ by the blow, and that the iritis which follows is due to a cryptic focus, it may be in the gastro-intestinal tract or elsewhere. The chief sources of iritis are syphilis, gonorrhœa, tubercle and infections from undifferentiated organisms of low grade. If these said iritides occur in a person of gouty diathesis they are unmodified by it clinically or pathologically, macroscopically or microscopically, save possibly in the direction of chronicity—a result, it may be, of those inherent peculiarities of tissue metabolism ingrained in a gouty subject, and in which presumably the iris shares.

And that which has been said of iritis in the gouty applies equally to other forms of so-called gouty ocular manifestations. There are no statistics available to show that there is any differential frequency in those who are gouty compared with those who are not. Authors have laboriously recorded cases of eye diseases which have waxed and waned in unison with podagrous toes, but the publication of these cases is in itself a confession of the rarity of the coincidence, a rarity which destroys the authenticity of any communal kinship. Coincidence is merely another name for the rigid and immutable law of chance, for a cycle of events which occurs with irregular regularity. If it could be shown that a diet rich in purins brought on an attack of ocular disease in gouty people, and if the experiment could be repeated with a similar result and sufficiently often to exclude all probability of coincidence, scepticism would no longer be justified. But until more definite evidence is forthcoming “gout” in the eye is nebulous.

In attempting to define the relationship of gout to ocular disease, there is one author to whose opinion we turn with the respect due to a master. Garrod’s judicial summing up supports the view that there is a connection between gout and ocular disease, but his cautious statement seems to imply that the affection of the eye is modified by rather than due to gout. His statement is as follows[56]:—

“Gout of the Eye.—A form of ophthalmia connected with gout has long been recognised, and appears to be tolerably well established, but as rheumatic inflammation of the eyes is equally allowed to exist, difficulties may at once arise in the diagnosis. I have witnessed many cases in which conjunctivitis and sclerotitis appeared to be distinctly connected with the gouty diathesis, and in two cases there existed deposits of urates on the surface; gouty iritis also occasionally occurs. I once saw a case of acute inflammation of the sclerotic coat and iris which supervened a few days after the operation for cataract in a gouty subject. By active treatment the disease was arrested, but distinct articular gout soon manifested itself.

“Our information on this subject may be thus summed up: patients having a well-marked gouty diathesis now and then experience attacks of inflammation of the different structures of the eye; and it is important to bear in mind the fact that the state of the habit considerably modifies and keeps up such affections, and also that treatment directed to the gouty condition of the system proves very effectual in curing the local mischief.”

It will be observed that Garrod tells us that his two important cases of sclerotitis “appeared to be distinctly connected with the gouty diathesis.” With the reticence of the careful and accurate observer, he does not say they were due to it even though there were deposits of urates on the surface. He would seem to recognise that cases of sclerotitis with uratic deposits were unusual events, and that generalisations cannot be based upon exceptional cases. A gouty man is gouty to his innermost cells, and the eye, like every other part of the body, is a potential uratic site. We must grant therefore that the course of an iritis, however caused, may be influenced, though not necessarily dominated, by the diathesis. Consequently it may be necessary that cases of iritis of undoubted gonococcal or other infective source occurring in gouty people should be treated by iodides, salicylates, atophan or colchicum.

From the academic point of view ocular gout may exist, but from the practical point we should invariably seek, and we shall probably find, some still more important source of infection requiring treatment.

Ocular Symptoms in Hyperuricæmia.—The popular view that gout depends upon uricæmia is so generally accepted that the expressions “uric acid diathesis” and “gouty diathesis” are tantamount to tautology. Nevertheless they are different, the first postulating the supposed cause, the second the inferred result. There is a commingling of cause and effect. Uricæmia is a normal condition of the blood, but in certain diseases—gout, leukæmia, plumbism, pneumonia, etc.—a considerable excess of urates is found. No form of ocular disease is included as an associate of hyperuricæmia unless one or other of the ancillary diseases is also present.

In leukæmia when severe there is an extremely pale fundus, with a yellowish tint; hæmorrhages, when they occur, are often pale; the choroidal vessels also, if they can be seen, are pallid; the veins in the retina are full and tortuous. There may also be yellow foci, and occasionally retinitis with white spots. In a word, the leaking vessels tell of vascular disease.

In lead-poisoning we find paralysis of ocular muscles, amblyopia, contracted fields of vision, papillitis and retro-bulbar neuritis. It is the nervous system upon which the stress principally falls.

In pneumonia we do not expect to find any ocular complications; in spite of the uricæmia, the eyes are scatheless.

It seems unlikely that hyperuricæmia can produce such widely different signs in the eyes. Rather, on the other hand, the ocular symptoms conform to the type we should expect to find associated with leukæmic blood in the first and with lead-poisoned nerves in the second.

In this congeries of ocular symptoms, marked by hyperuricæmia, we do not find iritis included, and yet this is a commonly accepted gouty affection of the eye.

False Gout.—It often happens that patients tell us that they are gouty although they do not claim to suffer from attacks in the old-fashioned way. With them there is a wide difference between the substantive “gout” and the adjective “gouty,” the latter apparently implying an attenuated form of the former. Such patients are seen at health resorts and are very frequently those in whom obesity and plethora are present to a marked extent. The full-blooded appearance involves the head, body and limbs, but the eyelids, for some unexplained reason, may escape. The patients have lived not wisely, but too well. On examination an increased quantity of uric acid in the urine is found, and is supposed to justify the diagnosis of gout. Sometimes the malassimilation, is associated with arterio-sclerosis, with diabetes, or with albuminuria. But the patient is almost invariably convinced that he has gout, that it is hereditary, that it has been handed down to him through a long line of ancestry from primeval days, and that an ascetic life would not have prevented it in his case.

Should such a one be attacked by iritis, the circularity of the argument is complete: he has iritis, therefore he is gouty; he is gouty, therefore he has iritis. But usually in the early days of this so-called gout we see no ocular changes; the time for organic disease (inflammatory and hæmorrhagic) has not yet arrived; auto-intoxication has not yet begun. But sooner or later with the maturation of disease come ocular degenerative signs, retinal hæmorrhages, and so on. The sequence is malassimilation, “goutiness,” sub-infection, ocular disease. Thus in diabetes melitus (omitting toxic and traumatic forms) we find pancreatic disease, nutritional changes, and not usually until late retinitis, cataract, iritis, etc. In renal disease retinitis is also late and often ushers in the final scene.

If in these cases of so-called gout we implicitly accept the patient’s nomenclature of disease, we shall find plenty of gouty iritis, but we may overlook the fundamental condition of his arteries, of his kidneys, and of other organs.

The sins of repletion in such patients may be relieved by the virtue of abstinence, not by colchicum.

Retinal Hæmorrhage.—That retinal hæmorrhage may be caused by gout was firmly maintained by Jonathan Hutchinson.[57] This opinion was shared by Gowers, who states that the “influence seems well-established.”[58]

Hutchinson pointed out that in cases of retinal hæmorrhage of renal origin, stellate white deposits occurred, whereas in gouty cases they were absent. By this criterion he classified his cases. In his first patient Hutchinson relates that he can only state from memory that there was no albumen, but that “he seemed in good health and that there was reason to suspect gout, although he had not had a definite attack.” In his second case, a woman who had suffered from rheumatic gout and true gout, there were numerous hyaline casts in the urine, but no albumen. In both cases the hæmorrhages were flame-shaped, and Hutchinson lays stress on the shape in gouty retinitis hæmorrhagica. The group consisted of fifteen patients, eleven men and four women. “Gout had been positively present in six, and was strongly probable in four or five others. In one the gout was complicated, and probably in part produced, by lead poisoning, and this is the only instance in which the urine contained much albumen. In another in which no history of gout was obtained, the patient, a man æt. 67, had diabetes, which was the probable cause of the retinitis.... In about a third of the cases albumen was found in the urine, but it was usually a mere trace and only present occasionally.... In four, including the case of diabetes, white deposits characteristic of renal retinitis were present in small quantity, and in all these albumen was found in the urine.”

Hutchinson sums up his cases with the catholic observation that retinitis hæmorrhagica is a malady the boundaries of which are very indefinite. And when we bear in mind the changes of modern medical opinion with regard to the influence of arterio-sclerosis on the retinal circulation and the effects of vascular hypertension the etiological difficulties regarding retinal hæmorrhages are hardly less illimitable than they were when Hutchinson penned his valuable contribution. In all his cases (as in those which we see now forty-two years later) there are many factors which may have been responsible for the hæmorrhages apart from gout.

In renal disease gout is widely recognised as a possible precursor. So we are again in the same quandary that we experience in considering the relationship of gout to iritis. Are the retinal hæmorrhages due to gout or to the resulting renal disease? The claim of gout to be the deus ex machina once more seems to be superfluous, for retinal hæmorrhages are an end result which may be reached by a variety of pathological routes. Gout may be one, but if so it acts viâ interstitial nephritis. In other words, hæmorrhagic retinitis is the apanage of nephritis and the appendix of gout.

It is impossible to affirm that a retinitis is gouty, for there are no distinctive features, but it occurs in gout when vascular disease has supervened, not gouty retinitis, therefore, but retinitis in the gouty. This is all that can be affirmed when we find albumen in the urine and tophi in the ears, eyelids, etc. Moreover, it is wiser in the interest of the patient to take this broad view. There may be a link between the kidney and the diathesis, but it is invisible.

Neither are we absolved from searching for some other cause of renal disease. The case may be fundamentally one of arterio-sclerosis with a secondarily induced sclerotic kidney, or, on the other hand, the hæmorrhages may be symptomatic of pernicious anæmia and due to toxins. With regard to prognosis it is helpful to remember that retinal hæmorrhages, especially when they are isolated, suggest the possibility of death ensuing suddenly from cerebral hæmorrhage; but albuminuric retinitis is itself frequently a terminal stage of chronic renal disease. We have not sufficient proof to call retinitis gouty, and we should adhere to the more catholic appellation “nephritic retinitis.”

“Commonly, of course, it occurs in association with albuminuria, yet it is met with apart from this even in cases where no very obvious cardio-vascular changes can be demonstrated in other regions. And thromboses in retinal veins, apart from cardiac hypertrophy and demonstrable changes in the arteries or in the blood pressure, are of frequent occurrence. In such cases gout is possibly—in many cases demonstrably—a very important factor in the etiology.”

The opinion that cases of neuro-retinitis may be gouty is based upon (a) the fact of the apparent absence of cardio-vascular disease elsewhere, (b) the lack of any other ostensible cause. Doubtless many cases of retinal hæmorrhage are seen for which we are unable to assign a cause; in some of these there is no suggestion of gout and nothing to support a postulation of a latent form of that diathesis. Taylor’s statement that gout in many cases is demonstrably a very important factor in the etiology cannot be lightly set aside, but as the appearances of neuro-retinitis are similar whether gout is present or absent, it is legitimate to question if the diathesis is really necessary.

Glaucoma.—Brudenell Carter, Hutchinson and Nettleship have claimed that gouty people are more apt than others to suffer from glaucoma, but no convincing argument has been brought forward in proof of any definite nexus.

The conclusion I would arrive at is that it is unwarrantable to speak of “gouty” ocular disease, for there is nothing in the character of the inflammation specific of gout. We renounce the prefix in order—

CHAPTER XXV OCULAR DISEASE IN THE GOUTY

Iritis.

CHAPTER XXV
OCULAR DISEASE IN THE GOUTY