Iritis.

Gout.Syphilis.Tubercle.Toxæmia.
Pathognomonic symptoms.0Gumma 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.”

James Taylor, writing on neuro-retinitis in the gouty,[59] states that—

“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—

(1) That we may not be lulled into false etiological security, and

(2) That we may approach the elucidation of the case and the treatment thereof free from preconceptions. The mouth and its accessory cavities are the primary sphere of our investigation. This is no mean task, including as it does the radiography of the teeth, even though these are apparently healthy. In the tortuous route of elimination we look for concealed dental roots, rarefying osteitis, buried tonsils, post-nasal infections, antral disorders.

The view that non-traumatic iritis is only a symptom imposes upon us a wide outlook in our search for a diagnosis. In this no viscus can be overlooked, no organ forgotten. All are members one of another, and the wise physician takes cognisance of their interdependence. The recognition of an inflamed iris is only the first stage in the diagnosis, for iritis is the sequel of a story written elsewhere. It is a question, not an answer.

But we know not what the future has in store, and though, with our present knowledge, I affirm that I can find no evidence that the eye is a locus signi for gout, the day may come when, either from bacteriological or other sources of progress, it may be shown that there is a mystic source of intercommunity. In other words, it may yet happen that the mysterious materies morbi of gout, whether microbic or chemical, may be demonstrated experimentally as capable of inducing, not only the arthritic phenomena, but also those inflammatory lesions in the eyes which provisionally are sometimes called “gouty.”

Lastly, I would enter a plea for more systematic, more scientific, investigation of the true link, if any, between iritis and arthritis. The war has taught us the value of “team-work”; it has taught us that the clinician must be reinforced by the bio-chemist, the bacteriologist and the pathologist. The work and the workers must be co-ordinated in our daily struggle with disease as we meet with it in our individual patients. The realm of medicine, with ever widening borders, is too vast for single control. In the foregoing pages I have said much about iritis, and it is a good example of what I mean. In justice to our patient, we may call for a Wassermann or a complement fixation test; we may require the teeth-roots made visible by an X-ray expert, or, it may be, the passage of a bismuth meal radiographed, hidden tonsils explored by the laryngologist, or the antrum illuminated; the fæces may need bacteriological examination. A gynæcologist may help us regarding a leucorrhœa or a possible ovarian abscess.

With many of our patients, alas! considerations of expense compel us to forego our aspirations.

What is the remedy? Is it not State help, central clinics staffed by highly trained experts engaged in research work? Here the poor could be examined and reports supplied to the attendant doctors free, and less impecunious patients at an inclusive fee. Centres such as these would do much to advance the science of medicine and thereby raise the standard of health and make the sick and ailing healthy citizens of a great empire.

Salus populi suprema lex.

CHAPTER XXVI
TREATMENT OF GOUT

Adaptation is the keynote to progress in therapy—adaptation of our therapeutic measures to the ceaseless advances of pathology. In the history of gout it has ever been so, the changing, oftentimes contradictory, vogues in treatment, always the reflex of equally mutable and conflicting views as to its pathogeny. For who can doubt that the facts of pathology supply the indices of rational as opposed to empirical methods of therapy?

Albeit, much remains to be done before we can claim to fulfil the demands of ideal treatment of gout. For we are still ignorant of its exact etiology, cannot yet boast of our control of the morbid potentialities that constitute the pathological groundwork of the malady. We cannot obliterate the diathesis, and must still deplore with Sydenham that “as for a radical cure, one altogether perfect, and one whereby the patient might be freed from even the disposition to the disease, this lies, like truth, at the bottom of a well; and so deep is it in the innermost recesses of nature that I know not when or by whom it will be brought forward into light of day.”

But although we cannot dissipate the inherent proclivities to the disorder, we can, I think, claim to fulfil the humbler rôle, viz., obviate their coming to fruition. Haply in the fulness of time we may be able to influence the endogenous factors that make for gout, may through the labours of the bio-chemist be able to translate or assess them in terms of functional inefficiency of this or that particular viscus. But meanwhile we must perforce content ourselves with the eradication or control of the exogenous factors of gout—the excitants whereby or through whose agency the malady from being latent becomes manifest and overt.