OCULAR DISEASE IN THE GOUTY
BY W. M. BEAUMONT
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 _sclera_ on rare occasions we find osteomatous degeneration.
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.
The _vitreous_ may sparkle with showers of cholesterin.
The _lens_ may contain both tyrosine and cholesterin.
The _aqueous_ shows similar crystals.
In the _iris_ degenerative calcareous or osseous deposits are
occasionally seen.
The _cornea_ may be affected by hyaline degeneration with deposition of
lime salts.
The _conjunctiva_ may be calcareous.
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:—
Tuberculous arthritis;
Syphilitic arthritis;
Gonococcal arthritis;
Certain forms of specific arthritis: malarial, dysenteric, etc.;
Infective arthritis of undifferentiated type, as yet unaffiliated to
specific germs.
In the following forms of arthritis iritis is less common:—
Acute articular rheumatism;
Acute gout;
Osteoarthritis (hypertrophic);
Rheumatoid arthritis (atrophic).
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.
_No Uratosis, no Gout._—If we pin our faith to the equation
Hyperuricæmia + Uratosis = Gout,
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_?
Applying these rules to gout, we find—
(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.
In the following table a comparison is made between types of iritis:—
IRITIS.
-----------------+-------+--------------+------------------+---------
| Gout. | Syphilis. | Tubercle. |Toxæmia.
-----------------+-------+--------------+------------------+---------
Pathognomonic | 0 |Gumma of iris.|Tubercles of iris.| 0
symptoms. | | | |
-----------------+-------+--------------+------------------+---------
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._