DEFINITION, CLASSIFICATION, ETIOLOGY, AND MORBID ANATOMY
DEFINITION AND CLASSIFICATION
Said Locke long since, “There are some words which will not be defined,”
and surely of these is gout; for reflection upon the proffered
definitions thereof is apt to leave one with the depressing impression
that the disorder is both “incomprehensible and infinite.”
But have we not by unjustifiable and unwarrantable assumptions
deliberately complicated the issue, in recklessly relegating to the
_gouty_ category a myriad affections of the intimate nature of which
we are as ignorant as we are of gout? Doubtless, this is in part the
outcome of a too slavish adherence to tradition, an undue reverence
for authority. In all deference, our forefathers were somewhat too
hasty in their speculations as to the causation of gout. Dominated by
the prevalent philosophy of their days, they strove to interpret the
phenomena of gout through its lights, endeavouring to reduce the study
of its pathology to philosophical order when the very elements of
philosophical order were lacking.
The same is reflected in the earlier, and to a lesser extent in the
latter day definitions or _descriptions_, as some of them more aptly may
be designated, notably that put forward by Sir Charles Scudamore.
“A constitutional disease, producing an external local
inflammation of a specific kind; the susceptibility to it often
depending on hereditary bodily conformation and constitution,
but with great frequency wholly acquired; almost never
occurring before the age of puberty, not frequently under the
age of five-and-twenty, and most commonly between the ages of
twenty-five and forty; affecting chiefly the male sex, and
particularly persons of capacious chest and plethoric habit;
in the first attack invading usually one foot only, and most
frequently at the first joint of the great toe; but in its
returns, affecting both feet or other situations, as the hands,
knees, and elbows; and not only in the articular structure,
but also in the other textures belonging to the moving powers,
different parts being affected together or in succession;
often accompanied with sympathetic inflammatory fever, which
is usually marked by nocturnal exacerbations and morning
remissions; much disposed to return at periodical intervals,
and for the most part preceded by some premonitory symptoms.”
In extenuation of this prolixity, Scudamore observed that, “In
an attempt to mark the general characters of gout, I feel the
necessity of entering into a description rather in detail,
instead of confining myself to a brief definition, because the
disease is too complex in its nature to be distinguishable with
certainty by a few signs alone.”
Trousseau, in his lectures on gout, refrains, perhaps wisely,
from attempting any definitions of the disorder, resting
content with the reflection that, “The production in excess
of uric acid is a pathological phenomenon, inherent, like
all others, in the disease, and, like all the others, it is
dominated by a specific cause, which we know only by its
effects, and which we term the _gouty diathesis_.”
Sir William Roberts defines gout “as a constitutional disorder
characterised by paroxysmal attacks of inflammation of the
joints, associated with the formation of chalk-like concretions
in and about the joints.”
Sir William Osler regards gout as “a nutritional disorder,
one factor of which is an excessive formation of uric acid,
characterised clinically by attacks of acute arthritis, by the
gradual deposition of urate of soda in and about the joints,
and by the occurrence of irregular constitutional symptoms.”
For myself, I would proffer the following definition, which, of course,
the reader must accept provisionally, viz., pending the perusal of
subsequent chapters, dealing with the pathology and clinical features of
gout, and the inferences drawn therefrom as to the nature of the disease.
_Definition._—Gout is an hereditary disorder, the _intrinsic_ element of
which is an inborn instability of nuclein metabolism which may remain
latent, but under the influence of _extrinsic_ factors, _infections_,
becomes manifest, as betokened by local inflammatory tissue reactions in
joints or elsewhere the specific character of which is attested by the
associated _uratic deposition_.
CLASSIFICATION
At the present time, under the most liberal interpretation, the word
“gout” comprises the following conditions, viz., acute and chronic
articular gout, and the so-called ab-articular forms. But it is clear
that not only the latter or _irregular_ manifestations, but even the
former or _regular_ varieties of the disorder seem destined to undergo
considerable pruning.
As to the classical podagra—_acute_ articular gout—no question can
arise as to the propriety of its retention in this category. But as to
the _chronic_ articular types we are on less certain ground, and to
discussion of this vexed question we now proceed.
Let us take, for example, Sir Dyce Duckworth’s classification of the
_arthritic_ types of gout. He distinguishes the following forms:—
(1) Acute articular gout.
(2) Chronic articular gout
the latter (2) further subdivided into—
(_a_) the “tophaceous” variety.
(_b_) the “deforming” variety.
Of these twain the “tophaceous” form need not detain us, and why? Simply
and solely this—the _uratic deposits_ stamp the seal of specificity on
the disorder. In short, the presence of _tophi_ places the “gouty” origin
of the arthritis beyond the pale of cavil.
Now, if we accept, as we must, the fact that _uratic deposition is the
solitary unequivocal clinical criterion of gout_, we are not, I contend,
justified in classing any _chronic_ arthritis as “gouty,” the victim of
which does not exhibit _tophi_ of articular or ab-articular site, either
clinically demonstrable or deducible from skiagraphic revelations.
Nevertheless, be it noted _tophi_ do but bespeak the “gouty diathesis,”
not necessarily the “_gouty_” nature of an associated arthritis. For
clearly tophi, of _ab-articular_ location, may coexist with an arthritis
of _gonococcal_ or other origin. But given uratic deposits, either in
the joint proper or its related structures, all reasonable doubts as to
the true “gouty” nature of the arthritis are disposed of. On the other
hand, in _the absence of tophi_, the diagnosis of an arthritis as “gouty”
is _presumptive_, not absolute. This even in acute classical outbreaks
in the _big toe_, viz., pending the finding or subsequent eruption of
_tophi_.
In saying this, I do not for one moment depreciate the diagnostic value
of the clue afforded by location of the initial outbreak of the disorder,
in the vast majority of instances, in the _big toe_. It is an invaluable,
but not an _infallible_ clue; for, unfortunately, acute arthritic
diseases other than gout may elect to announce themselves in the great
toe.
Moreover, there is nothing _specific_ in the external characters of
acute “gouty” inflammation, nothing in the objective changes which would
stamp them on sight as “gouty,” save only their _location in the great
toe_; nothing distinctive about the angry blush, œdema, and engorged
veins, all of which may be met with in _infective_ arthritis. There
may be, as Garrod with good reason affirms, a local _intra-articular_
deposit of urate of soda, but this lies beyond our ken, presumptive but
undemonstrable.
Let but the _initial_ outbreak of gout occur elsewhere than at the _big
toe_, say, _e.g._, in the _wrist_, _hand_, _ankle_, or _knee_, and we
are at once, diagnostically speaking, _en l’air_. In this _impasse_ how
impotent are we, and how painfully we realise that our diagnosis of
acute gout is largely _topographical_, not _etiological_! Not, strictly
speaking, etiologically diagnosable pending the eruption and detection
of _tophi_. In short, location _per se_ in the big toe is strongly
suggestive but not _diagnostic_ of “gout.” (_Vide_ Chapters on Diagnosis.)
If this be done in the green, what then shall be done in the dry?
In other words, if so precarious our diagnostic foothold in _acute_,
how much more so in _chronic_ articular gout! for in the latter
even _topography_ may wholly fail us, what then our diagnostic
criterion?—_tophi_ and _tophi_ alone—aye, and demonstrable at that.
Yet both Charcot and Duckworth would have us recognise not only a
tophaceous but a _non-tophaceous_ variety of chronic articular gout, for
that is what it amounts to. They apparently feel justified in labelling a
chronic arthritis as “gouty” even though _tophi_ “may not exist” or “be
invisible”! _Deformity_, say they, is its hall-mark, not _tophi_, and its
character forsooth, they add, is not only _not peculiar to gout_, but
clinically indistinguishable from the similar defacements met with in
_arthritis deformans_. Nor is Duckworth alone in his contention, for both
Ewart and Luff also recognise what they term “chronic deforming gout.”
_Tophi_, I contend, notwithstanding, are essential for the diagnosis of
gout. In their absence, the designation of an arthritis as “gouty” is
unjustifiable. Either tophi are, or tophi are not the sole pathognomonic
feature of gout. If the latter, then gout ceases to exist as a clinically
recognisable entity.
Holding tophi indispensable for the diagnosis of gout, I maintain that
Charcot and Duckworth’s plea for the recognition of a chronic type of
articular gout, apart from the _tophaceous_ variety, is untenable.
Fraught, moreover, with risk, as I am satisfied that their so-called,
“deforming” type is largely made up of the _atrophic_ and _hypertrophic_
forms of arthritis deformans.
SUGGESTED CLASSIFICATION OF ARTICULAR GOUT
For myself, as to the classification of the articular types of gout, I
would divide them into:
(1) Acute articular gout.
(2) Chronic articular gout.
Under the first group I would place not only the acute _localised_ type,
but also those acute varieties of _polyarticular_ distribution. As to the
second category, I would exclude therefrom, for the reasons cited, the
so-called “_deforming_” varieties of chronic articular gout, recognising
only the so-called _tophaceous_ form. But I would place a different
interpretation on this term in opposition to that generally accepted;
for, by most writers the word _tophaceous_ is apparently limited in its
application to examples which, so to speak, exhibit _tophi_ of phenomenal
size or number. Scudamore was the chief offender in this respect. As a
consequence, he found tophi in only 10 per cent. of his cases of gout.
Accordingly, he went so far as to postulate for such victims as did
present this peculiarity an _idiosyncratic_ tendency to chalk-stones!
In other words, he would seem to suggest that there is a gout within
gout, that one displays _chalk-stones_, the other _not_. By inference,
Duckworth and his followers, by differentiating _tophaceous_ gout,
tacitly concur, and so “confusion twice confounded” results.
This usage of the term “tophaceous” is unjustifiable and misleading.
The significance of tophi is _qualitative_ not _quantitative_. One
tophus bespeaks the “gouty diathesis” as surely as a myriad concretions.
Solitary though it be, the same, given elimination of all other sources
of arthritis, will suffice to establish the “gouty” nature of an
associated joint disorder. It is in this more catholic sense that I would
translate the term “_tophaceous_ gout.” The conclusion, then, to my mind,
is obvious—there is but one form of articular gout, and one only, viz.,
an arthritis, the victim of which exhibits _uratic deposits in situ or
elsewhere in his body_. On this and on no other grounds can a chronic
arthritis, with any show of certitude, be certified as truly “uratic” or
“gouty.”
This rigid attitude may not commend itself to some, but I feel convinced
that, only by holding on grimly to the tophus, shall we steer a safe
course through all the pitfalls that beset the diagnosis of the chronic
arthritides. Only in this way, too, can we preserve for ourselves a
clear conception of _gouty arthritis_ as a specific disorder, the
which otherwise loses its identity, submerged in a medley of joint
diseases. Prior to the differentiation of gout, on the one hand, from
_rheumatism_ and _arthritis deformans_, and on the other from the _nerve
arthropathies_ and the _infective arthritides_, such laxity might be
condonable, but not, we think, in the present stage of our knowledge.
In drawing to a close my remarks on the classifications of articular
gout, it will be noted that I have made no reference to that variety
known as _retrocedent_ gout, but to this I shall allude at a more
favourable juncture, viz., in the chapter devoted to the clinical
account of articular gout. Conformably, too, it will, I think, be more
convenient, to defer any criticisms of the term “irregular gout” to
the chapter I purpose devoting to consideration of the varied clinical
content of the same.
ETIOLOGY AND MORBID ANATOMY
To the antiquity of gout and no less its distinctive clinical _facies_,
when of classic type, we owe not a little. Its salient phenomena have
endured unchanged from the time of Hippocrates onward through the ages.
So it is that, even allowing for the enhanced powers of discrimination
of latter days, we are in no doubt that the gout of the ancients is the
gout of to-day. How signal the advantage thus accruing, when we come to
consider the conditions which engender or tend to engender the disease!
For, _quâ_ its broad etiological factors, we find ourselves in accord
with the physicians of old, our experience a confirmation of their
old-time findings.
Our forefathers, like ourselves, realised the innate complexity of the
problem, that in the development of the disorder both _heredity_ and
_environment_ played a _rôle_. In other words, that in the genesis of
gout not only _intrinsic_ but _extrinsic_ agencies were concerned. Of the
intrinsic influences the most important are age, sex, heredity, bodily
conformation, and individual peculiarities.
_Age._—Gout is slow in evolution, tardy of appearance, confined in the
main to the middle and declining years of life. Said Sir Thomas Browne,
“Leprosie awakes not sometimes before forty, the gout and stone often
later.” Experience but confirms the dictum, for, as Cullen long since
observed, it rarely declares itself under the age of five-and-thirty.
This relative immunity of youth is not the least striking feature of the
disorder; whence the Hippocratic aphorism, “Puer non laborat podagra,
ante veneris usum.” Both Sydenham and Heberden were also doubtful of its
occurrence before the age of puberty. Gairdner, however, records the
incidence of fits of gout even in _infants_ at the breast! and in one
death therefrom. Garrod, too, met with two cases of classical type in
_girls_, both of them under _ten_ years of age. But Scudamore states that
he never witnessed more than one example of a first attack before twenty,
or any after sixty-six.
For myself, I have never seen a case under thirty-five years of age,
and am sceptical as to the occurrence of _infantile_ gout of _regular_
type, believing with Scudamore that “the commonly asserted cases which
represent the existence of the gout in very early youth are really
examples of _rheumatism_.” Nor am I less but more inclined to cavil at
the claims of Comby and others, as to the frequency in _children_ of
_irregular_ manifestations. As Osler dryly observes, “The tendency in
some families is to call every affection gouty. Even infantile complaints
such as scald-head, naso-pharyngeal vegetations, and enuresis, are often
regarded, without sufficient grounds, I believe, as evidences of the
family ailment.”
To sum up, the majority of cases of gout ensue between thirty-five and
fifty years of age. But, given a strong _hereditary_ taint, it may break
out in _youths_ and _young adults_, or haply even in _children_. But
such, in my experience, are phenomenally rare. Indeed, it may be said of
gout that only exceptionally is it met with at either extreme of life;
though Garrod records several examples in which the initial attack was
postponed until nigh eighty years of age; while in one instance, a lady
experienced her first classical attack of podagra in her ninety-first
year.
_Sex._—In the matter of liability to gout the sexes stand in marked
contrast, the disorder being infinitely more common in males. Out of
eighty cases submitted to the French Academy, seventy-eight were men
and only two women; but according to other authorities, this is an
under-estimate. Thus in James Lindsay’s series of cases of gout, 84·7 per
cent. were males, 15·3 per cent. females, percentages which he notes “are
in accordance with the observations of other writers.” J. Lambert, out of
125 examples of gout, noted that 102 were men, _i.e._, 81·6 per cent.,
twenty-three women, _i.e._, 18·4 per cent.
From my own experience, the figures submitted to the French Academy
probably represent the ratio of incidence in males as opposed to females.
This certainly, if _regular_, in opposition to “irregular,” types of gout
be the criterion; for it must be admitted that regular gout does occur
in women, though exceptionally rare either prior or subsequent to the
climacteric.
As to the current opinion that the _regular_ manifestations of gout
in women are of _asthenic_ as opposed to sthenic character, this has,
I think, often proved a source of fallacy. At any rate, in many of
these cases the assumed _gouty_ inflammation resolves itself into one
of inflamed _bunion_. Again, in but too many instances, women, showing
_Heberden’s nodes_, are held to have gout or “rheumatic gout.” The latter
term, as Pye-Smith observed, “is a bad name for _osteoarthritis_,” to
which category Heberden’s nodes belong.
Judged by the one unequivocal diagnostic criterion, _i.e._, _tophi_,
gout in women is extremely rare. If to this be added the further fact,
viz., the rarity in their sex of classical attacks in the _great toe_,
we see clearly that the diagnosis of gout in women is often a matter of
_assumption_ rather than of certitude.
Moreover, having regard to the fact that the diagnosis of gout in women
is frequently based on so-called “masked and irregular manifestations,”
I must admit that, to my mind, statistics, purporting to indicate the
percentage incidence of gout in women and men, are not very convincing.
As to the why and wherefore of the relative immunity of _women_ it may be
due to the fact that their habits and mode of life are less calculated
to evoke the disorder. There is also the further possibility that the
_catamenial_ discharges to a certain extent are protective against gout,
for most authorities support Hippocrates’ aphorism, “Mulier podagra non
laborat nisi ipsi menstrua defecerint.”
_Heredity._—By the ancient physicians gout was held to be hereditary,
and even to-day most will agree that “From father to son its seeds are
transmitted, and bear fruit in exact proportion to the degree in which
circumstances prove favourable to their growth.” Cullen, indeed, went
further and held it _purely hereditary_; but, on the other hand, the
belief, that it is often _acquired_ is widely countenanced.
That gout is an _hereditary_ disease is, I think, beyond question,
and certainly, of all _arthritic_ disorders, gout furnishes by far
the greater number of instances in which _parents_ and _children_ are
victimised by the same articular affection. Scudamore in 522 cases found
that 332 could trace their disease to the father, mother, grandfather,
grandmother, or aunt. But in the remaining 190 no evidence of the
existence of gout in their forbears could be elicited. Out of eighty
examples submitted to the French Academy an hereditary predisposition
was established in thirty-four, and in the residue it appeared to have
been _acquired_. Garrod found that 50 per cent. of his hospital examples
of gout were hereditary, and of his private patients nearly 75 per
cent. came of gouty stock. Again, Sir William Roberts found that “fully
three-fourths of the cases of gout occurring among the easy classes, can
be traced back distinctly to a gouty ancestry.” Luff’s estimate is even
higher, inasmuch as analysis of a series of 300 examples disclosed a
“definite family history of gout in 81·3 per cent.”
Nevertheless, Garrod’s experience, he tells us, convinced him that “in
this country gout is frequently _acquired_ even at a moderately early
age, for in many most inveterate cases not the least hereditary influence
could be discovered.” For myself, I find it difficult to appreciate
the attitude of those who, like this observer, postulate _innate_ or
_static_ morbid proclivities on the part of the “gouty,” and in the same
breath, as it were, are equally insistent that it may be “acquired” _de
novo_. Now, in the taking of family histories _positive_ evidence is
more valuable than negative. Surely, therefore, in the light of Garrod’s
and Luff’s findings, it is obvious that _heredity_ plays not merely an
important, but an _essential_ and _indispensable rôle_ in the genesis of
gout. To my mind, accordingly, the balance of evidence is more in favour
of the same ancestral taint, though apparently undiscoverable, being
present in the remaining 20 or 25 per cent., than that the disease in
their instance was wholly and newly _acquired_.
Personally, I therefore question whether the alleged acquisition _de
novo_ of gout is not _apparent_ rather than real. My own opinion is
that the _innate predisposition_ thereto is _always inherited_, and the
predisposing factors, that we presume may originate gout, are in reality
merely _excitants_ or _determining_ agents. In other words, the remote,
the primary or essential cause of gout, is an _inborn_ morbid tissue
potentiality, and in the absence of this intrinsic warp the various
contributory or exciting causes are impotent to evoke the disorder.
Apart from _statistical_ proof of heredity, how else, save on the basis
of an _organic predisposition_ to the disease, can we explain the fact
that of a large number of individuals, of slothful habit, and given to
alcoholic and dietetic excesses, not one may get _gout_; while others
who lead literally “a godly, sober, and righteous life,” become martyrs
thereto. How escape then the conviction that in gout “breed is stronger
than pasture”? for, apart from gluttony and indolence, gout is much more
prone to arise in persons in whose pedigree it can be traced than in
others.
It is not gout, but the _predisposition_ thereto, that is inherited.
This proclivity, moreover, may descend to the children of those who,
in their own persons, have never suffered from the disease. In Luff’s
series it was so in 27 per cent. of the cases, _i.e._, the disease was
transmitted from grandparents to grandchildren without the fathers
or mothers suffering from “active gout.” In other words, the morbid
potentiality may lie _latent_ until _evoked_. Thus, the _females_ of
“gouty” families, infinitely more often than not, escape overt gout, but
hand on nevertheless their inborn liability thereto to their offspring.
Looked at in this light, I see no difficulty in accepting the fact that
gout may skip a generation. The son of a gouty parent, happily warned by
the excesses of his father, may remain immune, while in turn his son,
forgetful of his evil heritage, may bring it again to fruition.
The more one reflects on the essential cause of gout, the more inevitable
seems the conclusion that gouty individuals, as Walker-Hall contends,
“possess some inborn defect or alteration of nuclein metabolism.” And
the vague phrases “constitutional” or “nutritional,” as applied by older
writers to the disorder, are only explicable on the basis of _inherited
structural peculiarities_, with their correlated perversions of tissue
function.
That such constitute the pathological groundwork of gout, is, I think,
further indicated by the fact that _“gouty” inflammation_, in virtue
of its associated _uratic deposition_, is _sui generis_. No tissues,
other than the _gouty_, react in this _specific_ fashion. Does not this
seem to indicate that the _inborn tissue peculiarities_ dictate, so to
speak, the _character_ of the pathological reaction; this indifferently,
whatever the nature of the so-called _predisposing_ causes which, if our
assumption be correct, are merely _provocative_ of gout, in other words,
do but evoke or make _manifest_ what is already latent.
To sum up, on statistical, and more cogently, general clinical and
pathological grounds, my own conclusions are that—
(1) Gout is always an hereditary disease.
(2) The factors currently regarded as predisposing agencies are
in reality merely _determining_ agents, not the cause of gout,
but the _occasion of its appearance_.
(3) In the absence of an hereditary taint, these same are
powerless to evoke the _specific_ manifestations of true
_“gouty” inflammation_ as estimated by associated _uratic
deposition_.
_Bodily Conformation and Individual Temperament._—Of the hereditary
character of gout no doubt remains, but as to the influence of physical
build and temperament no such certainty prevails. Said Cullen, “Gout
attacks especially men of robust and large bodies, men of large heads, of
full and corpulent habit, and men whose skins are covered with a thicker
_rete mucosum_, which gives a coarser surface.” Doubtless, in its more
sthenic form, gout affects persons like Falstaff, of sanguine temperament
and corpulent habit. But its milder or more asthenic manifestations occur
often in men like Cassius, of lean and nervous type.[5]
Of objective stigmata, I know of none, save _tophi_, that can be truly
regarded as pathognomonic of the outward semblance of the “gouty.” The
skin of the face may be coarse, unctuous, and studded with ramifying
venules. Such appearances, though not always, betray the tippler. Indeed,
such stigmata as these are only of value as indicating the habits of the
individual, favourable or not, to the development of gout.
Again, it has become a tradition with us that gout produces
characteristic _teeth_. The mere fact that they are “ground down” so
as to display the dentine in section is held as evidence of a “gouty”
diathesis, or of lithæmia. The teeth of the gouty, it is true, often
appear long and square-topped; but the gouty, no more than others, are
immune from early _recession of the gums_. Again, we must recollect that
there are several causes which may lead to the teeth being worn down more
quickly than normally. Thus the _formation of the jaw_ may be such that
the upper and lower incisors meet edge to edge instead of overlapping.
This so-called “edge to edge bite” subjects the incisors to marked
attrition. Also we must recall that these effects may be aggravated by
the nature of the diet. All of us are familiar with the fact that in old
horses the teeth are ground down to the gums. The same also is observed
in races condemned to live on coarsely prepared flour and hard vegetable
food.
In conclusion, having regard to the marked frequency with which disorders
leading to early recession of the gums are met with in the “gouty,” and
the ease with which the early attrition of the teeth is explicable on
tangible mechanical reasons, I am inclined to refer such changes to their
combined agency, rather than to the nebulous “gouty” diathesis.
Again, despite Duckworth’s assertion that “the gouty throat is like no
other,” I am convinced that it presents no specific appearances. Nor
have I been able to satisfy myself that striated and fluted nails of,
it is usually affirmed, exceptionally brittle nature, are distinctive
of gout any more than the premature whitening of the hair so frequently
accredited to the subjects of this diathesis.
One point, however, I would emphasise is, the frequency with which
potentially gouty persons suffer from local _syncopes_ and _asphyxias_ of
the hands. They are precisely similar to those met with in _rheumatoid_
or _atrophic arthritis_, certain cases of which, as we shall see later,
have another affinity with gout, viz., _retardation in the output of
exogenous purin_.
_Locality, Race, Climate, etc._—As to the geographical distribution of
gout, the salient fact would appear to be the almost complete restriction
of the disorder to the _temperate_ zone. Among the natives of Africa
gout, according to Livingstone, is unknown. Neither apparently is it
to be met with in Turkey, China, Japan, Peru, and the Brazils. The
indigenous peoples of India, and the East Indian Archipelago, also seem
exempt, though the immunity does not extend to Europeans resident in
these tropical climes.
It is significant that Duckworth, inquiring of practitioners from foreign
parts as to their experience of gout, found that little or none was
forthcoming “save where Europeans have formed part of the community.”
This statement, to my mind, does but add cogency to my contention that
gout is always _hereditary_.
If we restrict our purview to the British Isles and the Continent, we
find that as a nation we have achieved the unenviable distinction of
being _facile princeps_ in point of the liability to and incidence of
gout. The bulk of examples, too, are met with in England, the disorder
being much less frequent in Scotland and Ireland. Moreover, in the two
latter countries, the disorder is practically restricted to the upper
classes. By contrast, in England it has extended to the lower orders
also, in respect of which peculiarity we stand unique as compared with
all other countries.
Reverting to the Continent, gout appears to be more common in France
than in Germany, Austria, and Italy. Indeed, it is said to be endemic
in Normandy, Burgundy, and the Rhone Valleys. In Holland, according to
Duckworth, there is practically no gout, and the same is true of Russia,
save in Petrograd and the Baltic Provinces.
In Belgium, also, gout is not common, and in Greece it is much less
prevalent than in France or England.
In regard to the incidence of gout, its greater prevalence in _temperate_
as opposed to tropical climes, and the disparities between different
countries, it would be unsafe to assume that the variations are the
outcome solely of _climate_. Thus the immunity of, _e.g._, strict
Mohammedans is attributable in part to their sobriety and the less highly
nitrogenous character of their food. But, if seduced into the ways of the
“infidel,” their exemption, it is said, ceases. Europeans, of “gouty”
heritage, may, if temperate, escape gout when resident in the tropics,
otherwise they fall victims thereto just as surely as at home.
Gout, indeed, is more a matter of _morals_ than climate. In the palmy
days of the Roman Empire, when luxury and indolence were rampant, gout
flourished, but declined following the installation of a republican form
of government. In like fashion and for similar reasons, the inhabitants
of modern Greece suffer infinitely less from the ravages of gout than of
yore. In short, the climate of Italy and Greece has presumably endured
unchanged, but the “habits” of their peoples have altered.
Formerly it was held that the incidence of gout in any country or
district varied according as to whether the population drank wine and
malt liquors, or distilled spirits. Where the taste for the latter
predominated, the disease was relatively rare, whence the comparative
immunity of Scotland, Russia, Poland, and Denmark. But what of the rarity
of gout in the wine-producing country Spain? Nor for that matter have I
ever seen it claimed that gout was especially prevalent in Portugal, the
home of “port,” that _bête noir_ of the “gouty.” In truth, dogmatism is
here out of place, for though overeating and overdrinking are undeniably
important factors in eliciting gout, they are not the _sole_ factors.
In reviewing the statements made as to the geographical distribution and
the race incidence of gout it is but too manifest that they are largely
provisional; indeed, such information as we do possess as to its relative
frequency in various countries, must be taken _cum grano salis_. Thus,
who can doubt that the various affirmations must have been very largely
influenced by the “personal equation,” that what one authority would
define as gout would by another be deemed inadmissible to this category.
Moreover, many of the original statements were made at a time when the
differentiation of arthritic disorders, as we now know it, was but in its
infancy. For obvious reasons, therefore, no researches in this sphere can
ever be satisfactory, until the opinion of the profession at home and
abroad be crystallised into some definite pronouncement, some precise
definition, of the exact criteria by which the diagnosis of gout stands
or falls.
In justification of these strictures, may I cite some opinions as to
the frequency of gout in the United States. In 1890, Sir Dyce Duckworth
affirmed that in America gout was “practically unknown.” But a few
years later, we find Sir William Osier convinced that gout was often
_unrecognised_ in the United States. More pertinent still, only twenty
years after Duckworth’s affirmation, Luff quoted the statistics of the
Johns Hopkins Hospital, Baltimore, from which it appeared that during a
period of fourteen years 0·26 per cent. of the total admissions thereto
were examples of gout. This he contrasts with the number of cases of gout
admitted to St. Bartholomew’s Hospital, London, during a similar period.
_Mirabile dictu_, the percentage was only 0·37, but a third more than
that of the Johns Hopkins Hospital!
Yet again, J. H. Pratt, of Boston, writing in 1916, observes “the
greatest confusion exists in the minds of many practitioners in America
to-day regarding this disease (gout) and its diagnosis. In some parts
of the country the diagnosis is frequently made in conditions that are
not gout; in other sections there seems to be a skepticism in the minds
of many practitioners regarding the existence of such a disease. In
New England I have found that chronic gout, even when tophi occur, is
often mistaken for rheumatism or arthritis deformans. Some physicians
of large experience assert that they see gout frequently. Enquiry has
shown that they mistake typical cases of arthritis deformans for gout,
and the swellings about the joints and even Heberden’s nodes for ‘gouty’
deposits.”
Can it for one moment be denied that even to ourselves, living in
England, the so-called “home of gout,” these trenchant criticisms are
but too applicable. So long, then, as such confusion exists as to what
does and what does not constitute gout, how can we, with any show of
scientific precision, presume to discuss, much less lay down, dogmatic
statements as to the geographical distribution and the race incidence of
gout?
_Food, Drink, and Occupation._—Gout, it has been well said, is the
“Nemesis of high living,” for, unquestionably _overeating_ is most
fertile in evoking any latent tendency thereto. Attempts to throw all the
blame on particular foodstuffs, _e.g._, red meats, etc., on the ground
that these highly nitrogenous substances engender excessive formation of
uric acid, have failed of their object. Even the much-maligned “purin
bodies” have of late been largely absolved of blame, and the virtues
of a “purin-free” diet, _e.g._, milk, are probably referable to the
_intestinal asepsis_ that such a regimen promotes.
My experience, like that of others, is, that it is not the quality, but
the _quantity_ of the food that is responsible. Moreover, I believe that
the _toxicity_ of the blood plasma thus produced exerts its evil effects
_indirectly_, viz., by lowering the _vis resistantiæ_ of the individual
to _microbic_ invasion. Nor have I any doubt that it is this same but too
common tendency to gluttony on the part of the “gouty” which is in part
responsible for the _cardio-vascular_, _hepatic_, and renal changes so
frequently associated with gout in its later stages.
Reverting to _alcohol_, there are many who regard it as _par excellence_
the predisposing cause of gout, and some even question whether gout would
have evolved had alcohol been unknown to mankind. But the interesting
point is, that _all_ forms of alcohol are not equally pernicious in
this respect, and the difference in their potency in this direction is
apparently little or at all referable to their _percentage content of
alcohol_. Port, madeira, sherry, burgundy, strong ales, and stout are far
more provocative of gout than distilled spirits. In England, where gout
is prevalent, malt liquors are the common drink, whereas in Scotland,
where the predilection is for whisky, the disorder is much more rare,
and the same applies to Ireland. In the Burgundian province of France
gout is common, but exceptional in the Rhenish district of Germany, where
hock is largely consumed. The why and the wherefore of these vagaries is
not as yet explicable; but of those forms of alcohol, most conducive to
gout, neither their _acidity_, _sugar content_, etc., can be impeached as
imparting to the alcohol its predisposing influence in this direction.
Incidentally, to those who advocate the primary _renal_ origin of gout,
one would propound the question, why is it that _distilled spirits_ are
less provocative of gout than wines, seeing these particular liquors are
so fruitful of _granular kidney_?
Again, if alcohol be such a potent factor in gout, why is it so rarely
met with in habitual drunkards, and how account for the comparative
rarity in gouty subjects of _hepatic cirrhosis_, or for that matter of
other disorders of alcoholic origin? Beset by these eccentricities of
behaviour, Sir William Roberts was tempted to regard gout as “rather an
incident of the legitimate dietetic use of alcoholic beverages.”
The relationship of _alcohol_ to gout is as erratic as it is to _atrophic
cirrhosis_. Thus an individual may drink hard through life, and escape
cirrhosis; another luckless wight, though he be quite temperate, yet
falls a prey thereto; still another, who may never have tasted alcohol,
acquires cirrhosis; lastly, cirrhosis is occasionally met with in the
lower animals, into whose diet alcohol does not enter.
In like fashion, an habitually intemperate man may pass through life
without incurring gout. Another, handicapped by his heritage, though he
be strictly abstemious, yet falls a prey thereto. Even a total abstainer,
when coming of gouty stock, may develop gout, haply through overeating.
To my mind, the only supposition deducible from these facts is that some
individuals are born with a tendency to gout, and that this tendency
may never assert itself as actual disease; that in others the dormant
proclivity, under the influence of alcohol, forthwith becomes manifest;
lastly, in some again, so nicely poised is the equilibrium of their
_nuclein_ metabolism, that the most venial alcoholic indulgence suffices
to evoke an outbreak.
I incline, therefore, to the view that alcohol _per se_ is not a cause
of gout; in other words, alcohol will not, in the absence of a _gouty
heredity_, produce gout. On the other hand, given an innate proclivity
thereto, alcohol, especially certain forms of it, will almost infallibly
evoke the disease; this often though the subject be conspicuously
moderate in its use.
That alcohol will produce the disorder even more swiftly and surely if
reinforced by _overeating_ also, cannot, I think, be gainsaid. As to the
_modus operandi_ of alcohol in inducing gout, I believe that it acts
_indirectly_, viz., by slowly sapping the protective mechanisms of the
body, and so paving the way to _infections_.
Much stress has been laid on the fact that certain _occupations_ conduce
to gout; but, if we exclude _plumbers_, _painters_, or other workers
in _lead_, no other callings in life can be held to entail a specific
predisposition to its development, save in so far as they promote
_overeating_, _overdrinking_, and _inactivity_.
It is well established that workers in _lead_ are specially prone to
develop gout. I take pride in noting that two of my predecessors at the
Royal Mineral Water Hospital, Bath, William Falconer (1772) and Caleb
Hillier Parry (1807), drew attention to the frequent occurrence of gout
in those exposed to the action of _lead_; nevertheless the major part
of our knowledge of lead as a predisposing cause of gout we owe to Sir
Alfred Garrod (1854). This authority noted that at least one out of
every four gouty patients that had come under his care at King’s College
Hospital had at some time in their lives been the subjects of _plumbism_,
and for the most part were plumbers or painters. Out of 136 undoubted
examples of gout, Sir Dyce Duckworth noted that of these twenty-five
males showed signs of lead poisoning, and were either plumbers, painters,
compositors, or workers in lead mills. My colleague, James Lindsay, out
of a total of 482 instances of males afflicted with gout, found that 108,
or 22·4 per cent., were workers in lead.
In light of these findings the question naturally arose as to whether
lead impregnation _per se_ could produce gout. It was then elicited
that the association of lead with gout was noticeably less frequent in
Scotland and in the North of England than in London. On this interesting
point Dr. T. Oliver observes, “We do not see in the north that intimate
relationship between gout and saturnine poisoning. Workmen from the south
develop it in the North of England. The natives of the north, though
equally exposed, seldom become gouty even when the kidneys are affected.”
Again, Osler tells us that in America lead-gout is comparatively rare,
though chronic lead poisoning is frequently met with in that country
in association with arterio-sclerosis and contracted kidneys. Again,
Frerichs, out of 163 cases of plumbism in the Berlin Hospital, found not
a single case of true gout.
Some remarkable instances illustrating the influence even of medicinal
doses of lead in determining outbreaks of gout are on record. In a
man aged 25-30, suffering from chronic diarrhœa, Sir Lauder Brunton
prescribed lead and opium pills. In less than ten days he returned with
gout in one of his joints, though he had never previously suffered from
an attack. My colleague, Dr. Munro, tells me of an even more striking
case. A lady under his care had used a hair wash, for many years, with
apparently no ill effects. She recommended a friend of hers to try the
same lotion, and within a few days she developed acute arthritic gout,
though she had never previously experienced the disorder. Analysing the
preparation, Dr. Munro found the clue in the contained lead.
As to proffered explanations of lead-gout some have sought it in the
production by this poison of _arterio-sclerosis_ and _chronic nephritis_.
But this is scarcely satisfying when we contrast the frequency of chronic
plumbism and associated arterio-sclerosis and contracted kidneys with the
relative rarity of lead gout.
The balance of evidence would appear to be in favour of the view that
lead _per se_ cannot produce gout. For the incidence of lead-gout is
scarcely appreciable, save in a population amongst whom from other causes
gout is prevalent. In short, lead in the absence of an hereditary bias,
is impotent to evoke gout.
As to its _modus operandi_, I think it exerts its effect through
derangement of the intestinal secretions, and so favours the migration
inwards into the system of pathogenic _bacteria_.
As for occupations other than those concerned with lead, it is certainly
notorious that gout is extremely frequent in those that are rich in
opportunities for overeating, overdrinking, and sluggish habits. This
point has never been more clearly illustrated than by James Lindsay,
whose analysis I take the liberty of transcribing.
Thus, out of 482 males the victims of gout, eighty-one were cabmen,
coachmen, grooms, stablemen, and bus drivers; fifty-one were draymen,
publicans, barmen, cellarmen, potmen, innkeepers, maltsters, coopers,
storekeepers, brewers’ travellers, and brewers’ labourers; twenty-five
butlers, men servants, ship’s stewards, and hotel servants; while
forty-five were labourers, and of the residue, although all kinds of
trades and occupations were represented, yet no other class reached ten
in number.
Of these various stations and occupations, it cannot be held that, in
themselves, these callings necessarily contain the “seeds of the gout.”
The banefulness resides in the _associated habits of living_; for but
too frequently repletion, intemperance, and indolence go hand in hand
with these vocations. In other words, dietetic excesses, overloaded
intestines, and too much alcohol, what more likely to impair the
digestive functions, to increase the toxicity of the intestinal flora,
and in turn to upset the equilibrium of general nuclein metabolism, with
its associated specific local reaction in certain tissues?
_Mental and Physical Over-exertion, etc._—Sydenham said of gout that it
destroys “more wise men than fools,” and in a letter to Dr. Short, he
complains, “I send you a short tract upon Gout and Dropsy instead of
the thicker volume, which in my own mind I had determined on, viz., a
history of such chronic diseases as my practice has most especially met
with. By applying my mind, however, to its utmost, and by bringing all my
powers of thought on the subject, I brought on a fit of gout, such as I
had never before suffered from; so that the fact itself warned me to lay
aside, even against my own will, such lucubrations, and to take care of
myself; well satisfied with having, in some measure, dealt with these two
diseases. Whenever I returned to my studies, gout returned to me.”
It is doubtful if, in the absence of an _hereditary_ proclivity,
intellectual strain would promote the development of gout. On the other
hand, there is, I think, no doubt that immoderate mental exertion will
indirectly precipitate an outbreak. I can well understand that the
illustrious Sydenham, absorbed in his life study, forgot to take a
normal amount of exercise. Perhaps, like the renowned Jenner, he would
have said, “I never walk at all except from my house into my carriage.
I hate walking, and if I could, I would get my servants to carry me to
bed.” Nevertheless, I doubt not that Sydenham’s intellectual efforts
necessarily entailed sedentary habits, which brought in their wake
digestive and intestinal derangements, whence his occasional gouty
outbreaks.
Gout, indeed, has taken its full toll of the “Intellectuals.” Thus
Scudamore tells us that “The late Mr. Pitt and his father had gout at
a very early period of life. The father was never a votary of Bacchus,
and neither of Venus (as we are told), but both were _ardent students_.”
Probably, in many instances, however, the evils of immoderate study are
reinforced by more reprehensible excesses. The ancients insisted on
sexual debauchery as favouring outbreaks of gout. Whence the Latin verse:
“Ut Venus enervat vires, sic copia vini,
Et tentat gressus, debilitatque pedes.”
Doubtless, in some instances of this supposed origin, a _gonococcal_
arthritis was confused with gout. Doubtless sexual neurasthenia with
diatetic excess favours the onset of gout. In the same way grief,
anxiety, and other depressing emotions are provocative of gout in that
they impair the digestive functions, lead to hepatic torpor, and sluggish
bowels.
SUMMARY
In conclusion, we have now dealt with those factors currently regarded
as _predisposing_ causes of gout. Personally, as I have before said, the
differentiation of the foregoing from the so-called _exciting_ causes of
gout is purely arbitrary. Thus even those who countenance such division
are forced to admit that many of the predisposing causes will, “if at any
time suddenly increased,” immediately excite a fit of gout.
In other words, the difference is _quantitative_ rather than qualitative.
Thus, a moderate drinker, if perchance he exceed his usual limits,
pays the penalty by an outbreak. Another habitually addicted to the
fleshpots eclipses himself, and a similar retribution is exacted. Or, he
exposes himself to a chill, with subsequent gastro-intestinal or hepatic
functional derangement. Yet again, the cessation of wonted exercise, and
more often the taking of it when unaccustomed, may determine the onset of
a paroxysm.
But far more arresting are the numerous and well authenticated instances
in which local _trauma_ not only determines an outbreak but also its
locality. How frequently, too, have blows, strains, sprains, _fractures_,
_dislocations_, or other trivial or severe injuries, been the signal
for an attack. Now, as we hope to show later, _local foci of infection_
are extremely _common_ in the _gouty_. Such are especially frequent in
the _teeth_, _tonsils_, _naso-pharynx_, etc. Is it not then extremely
probable that organisms may, _viâ_ the _blood-stream_, find their way
to a _joint_, the resistance of whose tissues has been lowered by a
_trauma_, however slight its degree? This I apprehend to be the true
explanation of the undoubted intimate connection between traumatisms and
arthritic outbreaks of gout.
Of similar significance, too, the numerous instances on record in
which acute attacks of gout have followed acute _tonsillitis_, acute
_pharyngitis_, acute _parotitis_, etc. How frequently, also, competent
observers, such as Garrod, noted that _boils_ and _carbuncles_ frequently
appeared to be excitant of acute attacks. But to this important point,
the intrusion of an _infective_ element in the genesis of gout, we shall
return in a later chapter entitled “Gout as an Infection.” It will
suffice here if we record our belief that—
(1) Heredity is the sole _predisposing_ factor in gout.
(2) That the differentiation between the usually cited
predisposing and exciting causes is unwarrantable.
(3) That both alike are merely _determinants_.
(4) That their influence as such in exciting outbreaks is
exerted through the medium of _infection_, this achieved either
directly or indirectly.
MORBID ANATOMY
It has been truthfully affirmed that we know more of the _results_ or
products of gout, and less of its _essential_ nature, than of almost any
other disease. Thus the post-mortem history of the disorder is concerned
almost exclusively with more or less graphic accounts of the _uratic
deposits_, their sites of predilection, and the changes that they induce.
Hence it is that the morbid anatomy of gout relates for the most part to
its _regular_ or _articular_ manifestations, for it is in and around the
joint structures that the deposits for the main part occur.
As to the assumed localisations of the disease in the _internal_ organs,
there is no _anatomical_ evidence that they are due to an invasion of
the “gouty” inflammation. Not even the _renal_ changes, despite the
attestation, as it were, of the gouty process by _uratic deposits_ in the
_papillæ_, can be held as distinctive of gout. Norman Moore found them
present in only twelve out of eighty cases. As Osler said, “The presence
of uratic concretions at the apices of the pyramids is not a positive
indication of gout. They are not infrequent in this country [U.S.], in
which gout is rare.... It is not possible to say in a given case that
the condition has been due to gout unless marked evidence of the disease
co-exists.”
If, then, nothing distinctive can be claimed of the _renal_, how much
less can we construe as “gouty” the anatomical alterations that may
or may not be met with in other organs in this disorder. In short, it
may be said of the _renal_ as well as the other _visceral_ lesions, so
often met with in association with gout, that they are met with even
more frequently in its absence, and most certainly fail to attest their
“gouty” nature by the appearances which they present.
The only morbid structural changes, therefore, that can legitimately be
defined as _specific_ of gout relate to its _regular_ or _articular_
lesions. As to the _anatomical_ alterations in the articulations, their
specificity depends essentially on the _uratic deposits_, rather than
upon the associated inflammatory and degenerative processes.
Given death during an _acute_ paroxysm, examination reveals the
usual tokens of inflammation, hyperæmia, effusion, and swelling of
the ligamentous tissues. The synovial lining is injected and spongy,
while the exuded fluid is thick, scanty and turbid, containing
polymorphonuclear leucocytes as well as _crystalline deposits_. Charged
therewith, not only is the synovia thick, but of a milky appearance.
Examined microscopically, it is found to contain the acicular crystals
of _sodium biurate_. The synovia has occasionally been found covered
with blood, but no _pus_ formation has ever been known to occur in
uncomplicated acute gouty arthritis. The reaction of the synovial fluid
is generally neutral or alkaline, but exceptionally Garrod found it acid.
Uratic deposit has a predilection for _cartilage_, and in some instances
is strictly confined thereto; but in the more _chronic_ forms it
permeates all the component elements of the articulation. In the synovial
membrane and fringes deposition takes place in the subepithelial and
subserous layers. It invades also the ligaments, the tendons, and even
the periarticular fibrous tissues become impregnated with biurate.
Moreover, like the synovial sheaths of the tendons, the neighbouring
bursæ are specially prone to deposits, which again encroaching upon the
subcutaneous connective tissues, infiltrate the skin itself, forming
chalk stones or tophi.
Inspected after death, the articular cartilages are seemingly overlaid
with a white mortar or chalk-like material, _i.e._, sodium biurate. Their
surfaces, however, though defaced by stains, streaks, or dull patches,
nevertheless, at any rate at first, retain their pristine smoothness.
This because closer scrutiny reveals that the deposit is not in reality
_upon_ the surface of the cartilage, but is located _interstitially_ in
its substance.
Microscopic examination of a vertical section, taken at the site of the
deposit, shows clearly that it is composed of felted masses of acicular
crystals. Lying in the matrix of the cartilage, they are more densely
packed just below its free surface. The crystals do not penetrate further
than one-third or one-half of the depth of the cartilage. Becoming more
and more sparse towards the deeper layers, those near the bone are
entirely free from deposit. This clearly indicates that the uratic matter
originated from the synovial fluid bathing the articular ends and was
precipitated therefrom.
As to the primary site of the deposition, it usually takes place at the
centre of the articular cartilage. Opinions differ as to whether the
cartilage cells are foci of deposition. Garrod thought so, but Duckworth
found no relationship between it and any histological elements, while
others locate it in the matrix.
While, as before stated, the cartilage at first retains its smoothness,
later it becomes pitted in patches. Ultimately the cartilage, through
atrophic changes and erosions, may disappear, the joint cavity becomes
filled with a plaster-like material, and the joint structures undergo
more or less disorganisation. _Pari passu_ with the central atrophy
of the cartilage, hypertrophic outgrowths form at its free margin.
In late stages the bones, too, undergo changes; their outer layers
become more dense through proliferative osteitis, while their spongy
tissue becomes rarefied, and the cells of the marrow fatty. Duckworth
held that uratic deposits might occur _primarily_ in the bone without
any similar implication of the related cartilage. On the other hand,
Garrod dissented, claiming that when the bone was involved, it was only
_secondarily_ to uratic deposition in the cartilage, of which indeed it
was but an extension.
In reviewing the foregoing findings, it must be admitted that morbid
anatomy fails to shed light on the _essential_ cause of gout. This, at
any rate, is true of the older studies with which, up to the present,
we have been engaged. Still, as Berkart’s more recent researches show,
our knowledge of even the _morbid anatomy_ of gout is as yet but in its
infancy.
_Histological_ examination of the _articular ends_ adjacent to gouty
joints reveals the presence of certain _cystic_ changes in the
_diaphyses_. Thereupon Berkart propounded an hypothesis, explanatory of
the acute phenomena of a paroxysm of gout. His view was that these cysts
in the bone, at first minute, gradually enlarge. Ultimately, through
concomitant thinning of the surface bone, there comes a day when the cyst
bursts into the joint, its content voided into the cavity thereof.
An interesting point noted by Berkart was that in many cases of “acute”
gout the articular cartilage was found apparently normal and devoid of
_uratic deposits_, and this although the attack had been sufficiently
severe. This would appear to contravene Garrod’s dictum that “gouty
inflammation is invariably attended with deposition of urate of soda.”
The same inference was drawn from a case of Sir Dyce Duckworth’s. The
subject had had two attacks of gout in the right great toe joint. Yet
at the autopsy neither toe joint contained a speck of uratic deposit.
Nevertheless, this does not prove that uratic deposition had not ensued
during the gouty attacks. All it can be held to prove is, that such
deposits are not always permanent, and that, under certain conditions,
they may undergo resolution. That this is so is almost certain, seeing
that tophi in the ear have been seen to come and go, and equally
certainly, after an acute attack, tophi in the neighbourhood of a joint
may lessen even though fresh ones form coincidently at another site.
Albeit, the importance of Berkart’s hypothesis and histological findings
resides in the fact that they suggest strongly that a pathological
process, more vital and biological than the mechanical uric acid theory,
is at the root of the clinical phenomena of a gouty paroxysm. It does
not put out of court Garrod’s assumption that uric acid is an invariable
_accompaniment_ of acute gouty inflammation, but it militates strongly
against his contention that uric acid deposition is the _cause_ of acute
gouty inflammation. It indicates the reverse, viz., that the uratic
deposition is the _consequence_ of a more vital underlying morbid process.
Let us revert now more in detail to Berkart’s findings. The bones
adjacent to gouty joints were fully prepared for microscopic examination.
Investigation of the first metatarsals, and in some instances of the
phalanges also, revealed the presence of _cystoid degeneration_. Its
starting point is in the _epiphyses_. Thence it extends to the articular
cartilage, through which it bores at one or more points. The contents
of the cyst then find their way into the joint through the fistulous
openings in the cartilage, with a resultant acute “perforative synovitis.”
The cysts, at first minute, may be either single or multiple. Small
in size, they are easily concealed by the fat marrow, unless the bone
is properly prepared for microscopic examination. The isolated cysts
eventually coalesce, and so lead to considerable excavation.
As to the contents of the cysts little is known, as, save through
accidents or surgical operations, they are rarely available for
examination. When of relatively recent origin they apparently consist
of a coagulable substance which later on become serous or hæmorrhagic.
So long as the fistulæ thus formed in the cartilage remain pervious, a
direct way into the articular cavity is provided, and through this, if
of sufficient calibre, the necrotic matter periodically gains entry into
the joint, with ensuing periodic outbreaks of acute synovitis. In other
instances in which the cysts are located in proximity to, or within, the
diaphysis they may fail to extend to the cartilage, and no perforation
ensues. In this event, through accumulation of its contents, the cyst
enlarges, and the bone is gradually expanded through pressure.
Berkart holds that the histological changes in the affected epiphyses
indicate that the cystoid degeneration is the outcome of an _anomaly_ of
the _vascular_ and _osseous_ structures. The degenerative area contains
an abundance of dilated and thin-walled veins, evidence of a condition
of chronic congestion. In consequence thereof, the trabeculæ undergo
decalcification, and the adjacent fat marrow becomes fibrous. The areas
of fibrosis thus formed, owing to thrombosis of the related veins, become
softened and transmuted into cysts.
Now, as we all know, some persons, after indulging in wine, almost
immediately experience sharp twinges in the small bones of their hands
or feet. Garrod attached diagnostic importance to such swift response
as a sign of gout. These pains he attributed to uric acid deposition.
In contrast, Berkart attributes the twinges to atony and consequent
over-distension of the related vessels, which lack the normal support
afforded by the osseous trabeculæ.
As far as we are aware, these findings of Berkart’s are as yet
unconfirmed. Nevertheless they provide us with a much more probable
explanation of the phenomena of acute gout than the older _uric
acid theory_, which, not to mention the many other obstacles to its
acceptance, has always laboured under the aspersion of being too
“mechanical” in conception.
Moreover, his studies clearly indicate that not only the intra-articular
surfaces but the adjacent _bone-ends_ and _marrow_ must, as the somewhat
rare opportunities present themselves, be exhaustively investigated.
For myself, I cannot believe that so passive an agent as an “anomaly of
the vascular and osseous systems” is the _fons et origo mali_ in gout.
Some more vital element must, I feel convinced, intrude, and I incline
to think an _infection_. Berkart himself brings forth evidence in favour
of this contention, inasmuch as he noted the frequent co-existence of
_lymphangitis_, so pronounced that the whole of the affected leg became
the seat of a _leuco-phlegmatic œdema_.