CLINICAL DIAGNOSIS (_continued_)
CHRONIC ARTICULAR GOUT
If the diagnosis of acute types of articular gout often presents
difficulties, these same are, if anything, accentuated when we approach
its chronic manifestations. For, _apart from uratic deposits_, the
anatomical lesions that ensue in joints the seat of long-continued gout
have no _specific_ character. In short, there is nothing pathognomonic of
gout in the changes produced, and which, as a matter of fact, we know to
be capable of production, by many different morbid agencies. Surely this
lack of specificity in its structural lesions should make us very chary
of admitting to the category of chronic articular gout any examples of
arthritis _destitute of uratic deposits_.
In our chapter on _classification_ we emphasised the desirability of
restricting the usage of the term chronic articular gout to that type
long since known as _tophaceous_ gout, this because there is little,
if any, doubt that that variety known as chronic deforming gout (syn.
arthritis deformans uratica) is largely made up of examples of rheumatoid
or atrophic arthritis and hypertrophic arthritis or osteoarthritis.[41]
As to _osteoarthritis_, I do not for a moment deny that _uratic
deposits_ may be met with in its victims. One frequently meets with
patients, the subjects of osteoarthritis of the hip, who at the same time
exhibit tophi in the ears.
But such to our mind are to be regarded as merely instances of
_osteoarthritis_ occurring in subjects of “gouty diathesis.” This
apparent blending of the two disorders must not be allowed to impair
the clarity of our conception as to the essential distinctness of gouty
arthritis and osteoarthritis.
Sir W. Hale White has some pregnant observations on this point. Many
patients, he says, “with chronic arthritis are quite wrongly said to have
gout; usually they have osteoarthritis. The presence of bony outgrowths
is strongly against gout, though it is not conclusive, for such may occur
in true gout either more or less all round the joint or in the form of
little nodules, but they never attain the considerable size common in
arthritis,” and he adds: “If no urate of soda is visible anywhere the
diagnosis may be very difficult.”
To proceed, the general and local phenomena of chronic articular gout
are such as scarcely lend themselves to succinct definition, and for
their description we would refer the reader to the chapter dealing with
its clinical aspects. As that careful observer Sir Alfred Garrod states:
“Chronic gout is at times confined to one or two joints, but sometimes
numerous articulations are involved.” In other words, chronic articular
gout may be mono-, oligo-, or poly-articular in distribution; and
naturally the process of differentiation is modified accordingly.
This being so, I purpose dealing in the first instance with chronic
monarticular gout, and in succession with the types of oligo- and
poly-articular location.
CHRONIC MONARTICULAR GOUT
Occasionally gout in its recurrences clings obstinately to the great
_toe_ and _tarsal_ joints. But since the advent of _radiography_
there should be little or no difficulty in differentiating a chronic
gouty arthritis of the great toe from the only other arthritic
lesion with which it is likely at this stage to be confounded, viz.,
_osteoarthritis_. But at the same time we would refer the reader back
to the chapter dealing with the differential diagnosis of the localised
variety of acute gout, as therein we dealt fully with other possible
sources of fallacy, _i.e._, _static deformities_, etc. We shall therefore
now proceed to discuss those exceptional cases in which chronic gout
is located not in one of the small, but in one of the _larger_,
articulations.
MONARTICULAR GOUT IN LARGE ARTICULATION A RARITY
Given a chronic arthritis of one of the larger joints, say the ankle,
knee, or elbow, we should be careful not to jump too readily to the
conclusion that it is of “gouty” nature. The more obscure it appears the
more need for caution. Needless to say, if the objective changes be but
minimal and the condition be, so to speak, practically a mere arthralgia,
there rests upon us the paramount necessity of careful discrimination
before labelling it as “gouty” in kind.
Thus, if it be the knee, it may be a referred pain due to hip disorder,
_e.g._, _osteoarthritis_ or _tuberculous_ disease, or it may be
symptomatic of an inflammatory process, or, having regard to the usually
mature or advanced age of the subject, it may be a _neoplasm_ in the
bones.
On the other hand, suppose the subject come complaining not much of pain
in his joint, but more troubled because of its _enlargements_. If now
on examination we find also that there is little or no tenderness, but
simply a condition of _peri-articular thickening_ or _intra-articular
effusion_, what shall be our method of procedure? Certainly not to leap
forthwith to the conclusion that it is gouty. No, not even if he exhibit
_tophi_ in his ears.
Now, as to pain and tenderness, it is a blessed feature of gouty
arthritis that, generally speaking, in the chronic forms pain becomes
much attenuated. But let us at the same time recollect that _syphilitic_
arthritis, both secondary and tertiary, is relatively _painless_. But it
is the much rarer _tertiary_ form, be it remembered, which is usually
_monarticular_. By the bye, too, we should never forget that a _Charcot’s
joint_ is also painless.
Coming now to the _objective_ phenomena, is the case predominantly one
of peri-articular infiltration or intra-articular effusion? As to the
former, while you never know, still _tuberculous_ joint disease is
exceptionally rare at the age at which we usually meet gout. On the
other hand, _gummatous synovitis_, with or without osteoperiostitis,
is occasionally met with. It is just such a case as this that may be
confounded with gout, the irregular lumpy thickening of the sub-synovial
tissues with effusion being wrongly attributed to a gouty process with
uratic deposits. Do not be misled if a history of injury be forthcoming
in such cases, for it is not uncommon and may be given in good faith.
Now what if synovial effusion of chronic or recurring form be the
striking objective feature of the case under review? In this event always
recollect that of all the causes of _monarticular_ disorder _injury_
is far and away the most frequent. Not a few cases of monarticular
joint disease come annually to the Royal Mineral Water Hospital,
Bath, under the diagnosis of “gout” and “rheumatism.” But in all
too many the symptoms are referable in truth to ligamentary strain,
displaced cartilage, or foreign bodies, lesions always to be sought for
and excluded in monarticular joint affection. Duckworth has it that
_hydrarthrosis_ is met with in chronic articular gout, in his deforming
variety. He states that “hydrarthrosis is less commonly due to gout than
to rheumatism,” but, we would remark, apart from traumatic lesions, more
commonly due to _gonorrhœa_ or _syphilis_ than to either of them.
But the reader may say, this dissertation notwithstanding, Where does
_gout_ come in? Precisely so, and if his experience tallies with mine, he
will find that chronic articular gout localised in _one_ of the _larger_
joints, and one only, is exceptionally rare. Personally, I should never
feel justified in making the diagnosis unless I had elicited a history of
(1) recurring classic outbreaks in the great toe with (2) an absence of
traumatic infective and nerve arthropathies and, on the other hand, (3)
demonstrable existence of _uratic deposits in situ_ in the peri-articular
tissues, the cartilage or bones as revealed by _skiagraphy_, or in the
related bursæ.
In conclusion, if all these various pitfalls have been avoided, it will
almost without exception be found that the final differentiation in
doubtful cases will rest between gout and _osteoarthritis_; and in the
vast majority, I had almost said all, it is the latter morbid process
that will be found responsible.
This all too lengthy disquisition will not have been in vain if it instil
caution. For it is in the monarticular types of joint affection that
errors of catastrophic proportion occur more commonly than in any other
form of joint disorder.
CHRONIC GOUT OF OLIGO-ARTICULAR DISTRIBUTION
The course of chronic articular gout, as has been observed, may be
chequered by acute outbreaks involving three, four, or more of the larger
joints. But, apart from this, there are those so-called _asthenic_ and
_afebrile_ types of gout in which two or more joints may be the seat of a
chronic gouty arthritis. In my experience it is the _knees_ that are most
frequently attacked. The joints are enlarged, the seat of more or less
effusion, but the distinctive feature is the presence of deformity due to
the irregularly rounded or ovoid swellings produced by _uratic deposits_.
Enlargement of the patellæ is also present, and they lose their sharp
edges, and sometimes they as well as the neighbouring articular ends are
studded with small bony outgrowths, but of minimal size compared with
those met with in _osteoarthritis_. The related _bursæ_, too, are often
the seat of _deposits_, a valuable clue to diagnosis. Needless to say,
such marked cases are nearly always the outcome of oft-repeated attacks,
the ultimate deformity being the result of successive accretions of urate
of soda laid down in the trail of the exacerbations.
ITS CONFUSION WITH CHRONIC VILLOUS SYNOVITIS
The frequency with which this misconception occurs is very noticeable. If
a _middle-aged_ woman of florid complexion and _corpulent_ habit begins
to complain of pain and stiffness in her knees with more or less swelling
thereof, there is a very prevalent tendency to attribute not only her
joint disorder to _gout_, but any gastric or nervous symptoms that she
may simultaneously complain of are translated as being confirmatory of
the assumption. It gathers weight too from the traditional and widespread
belief that “the change of life” is the period _par excellence_ at which
women develop the morbid vagaries associated with “irregular gout.”
Now, as Bassett Jones and I have pointed out in a previous work, this
condition, _symmetrical villous synovitis_ of the _knees_, is a very
common joint disorder in _women_ at or near the _menopause_. Frequently
they give a history of numerous _pregnancies_, or of _rapidly increasing
obesity_, while with or without this latter they display a _faulty
postural attitude_, indicative of lowered muscular and ligamentary tone.
Following in the wake of these, the subject develops a _symmetrical
flatfoot_, which, according to the stage at which it is seen, may be of
flexible or rigid type.
Now, such is the mutual _static interdependence_ of the component parts
of the lower limb that this condition of flatfoot promotes or favours
the incidence of _villous overgrowths_ in the proximal joints, the
_knees_. As to the _modus operandi_ we have put forward the following
explanation: “The everted foot, with its sunken arch, as before stated,
determines an alteration in the normal coaptation of the articular
surfaces in the knee, and this incongruence is revealed in skiagraphs by
the marked prominence laterally of the external tibial tuberosity beneath
the external femoral condyle. Coincidently, and for the same reason,
additional strain is thrown upon the internal lateral ligament. This in
turn favours a state of passive congestion or hyperæmia of the synovial
membrane, which becomes relaxed and thrown into folds, especially at its
reflexions near the edges of the cartilages. If, as often happens, the
individual is the subject of _varicose veins_ or suffers from a _general
lack of tone in her muscular or ligamentary structures_, this tendency to
venous engorgement of the knees is much enhanced.”
“Under the influence of these mechanical factors and their associated
circulatory disturbances, _thickening and enlargement of the synovial
fringes ensue_. The inflammatory condition thus produced tends to
increase automatically, as, owing to the articular incongruence, the
enlarged fringes are very prone to become caught between the joint
surfaces; in other words, a vicious circle is produced, as with the
increasing villous hypertrophy the liability to internal traumatisms
increases _pari passu_.”
VILLOUS SYNOVITIS STATIC AND NON-GOUTY IN ORIGIN
In short, the joint disorder is fundamentally of _static or mechanical_
origin, and, this being so, the results of _anti-gouty_ treatment are
open to a further misinterpretation. The victims, as we have said,
exhibit very generally a tendency to _obesity_. Now, Ebstein and many
others hold the view that _obesity and gout have affinities_. Ebstein,
moreover, believes that treatment directed to the reduction of body
weight will check the appearance of gouty arthritis or ameliorate the
same when avowed. What happens is this: these corpulent subjects are
placed on a special dietary. Hydrocarbon foodstuffs are limited, bread,
amylaceous food and liquids being also restricted. Naturally, _pari
passu_ with reduction in their body weight, their overburdened joints
become more equal to their office. But those who assume that the chronic
arthritis is of _gouty_ origin attribute, and, we think, wrongly, the
beneficial results attained to correction of the underlying “gouty” habit.
We prefer to subscribe to the simpler or mechanical theory, and in view
of the widespread and, as we believe, erroneous belief in the gouty
nature of this arthritis, we take the liberty of appending the salient
features of these cases, while adding further a few remarks on the
differential diagnosis of other symmetrical affections of the knees which
may also be wrongly attributed to gout.
CLINICAL SYMPTOMS OF VILLOUS SYNOVITIS
The onset is gradual and insidious. Stiffness is the salient symptom,
but sometimes the subject is more distressed by a sense of weakness,
distension and unreliability. Pain is slight or absent, save when during
walking pseudo-locking occurs. The mobility of the joints is usually
unimpaired, and if any limitation exist it is the power of full extension
that is usually restricted.
Objectively the joint shows either general enlargement or swelling
localised to the _supra_- or _infra-patellar_ regions. Intra-articular
effusion which comes and goes is a very characteristic feature. On
palpation a peculiar soft silken crepitus will be heard and felt as the
patient alternately flexes and extends the limb. The enlarged fringes
are also easily to be felt as knots or nodules which can be moved up or
down on the underlying bone. The ease with which they can be appreciated
depends upon the degree of effusion present at the time. Judging from
their symptomatology, it seems probable that some of the cases included
in Sir Dyce Duckworth’s category, chronic deforming gout, are of this
description.
The diagnosis of villous synovitis should not be considered complete
without _skiagraphy_ being undertaken to reveal or exclude osteophytic
outgrowths. For the subjective symptoms and signs of _early_
osteoarthritis are practically identical with those of villous arthritis,
and although the presence of osteoarthritic lesions elsewhere would be
suggestive, skiagraphy alone will enable us to effect a differentiation
with certainty. Indeed, Bassett Jones and myself are strongly of the
opinion that the life history of osteoarthritis involves two stages: (1)
a _primary_ or _pre-osteophytic_ phase, often of prolonged duration,
whose clinical characteristics are those of villous hypertrophy; (2)
a _secondary_ or _terminal_ stage, in which bony and cartilaginous
outgrowths make their appearance.
Other symmetrical disorders of the knees that may be wrongly ascribed to
gout are hydrarthrosis and gummatous synovitis.
_Bilateral Hydrarthrosis._—Given effusion into both knees which is
_passive_, _copious_, and _persistent_ rather than recurrent, then its
possible _infective_ origin must be carefully canvassed. The common
sources are _gonorrhœa_, _syphilis_, and _tubercle_. The history or
presence of an urethral discharge and detection of the gonococcus will
identify the first named. In syphilis the existence of other lesions, the
response to Wassermann’s test and specific treatment are the points on
which to rely, and in tubercle, the detection of visceral foci and the
sero-reaction will give the clue.
As to the _intermittent_ type of hydrarthrosis, the remarkable
_periodicity_ in incidence of the effusion will suffice to obviate any
possibility of confusion.
_Peri-synovial and Peri-bursal Gummata._—Affecting as they do commonly
the knee joints of adults, these may, in the absence of a history
of infection, be a source of error. The uneven and nodular swelling
may quite easily be confounded with uratic deposits. Pain is slight
and mobility but little impaired. The presence of neighbouring
scars, a positive Wassermann reaction, and a favourable response to
anti-syphilitic therapy will clear up the diagnosis.
CHRONIC GOUT OF POLYARTICULAR DISTRIBUTION
The clinical portrait of tophaceous gout when of widespread distribution
is one of the most striking to be met with in the whole domain of
medicine, but for the broad outlines of the picture presented we would
refer the reader to the chapter dealing with the clinical description of
chronic articular gout.
In these polyarticular forms the most distinctive joint deformities are
those met with in the _hands_ or feet, more particularly the former. The
excrescences produced are the outcome of successive _uratic deposits_.
These latter when massive can scarcely be confused with any other
disorder, for the superjacent skin, distended by the ever-increasing
underlying uratic deposits, becomes thinned and purplish red in hue, and
occasionally ulcerates. I have at present in my wards a case of this
nature, and the subject hoards up the exuding “chalk” in a small bottle.
Fortunately such marked examples are relatively rare, though easily
recognised; but it is the less marked types that occasion difficulty
in diagnosis. The point at issue of course is the differentiation of
moderate-sized or small tophaceous swellings from bony outgrowths.
Frequently the task is impossible of achievement without resorting to
puncture, when, if anything can be withdrawn, microscopic examination may
reveal the presence of _biurate_ crystals.
For the rest, attention to the following points will prove helpful in
enabling us to differentiate clinically between gouty arthritis and other
chronic joint disorders attended by deformities:—
(1) Tophi when of recent incidence are _soft_, and when of long
standing are never so dense or so hard as bony outgrowths.
(2) The overlying skin is thin, and through its substance the
subjacent white concretions may sometimes be discerned. It may
be adherent, or the seat of ulcers.
(3) Uratic deposits are _not located exactly at the level of
the articulation_. They do not adapt themselves to the contour
or shape of the bone-ends.
(4) Unlike osseous growths, they may be slightly movable in
lateral directions.
(5) Tophi may _soften_ or _disappear_ after exacerbations of
arthritis.
DIFFERENTIAL DIAGNOSIS
The conditions likely to be confused with chronic polyarticular gout are
osteoarthritis, rheumatoid arthritis, and the multiple arthropathies met
with in affections of the central nervous system.
OSTEOARTHRITIS
Its chief characteristics may be summarised as follows:—It is a disease
rarely met with under forty years of age. The mode of onset is generally
insidious, never really acute. In this respect it contrasts with gout,
the initial outbreak of which is invariably acute. Osteoarthritis
attacks both sexes equally. Although it may be polyarticular, its
specific tendency is towards a mono- or, more accurately speaking,
oligo-articular distribution, with no marked leaning to symmetry. It has
a pronounced predilection for attacking the _hip_, the _shoulder_, and
the _spine_—sites rarely, if ever, attacked by gout.
Unlike gout, constitutional symptoms, pyrexia and so forth, are generally
absent; muscular atrophy is slight, hardly ever pronounced, likewise
muscular spasm and contracture.
LOCAL CHARACTERS OF JOINT SWELLINGS
These are best appreciated in the small joints of the hand.
Osteoarthritis has an affinity for _terminal_ joints—the so-called
Heberden’s nodes. Another favourite site is the carpo-metacarpal joint of
the thumb, while the preference of gout is for the metacarpo-phalangeal
joint thereof and for the same articulation in the other digits.
The overlying skin, as a rule, is unchanged, and never assumes, as in
gout, a dusky red or purplish hue. The margin of the articular surfaces,
instead of being smooth and rounded, is broken and irregular, its nodular
contour being due to osseous outgrowths studding the line of junction of
the bones entering the articulation.[42]
In this respect they contrast with tophi, which are located near to,
but not at, the level of the joint fissure. Again, unlike tophi,
bony outgrowths are fixed, immutable, undergoing no change save in
the direction of progressive enlargement. While the tendency of an
osteoarthritic joint is to expand and increase, still the enlarged and
gnarled joints never attain the colossal bulbous appearance presented by
inveterate examples of tophaceous gout.
RHEUMATOID ARTHRITIS
This affection differs from the foregoing disorder as well as gout
in that it is most commonly met with in persons under forty years of
age. Moreover, it attacks women much more frequently than men. Of
polyarticular distribution, it evinces a marked tendency to symmetrical
invasion. Like gout, it has a pronounced preference for the smaller
joints, while, similarly, it avoids the hip and shoulder.
Constitutional symptoms are conspicuous: pulse quickened, temperature
raised, extreme wasting not uncommon. Intense and widespread muscular
atrophy with contracture is a prominent feature, also trophic
disturbances of varied nature and degree.
LOCAL CHARACTERS OF JOINT SWELLINGS
In early stages the skin over the joint is waxy white or semi-asphyxial
in tint, outline of joint smooth, rounded, and spindle in shape, with, as
a rule, no irregular bony projection at the level of the articulation.
If seen at a later stage, the swollen joint will be found shrunken from
atrophy of all the articular structures as well as the skin. Ultimately
it becomes reduced even below its normal size, the small “end-joint” of
atrophic or rheumatoid arthritis. The deformities due to muscular spasm
are usually in the direction of luxation and hyperextension, and differ
from those of gout and osteoarthritis, in which there is more generally
lateral displacement.
NERVE ARTHROPATHIES
The joint disorders incidental to tabes and syringomyelia do occasionally
find their way to spas for treatment under the mistaken conception
that they are instances of “gout,” “rheumatism,” or “rheumatic gout.”
In the case of tabes the mistake is often referable to the confounding
of its lightning pains with “gout” or “rheumatism,” with subsequent
relegation of the swollen joints, whether single or multiple, to one
or other of these categories. In the syringomyelic it is, I think, the
close resemblance that obtains between the joint lesions and those of
osteoarthritis or so-called “rheumatic gout” that accounts for their
uncalled-for and utterly useless transference to spas. I have known a
case of syringomyelia with multiple arthropathies in the hands sent to
Bath under the mistaken idea that they were of “gouty” origin.
These remarkable joint affections will be distinguished by their
fulminant onset with marked effusion and absence of _pain_, tenderness,
and heat. In addition, associated phenomena will be present, viz., ataxic
pupillary changes and lost knee-jerks in tabes, while syringomyelia is
characterised by dissociated anæsthesia, trophic disturbances of bones,
progressive muscular atrophy with paralysis.
HÆMOPHILIC ARTHRITIS
It will be recalled that Rieken held the view that so-called “bleeders”
were prone to attacks of gout, and that sometimes these alternated
with intra-articular hæmorrhages. Nor was he devoid of supporters, for
Sir Dyce Duckworth maintained that a definite hereditary relationship
obtained between gout and hæmophilia, while that astute observer Jonathan
Hutchinson also contended that the vascular weakness was the outcome of
gout and aggravated by serial hereditary transmission. Wickham Legg,
however, in his masterly contribution questioned the correctness of
Rieken’s proposition.
Personally, I cannot out of my own experience confirm or rebut the view
that “bleeders” come of gouty stock, nor have I ever met an avowed
gouty subject who was likewise the victim of hæmophilia. _Quâ_ its
joint complications, hæmophilia to our mind would appear to display
closer affinities with peliosis rheumatica than with gout; but, in
view of Duckworth and Hutchinson’s claims, it were wiser on our part
to withhold judgment, while paying them the deference of being alive
to the possibility of there being some obscure connection, though not
proven, between the two disorders. Again, as emphasising the necessity
for discrimination, we would draw attention to the fact that Konig
recognised three stages in hæmophilic arthritis: (1) hæmarthrosis; (2) an
inflammatory process, with pyrexia and spindle-shaped swellings apt to be
confused with tuberculosis; (3) extensive arthritic changes reminiscent
of arthritis deformans. Confusion with gouty arthritis clearly is only
likely in the second or third stages, and in the matter of diagnosis the
_personal and family tendency_ to hæmorrhages is the most important clue.