CLINICAL ACCOUNT (_continued_)
CHRONIC ARTICULAR GOUT
In delineating the features of the _acute polyarticular_ variety, we have
to a certain extent trenched on the clinical territory of the _chronic_
form; this is scarcely avoidable, inasmuch as the line drawn between
acute and chronic gout is purely arbitrary. Thus one authority remarks
of acute gout: “If the disease continue beyond three or four weeks, it
is to be considered as persistent or chronic” (Flint). Trousseau, again,
discussing the acute variety, more particularly the acute polyarticular
type, states that it “may last for some weeks, or even for three months,”
adding: “Should it extend beyond that period, it is no longer acute gout;
it is chronic gout.”
The truth is that articular gout in this respect is very prone to
vagaries. Thus, in rare instances an attack of _acute_ or _sub-acute_
gout, more particularly the latter, may merge without break into the
_chronic_ form of the disease.[35] Far more commonly the tragedy is more
slowly played out. The unfortunate victim, after passing through several
more or less classical attacks, finds that the intervals become shorter
and shorter until they merge, as it were, one into the other. Fortunately
its course is not one of continuous uniform severity. _Remissions_, but
not complete _intermissions_, occur, and every now and again intercurrent
acute attacks take place.
But, the reader may observe, surely this is very reminiscent of _acute
gouty polyarthritis_, with its serial content of acute paroxysms?[36]
Quite so; but there is this difference, that, although such may last six
weeks or three months, still there is a period put to the sufferings.
A respite of months or years of immunity, and relative health may then
supervene.
Not so, unfortunately, when such paroxysmal waves sweep over the subject
of long-standing or _chronic gout_. Not only do the recurrent acute
outbreaks occur with _increasing frequency_, but also with _increasing
length of duration_. It is here no longer a question of the intercurrent
acute attack lasting days, but _weeks_. Also during such exacerbations
either four, five, or six joints are simultaneously attacked, or in such
rapid sequence that before one joint is free another is involved.
But a word here as to the variations in _distribution_ of the _articular
lesions_ in _chronic gout_. The well-marked _penchant_ of _acute_
gout for the _great toe_ continues throughout the life history of the
disorder, the predilection for this site being equally a characteristic
of the _chronic_ type. As to the subsequent articular involvement, Garrod
held the sequence to be as follows: _heels_; _ankles_; _knees_; the
smaller articulations of the _hands_; lastly, the _shoulders_ and _hips_.
It has never been my lot to see either the shoulders or hips involved;
but I have seen _osteo-arthritis_ of the _hip_ in _men_ displaying
_auricular tophi_, and I am inclined to think that, in the presence of
the latter, it has sometimes been assumed that the hip mischief was of
_gouty_ nature—the “hip gout” of the older authors.
Moreover, the _order of sequence_ is by no means invariable, for
oftentimes a local circumstance, _i.e._, _injury_ or _sprain_, determines
the location. Again, chronic gout is very erratic in respect of the
_number_ of joints implicated. In some almost all the joints may be
affected, while in others, no matter how ancient the disorder and how
oft its recurrence, it remains localised to but a few joints; or it may
progress after a leisurely fashion, with each attack invading different
joints in succession.
Naturally, if the disorder confine itself to a few joints, and these, and
these alone, are the seat of the oft-recurring attacks, permanent changes
sooner or later make their appearance. Nor are the morbid effects limited
to the joints, but they invade the continuity of the limb, for the
oft-repeated inflammatory reactions lead to engorgements of persistent
nature. The contour of the affected members is distorted by the œdematous
tumefaction, which, more pronounced at the level of the joints, extends
in lesser degree beyond their confines. The skin, too, especially over
the fingers, undergoes a change in texture, often becomes smooth and
glossy, and through its dusky pink subjacent uratic deposits may be
discerned.
Old gouty subjects are often of sallow or parchment-like complexion.
The _blood_ in these cases of polyarticular gout conforms in attenuated
degree, in the matter of leucocytosis and secondary anæmia, to that
observed in the more _acute_ types, as witness the following blood
pictures.
All were males, the subjects of chronic articular gout of many
years’ standing. They all exhibited _tophi_, which were verified
microscopically. The examinations were conducted during the
inter-paroxysmal periods.
(1) BLOOD COUNT.
Red corpuscles, per c. mm. 4,832,000 = 96·6 per cent.
Hæmoglobin = 64 ”
Colour index = ·66 ”
Leucocytes, per c. mm. 11,000
DIFFERENTIAL COUNT.
Lymphocytes 42 = 4,620
Large mononuclears 4 = 440
Polymorphonuclears 52·5 = 5,775
Eosinophils 0 = 0
Mast cells 1·5 = 165
(2) BLOOD COUNT.
Red corpuscles, per c. mm. 5,040,000 = 100·8 per cent.
Hæmoglobin = 72 ”
Colour index = 0·72 ”
Leucocytes, per c. mm. 13,400
DIFFERENTIAL COUNT.
Lymphocytes 15 = 2,010
Large mononuclears 2·5 = 335
Polymorphonuclears 78 = 10,452
Eosinophils 1 = 134
Mast cells 3·5 = 469
(3) BLOOD COUNT.
Red corpuscles, per c. mm. 4,280,000 = 85·6 per cent.
Hæmoglobin = 66 ”
Colour index = 0·77 ”
Leucocytes, per c. mm. 12,000
DIFFERENTIAL COUNT.
Lymphocytes 23 = 2,760
Large mononuclears 3 = 360
Polymorphonuclears 74 = 8,880
Eosinophils 0 = 0
Mast cells 0 = 0
In these chronic forms, save during exacerbations, there may be little or
no febrile movement, and local pain, heat, and redness may be slight or
wholly lacking. But the articular swellings never wholly disappear, and
the mobility of the joints is never entirely regained. The articulations,
few or many, become stiff, ankylosed, and deformed, by the growth of
_tophaceous deposits_. But to detailed description of these latter we
shall return later.
In inveterate cases of this nature the victim grows more and more
crippled and infirm, the inroads of the disease upon the constitution
more and more palpable. Pelion is heaped upon Ossa, as one ailment sets
in after another, now of the digestive organs, now of the heart, or of
the kidneys. These subjects of chronic gout are more often than not
dyspeptic, show signs of _arterio-sclerosis_. Their _blood pressure_ is
_raised_, their vessels tortuous and thickened, and the left ventricle
enlarged.
As to the _variations in uric acid excretion_, these, as before remarked,
show no appreciable deviation from normal. Occasionally, however, there
is a tendency to _uric acid gravel_. Of more sinister significance,
albeit, is the fact that in many of these cases the urine is copious,
of low density, paler than normal, and shows a trace of _albumen_ with
hyaline casts.
As the disease marches to its fell end the appetite becomes impaired,
gastric catarrh and diarrhœa may sap the waning strength, or
palpitations, fits of dyspnœa, or angina-like attacks, sometimes
fleeting, but often of organic source, may portend a fatal issue. Ripe
for the sickle, a kindly “stroke” perchance puts an end to his protracted
misery. Or symptoms, long since manifest, of progressive _renal_
failure may usher in the closing scene, and happy the victim if he pass
muttering, half conscious, into that dream-like stupor drifting by
insensible graduations to death.
“The life of all his blood
Is touched corruptibly, and his pure brain
(Which some suppose the soul’s frail dwelling-house)
Doth by the idle comments that it makes
Foretell the ending of mortality.”
_Shakespeare._
So much in attempted portraiture of the long-drawn-out tragedy of
inveterate chronic gout. But, fortunately, it is not always thus, and
nowadays, at any rate, the evils wrought on the constitution by the
malady are seldom so malignant. For not only, as before stated, has
gout become less frequent, but its virulence also much attenuated.
States of so-called “gouty cachexia” were, however, more familiar to our
forefathers. It more commonly ensues in subjects of strongly _hereditary_
tendency, and particularly in those in whom the _initial_ attacks ensue
before thirty years of age. I recall the instance of a colonel who
sustained his first attack of gout when a subaltern of but eighteen,
brought on, as he thought, through exposure while shooting snipe in
Peshawur. It is in such cases that this so-called “gouty cachexia” may
overtake a man while yet in his prime, and vest him untimely “with all
the characters of age.”
As to the milder types of regular chronic gout, such usually arise, not
in youth, but in men past the meridian of life. In their instance the
recurrence of gouty paroxysms is often erratic. Periodicity becomes less
pronounced or wholly lost. The life history of the disease may be summed
up in a few sporadic outbreaks, occurring irregularly throughout a long
life. Even when at first the attacks occurred regularly in the spring and
fall the rhythm of incidence becomes broken. An attack comes before its
time, is belated, fails of appearance wholly, or an intermediate paroxysm
comes as a surprise. Moreover, in many such the gouty manifestations with
the passing years tend to become more and more attenuated, maybe even to
extinction. Thus, a man who in the middle decades was a martyr to gout in
old age gains freedom from its visitations, the disease having apparently
exhausted its vicious potentialities.
Reviewing articular gout as a whole, one cannot but realise that it does
in respect of the recurrence of gouty paroxysms exhibit inexplicable
vagaries, inexplicable in that, as Sir William Roberts long since said,
“in many instances they are dependent neither upon medical treatment nor
upon altered dietetic habits, but are due to spontaneous changes in the
constitution. They form part of the natural history of gout; and it is
important to bear their existence in mind when we seek to estimate the
value of therapeutic means in order to prevent ourselves from becoming
the dupes of misinterpreted sequences.”
Albeit, we would not end on too sombre a note. For, in respect of the
graver consequences of gout, it is unquestionable that right living,
aided by efficient therapy, may arrest the course or mitigate the
severity of the disorder. Moreover, as long as the attacks do not follow
quick upon each other, but are separated by long intervals, there is
little fear of a cachectic condition supervening. Life may not be
appreciably shortened, and such textural degenerations as may ensue,
though frequently attributed to gout, may often with at least equal
plausibility be assigned to advancing years, but this with reservation,
for, as Duckworth says, “the wilful libertine is likely soon to become
cachectic, while the prudent man may altogether avoid this state or avert
its evils for many years or decades of years.”
THE JOINT DEFORMITIES OF CHRONIC GOUT
The palpable changes in the affected joints differ widely in different
cases, and why is not apparent. Thus, the first attack, if of prolonged
duration, may bequeath a legacy of crippledom comparable to that met with
after repeated paroxysms. On the other hand, some, although they have
suffered from the disorder off and on throughout their lives, yet escape
those consecutive deformities which in others deform and cripple the
hands and feet, though the disease may be of relatively brief duration.
But in the less fortunate cases the continued ravages of gout lead to
a pitiful disablement of the affected limbs, reaching its acme in the
_hands_ and _individual fingers_, flail-like and semi-paralytic as they
so frequently become.
Not only are the digits variously distorted, their joints more or less
ankylosed, but the overlying skin, distended by the ever increasing
subjacent uratic deposits, becomes thinned and purplish red in hue,
and occasionally ulcerates. Similarly at ankle, knee, wrist and elbow
thickening and deformity ensue as the concretions accumulate in and
around the affected joints, these further accentuated by the correlated
inflammatory and degenerative processes. Coincident deposits in the
tendon sheaths and related bursæ contribute their quota, and at knee and
elbow the bursal masses may reach extraordinary dimensions. Not only do
the joints become deformed, but distorted also, through reflex muscular
spasm and instinctive adoption of unnatural attitudes for the avoidance
of pain.
So much for the broad outline of the picture presented, but a still
closer scrutiny is called for. The deformities produced are the outcome
of uratic deposits, which, as Charcot long since pointed out, take on the
shape of “irregularly rounded or ovoid swellings, bunched, and either
large at the base or just the opposite, _i.e._, provided with a pedicle.”
As shown in the coloured plate, the favourite site for their
development is the _dorsum_ of the _hand_ or the vicinity of the
_metacarpo-phalangeal_ or _mid-phalangeal_ joint. The resultant
disfigurement of the hand is very characteristic. Irregular tuberous
swellings surmount the knuckles, and spreading laterally, obliterate the
fossæ between them and their fellows. The same extend forward over the
first phalanges, from nigh the distal end of which again arise similar
bossy excrescences over the mid-phalangeal joints. Encroaching thus
upon the length of the first phalanx from either end, but little of its
shaft is ultimately left exposed. In like fashion the mid-phalanx may be
buried in uratic deposits, its contour wholly lost; and, the terminal
phalanx participating, the digits become almost pedunculated, the nails
projecting from the ends thereof—the “parsnip hand” of Sydenham. Such is
the appearance presented in inveterate chronic gout.
Fortunately such examples are relatively rare, and a study of the
condition in its earlier stages reveals some interesting features. The
uratic deposits, it is important to note, _are not located exactly at
the level of the articulation_. Unattached as they are to the _articular
ends_, they are not compelled to, nor do they in any way, adapt
themselves, as it were, to the contour or shape thereof. In short, the
tophaceous formations are _erratic_, are not like _osteo-arthritic_
nodules, erupted from and continuous with the articular bone ends. Again,
relatively independent of the contiguous tissues, they, unlike osseous
outgrowths, are slightly _movable_ in lateral directions.
When of _recent_ incidence, their consistence is _soft_, and, be they
never so ancient, they do not attain the _density_ and _hardness_ of
_bony outgrowths_. The overlying skin, to which they are sometimes
adherent, takes on a peculiar glossy and satin-like texture, its dusky
pink blotched with spots of dead white colour, _i.e._, subjacent uratic
deposits.
In other particulars also they differ from bony outgrowths. The
tophaceous masses may _soften_ and _disappear_ after exacerbations of
_arthritis_, and others may form at different sites. Following such
absorption or difference in their location, some increase in joint
_mobility_ may happily ensue. This same fortunate occurrence may follow
discharge of the uratic masses through _ulceration_ and _perforation_ of
the skin.
TOPHI: THEIR EVOLUTION AND DISTRIBUTION
In our chapter on _Uratosis_ we dealt with the chemical nature and mode
of formation of tophi. Also we affirmed our belief that tophi, whether
_articular_ or _ab-articular_ in site, were always _preceded by local
inflammatory reaction_, and to the clinical tokens of their impending
eruption we need not recur. Albeit this point, _i.e._, _antecedent_
inflammation, is of such prime importance that we have not hesitated to
append to our text a lengthy footnote,[37] this because, as Garrod, who
quotes the same _in extenso_, rightly claims, the genesis and evolution
of tophi has never been so graphically depicted as in Moore’s description.
It will be seen that this observer holds that tophus formation “is
usually preceded and accompanied by inflammation.” Garrod, as we know,
believed uric acid to be the _cause_, and not the consequence, of gouty
inflammation. But he emphasises the fact that the phenomena attendant on
the eruption of auricular tophi are “exactly the same as when a joint is
affected, and constitute, in fact, a true gouty paroxysm, commencing with
infiltration of the tissue and subsequent inflammation.” Still, though
venturing to differ as to the sequence of events, we gladly invoke this
authority’s observations in proof of the fact that the _inflammation_
even in the _ear_ is not always of negligible grade: “I have seen many
cases in which the ear symptoms have proved very annoying, so that
patients have been unable to rest their ears on the pillow.” _Subacute
gout_ sometimes occurs in the ears, says Duckworth, who furthermore
believed that the _indurations_ in the _cartilage_ observed by him
in _gouty_ subjects were the outcome of such attacks. Laycock, too,
long before noted that the ears of gouty subjects often appeared to be
“soldered.”
_Pain or discomfort in auricular tophi often presages an oncoming
articular paroxysm._ “Those gouty persons,” said Scudamore, “who are
affected with concretions (chalk-stones), experience for a short time
before the fit pricking pains in the parts where they are situated. This
is described even by those who have minute points of concretions in the
lobes of the ears and in no other parts of the body.” Hence tophi have a
_prognostic_ as well as diagnostic valency in that the incidence of pain
at their site may foretell the oncoming of _articular_ outbreaks.
While, as before emphasised, the eruption of tophi may _antedate_ the
occurrence of _articular_ gout, on the other hand tophi may be present at
the joints, but lacking in the ears and all other _ab-articular_ sites.
Auricular tophi, extracted occasionally by patients, are sometimes shed
_spontaneously_. According to Duckworth’s statistics, in one-third of
all well-marked cases of gout the ears present tophi in the _helix_, the
_anti-helix_ and its _fossa_ and the _lobule_, and in some cases they may
be situated on the _posterior_ surface of the _pinna_.
OTHER SITES OF TOPHI
Apart from the external ears, tophi are apt to form in various
localities. Most frequently they are situated in the vicinity of the
_joints_ and _bursæ_, especially that over the _olecranon_. As attack
follows attack at short intervals the tophaceous matter is heaped up
around the joint, and in this way many articulations may be involved,
even all of them, says Trousseau, “as happened to Gordius, who composed
on himself the following jocular epitaph:—
“‘Nomine reque duplex ut nodus Gordius essem.’”
Uratic deposits sometimes attain a prodigious size. I have seen them the
equivalent of a small hen’s egg. The largest tophi are invariably found
in the neighbourhood of some joint, and the upper extremities furnish the
most marked examples. But even when of considerable magnitude they may be
non-adherent, the skin gliding freely over their surface. As John Hunter
wrote: “The chalk shall remain for years without producing inflammation,
and seldom produces it at all but from quantity.”
Often, however, their presence at length induces irritation of the
overlying integument. As they approach the surface the skin assumes a
purple hue, becomes thin, and ulcerates. The uratic ulcers thus formed
have generally an indolent fungous base. As the deposits extrude or are
removed they are continually redeposited, and in this manner ounces
of urates may be discharged. The same is followed by great relief and
diminution of deformity.
Discussing such lesions, John Hunter tells us that “when the interior
surfaces are exposed they hardly take on common inflammation and
suppuration, healing more readily than a sore of the same magnitude from
any other cause; even a joint shall be exposed, yet common inflammation
shall not come on, nor shall it suppurate: only a watery fluid shall
come out, bringing the chalk with it occasionally, and it shall heal up
kindly.”
A glance, too, at the preceding footnote shows that Moore also agreed
with Hunter as to the absence of common inflammation and suppuration.
Moreover, even of recent years it has been suggested that, because
gouty tophi do not suppurate even when ulcerated through the skin,
the _urates_ have _antiseptic_ properties. But Bendix (_Zeit. klin.
Med._, 1902) failed to demonstrate such qualities experimentally. The
truth would appear to be that, though gouty inflammation never ends
in _suppuration_, yet _abscess formation_ very commonly occurs in the
_peri-tophal_ tissues. Such more often ensues in subjects of frail health
or of definitely cachectic type. Garrod saw as many as five or six open
at one time in each hand, and others on the feet. In his experience they
give rise to but little constitutional disturbance. Scudamore, speaking
of the same, says the sores produced are “unusually tender, aching, and
sometimes very painful as the fit is making its approach.”
Ultimately the gouty ulcers thus formed dry up, and this indifferently
whether or not the uratic deposits are wholly extruded in the discharging
pus. The wound then closes, leaving a small scar, which, however, given a
fresh attack of gout, is but too likely to break down, and this process
may occur repeatedly. Bursal sacs containing tophi not infrequently
suppurate, constituting abscesses containing urates.
An interesting fact noted by Garrod was that so long as such abscesses
were discharging freely the subjects enjoyed comparative immunity from
overt gout. But, given healing of the same, in several instances he had
seen it the signal for a sharp outbreak. Duckworth, too, states that
“whenever ulceration and flow of tophaceous matter occurs it is rare to
meet with paroxysmal attacks anywhere in the body. With the cessation of
the discharge renewed fits may intervene.”
While they tend to aggregate themselves round the joints, yet tophi
sometimes invade the _integument_ of the _limbs_. They have been seen in
the skin over the _ulna_ and _tibia_, and commonly over the _olecranon_
and _patella_. Pye Smith recalls the instance of a man in whom a number
of small ulcers, discharging urate of soda, formed in the middle of his
_thighs_ and _legs_. The case is not an isolated one, but the incidence
of subcutaneous uratic deposits in the limbs, save over _articulations_,
is exceptional.
In the _palms_ of the _hands_ and the _pulps_ of the _fingers_, the
knuckles and phalanges, tophi are found not infrequently; and Trousseau
tells of a lady of sixty in whom the cutaneous _palmar folds_ of both
hands were “marked with radiating white lines such as are seen in those
who have long been employed in tempering plaster.”[38] Similar deposits
have been noted in the _plantar surface_ of the _feet_.
Reverting to the _trunk_, uratic deposits have been found in the
_scapular_ region, also in the _perineum_. I have twice seen tophi
in the _corpora cavernosa_ of the penis. In the face, apart from the
ears, they have been found in the _alæ_ of the nose. In the _eyelids_
Duckworth noted uratic deposits in streaks resembling xanthoma; they
were chemically tested, and proved to be of this nature. Speaking of
“gout in the eye,” Garrod states: “I have witnessed many cases in which
conjunctivitis and sclerotitis appear to be distinctly connected with the
gouty diathesis, and in two cases there existed _deposits_ of _urates_ on
the surface.”
As before stated, we recognise only one type of gout, viz., the
tophaceous variety. But even so it must be noted that in some instances
the process of tophus formation is greatly accentuated. In other words,
the tophi may not only be of prominent size, but of unusually widespread
distribution. Indeed, poetic exaggeration has it that one Baylas and
one Acragas were entombed while alive in their own uratic deposits.
But, apart from such imaginative flights, there are unquestionably some
cases in which tophi are most widely diffused. Thus Plater tells of a
patient whose whole body, even the eyelids, was studded with them: “ex
toto corpore, per poros, adeo ut etiam palpebræ oculorum non exemptæ
fuerint, ejusmodi materia gypsœa, circa poros cutis mox in tophos mutata,
prodisset.”
These cases of multiple tophi are far more common in men. Duckworth met
with some well-marked cases in women. They may occur also in persons who
have been lifelong abstainers. Sometimes trauma seems to have played
a part in determining their localisation. Garrod held that, given
prodigious uratic deposition, the kidneys might be held as unsound and
undergoing sclerosis; and, according to Duckworth, the rule commonly
holds good.
AFFINITIES BETWEEN GOUT AND OTHER DISEASES
Whatever be the explanation, no fact in practical medicine is better
established than this, viz., that certain disorders are peculiarly liable
to arise in gouty subjects. Of these the more noteworthy are glycosuria,
phlebitis, certain cutaneous disorders, and nephritis. While, for
myself, I prefer to regard these affections as merely diseases to which
the gouty are especially subject, nevertheless each and all of them,
by one authority or other, have been classed as among the _irregular_
manifestations of gout.
This, on the assumption that these several morbid entities may precede,
alternate with, or follow arthritic seizures, frequently also on the
basis of their alternation in hereditary transmission with arthritic
gout. Thus, in a family of marked gouty proclivity, while one son,
despite a temperate life, may have severe articular gout, on the other
hand his brother may suffer only with _irregular_ manifestations, _i.e._,
phlebitis, eczema, etc.
As to whether these particular disorders, phlebitis, glycosuria, etc.,
are directly caused by the toxin of gout, or whether their not infrequent
association with gout is merely accidental, is a moot point. But to the
sources of fallacy in this connection we shall allude more in detail when
dealing later with irregular gout. Meanwhile extended knowledge of the
intimate etiology of phlebitis, glycosuria, etc., tends to an attitude
more critical than that of our forefathers, who, _faute de mieux_,
relegated a large number of conditions whose pathology was inexplicable
to the nebulous domains of irregular gout.
GOUT IN RELATION TO GLYCOSURIA
That some obscure link existed between glycosuria and gout was long since
suspected. Prout noted it as far back as 1843, and Bence Jones discussed
the subject under the title “Intermitting Diabetes” (1853), while in the
following year Gairdner announced that he had long surmised the kinship
between the two disorders. About the same time Claud Bernard remarked
that gout and glycosuria might alternate, and so did Trousseau, and many
since that day have ranked glycosuria as one of the forms of _irregular_
gout, whether legitimately or not is an open question, but at any rate it
does not affect the established clinical fact that glycosuria occurs with
significant frequency in gouty individuals.
Gouty glycosuria is more common in males than females. The subjects
are usually robust, middle-aged, and of full habit. Sugar is found
intermittently in their urine in small amounts, but no acetone bodies. It
is as a rule unaccompanied by thirst or wasting. It quickly responds to
dietetic restrictions. As Gull long since observed, gouty glycosuria does
not “discover itself,” but is “not uncommonly discovered.” This tersely
sums up the clinical difference between this affection and true diabetes,
albeit, as in all glycosurias, there is always the risk that carbohydrate
excess, mental strain, or other adverse circumstances may aggravate the
disorder and the case merge into one of true _diabetes_.
Following the installation of glycosuria, the tendency to paroxysmal
_articular_ outbreaks often ceases. The converse also has been observed,
viz., that when, in sequence to dietetic restrictions, the sugar
disappears, the articular pains may reappear. The fact that attacks of
glycosuria may alternate with attacks of gout led to the assumption that
a positive antagonism existed between the two disorders. Hence the phrase
“the more sugar the less gout,” and _vice versâ_. This, however, with
reservations, for a fugitive glycosuria has been seen during an acute
articular paroxysm, and a classical outbreak in the toe has been known to
supervene in the course of a well-established glycosuria.
It is generally held that glycosuria is most commonly associated with
_irregular_ forms of gout. But, in view of our ignorance of the intimate
nature of even _regular_ gout, I should myself deprecate affixing the
prefix “gouty” to any glycosuria other than one that has supervened in
sequence to, or alternates with, gouty _arthritic_ seizures. Moreover,
the glycosuria of gout is usually the alimentary glycosuria of fat
elderly people, in whom the sugar excreted represents the unconsumed
surplus of carbohydrate food. But fat elderly people are not necessarily
“gouty,” neither is every so-called benign glycosuria inevitably linked
on to a gouty diathesis. In fact, the relegation of glycosuria to the
gouty category is but too often not a matter of diagnostic certainty, but
rather an inference. Hence my plea that the prefix “gouty” would best be
restricted to glycosurias occurring in individuals who suffer _regular_
attacks of gout, or those displaying those objective tokens pathognomonic
of the disorder, _i.e._, _tophi_.
Again, James Taylor has recently reminded us that, if nerve affections
are relatively common in true _diabetes_, the same may be met with in
_gouty glycosuria_, even when of temporary duration. Thus symptoms
indicative of _peripheral neuritis_ may occur, _i.e._, lost knee jerks,
paræsthesiæ, and paresis of the lower limbs. Now, as this authority
pertinently observes, the subjects of _gouty glycosuria_ are frequently
given to _alcohol_. Consequently the question whether or not the
symptoms are due, not to sugar, but to _alcohol_, arises forthwith.
In some undoubtedly the alcoholic factor plays a _rôle_, but such
symptoms may, on the contrary, arise in very abstemious individuals.
This notwithstanding, James Taylor holds that the clinical complex
differs substantially from that met with in true _alcoholic neuritis_.
It is slighter in degree, the paresis usually restricted to lower limbs,
while the exquisite tenderness to pressure on nerve trunks so typical
of alcoholic neuritis is little or not at all in evidence. Nor is
there the same tendency to contractures in muscles as met with in the
alcoholic variety, and withal there is an absence usually of the mental
changes—loss of memory—associated therewith. Accordingly Taylor holds
that we must recognise the existence in the _gouty_ of a true _glycosuric
peripheral neuritis_ quite independent of _alcoholic peripheral neuritis_.
Other concomitant nerve troubles noted in this association are _severe
intercostal neuralgia_ and, even more commonly, _neuralgia_ of the _fifth
nerve_, and to this may be added _migraine_ and that other neurosis
_asthma_. Intense mental irritability and depression is not an infrequent
sequel in gouty glycosuria. According to James Taylor, melancholia even
may result, especially if the glycosuria have merged into true diabetes—a
sequel, he says, especially prone to occur in Jewish subjects.
Having seen and suffered many painful disillusionments through too
flippant relegation of neuralgias or neuritides to diatheses “gouty”
or “rheumatic,” I would emphasise the necessity for great caution. In
other words, before labelling a neuralgia or neuritis as “gouty,” all
possible causes, _infective_ or _other_, should be excluded, this always,
but pre-eminently so in _brachialgia_, _sciatica_, and _trigeminal
neuralgias_. Nor even, should there be a history of classic _outbreaks_
or blatant _tophi_ present, should we be less vigilant.
By all means recognise the _gouty diathesis_. It often avails much
in treatment, but not if, _e.g._, _dental caries_, _antral disease_,
_cervical rib_, or _pelvic growth_ be overlooked, not to speak of recent
or concurrent sources of _infection_ or _toxic absorption_.
Lastly, we should always recollect that gouty glycosuria, as Gull said,
“does not discover itself”; it is not writ large on the subject like
true diabetes. But given the incidence of _nerve_ troubles in a _gouty_
person, _i.e._, a paræsthesia, itching, neuralgia, etc., we should always
suspect its presence.[39] Incidentally our search may reveal not only
sugar, but also _albumen_, and the latter may explain much that appeared
inexplicable.
GOUT IN RELATION TO PHLEBITIS
It is to Sir James Paget that we are indebted for recognition of the fact
that phlebitis occurs with significant frequency in gouty subjects. This
great surgeon held that the disorder was the outcome of a modification
or transformation of gout, the result of “morbid conditions changing and
combining in transmission from parents to offspring.” At the present time
some regard it merely as a complication of gout, others as one of the
_irregular_ manifestations of the disease.
It occurs most commonly in men, women being rarely the subjects of
gouty phlebitis. It may install itself insidiously with but mild local
discomfort, and yet on examination a cord-like hardness is detected. In
others it announces itself with pain, in rare instances intense, this
more commonly if the deep veins of the calf are its seat.
Its predilection is for the veins of the lower extremity, the superficial
rather than the deep vessels. If the former, a faint blush over the
affected veins may be seen, but if the deep veins, then œdema and
tenderness may be the sole token of its presence.
Frequently the phlebitis is patchy in distribution and migratory. Thus,
as Paget says, it may on one day be located in a short length of the
saphenous vein, flitting the next day to some other portion thereof, or,
it may be, to the corresponding vein of the opposite limb. This tendency
on its part to metastasis and symmetry led Paget to the conclusion that
“the essential and primary disease is not a coagulation of the blood, but
an inflammation of portions of the venous walls.”
Its duration is not uncommonly prolonged, and it displays a marked
tendency to recurrences, the latter determined by blows, unusual
exertion, or, according to some, exposure to cold. Most cases end
favourably, but death from embolism sometimes occurs. Occasionally, given
occlusion of the large veins, some degree of swelling lingers permanently.
The instances most indicative of a _gouty_ origin are those in which the
veins of a limb, the seat of _acute gout_, are simultaneously attacked
by phlebitis. In three cases of this nature recorded by Garrod, the
subjects, despite their suffering from acute articular gout, persisted in
leaving their beds to record their votes in the parliamentary election
of 1884. This type of case, according to Garrod, is usually confined
to men, and, with the exception of the cases above noted, a _varicose_
condition of the veins of the legs of long standing existed in his series
of examples.
Garrod recognises in addition a second type, in which phlebitis,
“usually of a much less acute character, ensues without the previous
development of gouty inflammation in the neighbourhood of the part.”
Here we may recall that, according to Paget, the incidence of phlebitis
in an elderly person without any external cause warrants the suspicion
of gout. Perhaps the chief justification for such an assumption rests on
the fact that phlebitis appears sometimes to be _hereditary_. Paget cites
the instance of a man who suffered from phlebitis of both saphenous veins
during an attack of acute gout. On the maternal side his mother, two
uncles, a grandmother, and two cousins had been the subjects of phlebitis.
In conclusion, for myself, I would suggest that the term “gouty”
phlebitis be restricted to those instances in which a limb, the seat of
_acute articular gout_, is complicated by _phlebitis_ of the veins of the
affected part. Here we are dealing with what is palpably an extension
of the gouty inflammation from the affected _joint_ to the _veins_, and
which, I venture to assert, is strongly confirmatory of the view that
an _infective_ element intrudes in “gouty” arthritis. We may recall
that, _e.g._, _gonorrhœal phlebitis_ of the lesser saphenous veins is
not so uncommon, while the frequency with which phlebitis complicates
_infections_ calls for no emphasis.
Leaving aside these rare instances of _acute gout complicated by acute
phlebitis_, I think there is a too flippant tendency to regard any
phlebitis occurring in middle-aged or elderly subjects as being of this
nature, this often in the absence of any evidence, hereditary or other,
of a gouty element in the case. Frequently, too, the subjects are women
with _varicose veins_ of long standing, and _ipso facto_ potentially
liable to phlebitis. But why, in the absence of ancestral or acquired
gout, dub such cases forthwith as “gouty”? We may, it is true, as in
Paget’s classical instance, elicit a _familial_ tendency to phlebitis,
but even so I doubt the legitimacy of the inference that the phlebitis
is necessarily “gouty.” Is it not equally true that the tendency to
_varicose veins_ is hereditary, and _ergo_ predicates an enhanced
liability to phlebitis?
CUTANEOUS DISORDERS
The incidence of tophi in the skin naturally engendered the conception
that gout was responsible for many and diverse types of cutaneous
affections. In accordance with this, every effort was made to prove that
they were the outcome of uratic infiltrations, but in vain.
Objective proof of this nature being lacking, the older clinicians
found their justification in the alternation of arthritic attacks with
cutaneous disorders, and their alternation in inheritance was laid great
stress upon, this especially by French dermatologists, notably Bazin,
but at the present day Jacquet’s non-committal pronouncement is probably
representative of the attitude of the French school as a whole towards
“arthritic” affections of the skin: “Le lien admis entre le groupe de
maladies dites _arthritiques_ est très mal connu dans son essence, mais
il serait tout aussi contraire à l’esprit scientifique de le nier avec
rigueur que de l’affirmer avec presomption.”
As to the skin disorders associated with _acute_ types of gout, perhaps
the most interesting and well ascertained is _herpes_. It may precede
an acute attack, may alternate with it, or be a sequel thereof. Rendu
noted that acne, boils, and carbuncles also might occur prior to, in
alternation with, or in sequence to acute attacks, and Scudamore noted
the same in respect of erysipelas.
The noteworthy liability of the gouty to these disorders is but another
proof that gout predisposes its victims to _infections_. The fact that
acute gouty arthritis might follow acne, boils, etc., lends colour to our
contention that the same may be of infective origin. But unfortunately
the suspicion also intrudes that some of the arthritides occurring in
such association may, on insufficient grounds, have been diagnosed as
“gouty,” this especially if the joint disorder were located anywhere save
at its classic site, the _big toe_.
Passing to skin affections associated with _chronic_ gout, it must be
admitted that as a whole the contention that they are “gouty” in origin
is, to say the least of it, doubtful. French dermatologists claimed
that the cutaneous eruptions of the “gouty” might be recognised by
their polymorphism, circumscribed location, etc., but these are no more
distinctive peculiarities than the concomitant pricking, hyperæsthesia,
and hyperalgesia upon which Bazin laid such emphasis in their diagnosis.
In short, sequences, coincidences, and alternations are the basis of
much that has been written upon so-called “gouty” cutaneous affections,
criteria all of them fruitful sources of fallacy.
As to _psoriasis_, I have met with it so frequently in association with
non-gouty arthritides that I have never felt justified in claiming any
example as “gouty.” So-called “gouty” _pruritis_ and _prurigo_, these
when they occur in the “gouty” are frequently referable to an associated
glycosuria, and when this is not the case, it is frequently a senile
prurigo. The claim that urticaria is “gouty” may be dismissed without
comment.
As to frequency of incidence in the “gouty,” _eczema_ undoubtedly must be
awarded the palm. But whether the scaliness of skin on extensor surfaces
of arms and legs and back of neck, which ultimately, under the influence
of skin infection through scratching, develops into a dermatitis which
assumes the character of eczema, can be, strictly speaking, held as of
“gouty” origin, is questionable. Certainly, whatever be the origin of the
pruriginous scaliness of the skin, there can be no doubt that the later
dermatitis is the outcome of infection by skin organisms. Frequently the
presumption that the eczema is “gouty” rests upon general rather than
specific grounds, on “goutiness” rather than “gout.” Accordingly I think
it would be wiser to regard eczema as an occasional complication of gout
rather than an integral element thereof.
Lastly, there can be no doubt that many of the so-called “gouty”
cutaneous disorders ensue at what may be called the arterio-sclerotic
stage of life. It is when renal and cardio-vascular changes are
present that we meet with exudative erythema, pityriasis, exfoliative
dermatitis, and purpuric eruptions. All these have at one time or another
been foisted upon gout, whereas they are far more closely related to
the cardio-vascular and renal changes with which the disorder is so
frequently associated.
GOUT AND NEPHRITIS
The association between gout and renal disease is admittedly intimate,
in so far as gouty subjects often have granular kidneys, while gout is a
frequent complication of this type of renal disorder. Nevertheless, the
clinical relation between the two diseases is ill defined and, moreover,
somewhat erratic. In most instances the renal defect is engrafted
upon the antecedent gout, or the sequence is reversed; and, again,
the two conditions may arise contemporaneously. Lastly, in sharp and
disconcerting contrast to this mutual overlapping of the two disorders,
we have the awkward fact that more commonly _gout_ and _granular kidney_
run to their fell end quite _independently_ of each other.
Thus, Sir William Roberts observed: “It is quite common to see articular
gout, even of chronic and inveterate character, run its entire course
without any accompanying signs of structural disease of the kidneys.” The
same, to be sure, is equally true of _granular kidney_, which may pass to
its close without any suspicion of gout.
Now, as we have seen, the primary _renal_ origin of gout fails of
demonstration. Is _gout_, then, _causally_ related to _granular kidney_,
or is there some less direct relation between them?
As to this, to begin with, it is extremely rare that a “gouty” subject
develops _acute_ nephritis. In the exceptional instances when it
does occur it is either purely accidental or else the outcome of an
_exacerbation_ of a _previously existing interstitial nephritis_.
The question then arises, Can gout when long continued originate _per
se_ the condition we are pleased to term “gouty kidneys”? As seen above,
such renal lesions are by no means an inevitable sequel or concomitant of
long-standing gout. Moreover, there is nothing _specific_ of _gout_ in
the so-called “gouty” kidney. It is an _interstitial nephritis_, which
may assume the appearances of the ordinary “contracted kidney” or the
“arterio-sclerotic” type. There may be _uratic_ deposits at the apex of
the pyramids, or even an _uric acid calculus_; but even so that of itself
constitutes no proof of the renal changes being “gouty” in origin. In
short, the prefix “gouty” as applied to these types of renal lesion is
just as unscientific and unwarrantable as used in regard of “phlebitis,”
“eczema,” and so forth.
Nor, _quâ_ _gout_ as a _causal_ factor, are we in better case if the
renal disorder be of the “arterio-sclerotic” type. No direct relationship
is established between gout and arterio-sclerosis beyond the fact that
both are usually met with in middle-aged or elderly people. Moreover,
a man may develop arterio-sclerosis and arterio-sclerotic kidneys, yet
never have any vestige of gout.
There being nothing _specific_ of _gout_ in the lesions of so-called
“gouty” kidneys, we must revert to the clinical findings to refute or
establish any _causal_ connection between gout and the renal disorder.
Now, gout is a disease of middle and late life, and rarely of itself
proves mortal. On the other hand, it appears increasingly probable that
the seeds of granular kidney are laid in earlier life, and, on the
average, its course is shorter than that of gout. Also the two disorders
have clinical _facies_ absolutely distinct the one from the other.
From the above considerations it is, I think, clear that, whatever the
hidden nexus between gout and “granular kidney,” it is neither essential
nor constant. It is rather, I believe, of the nature of a coincidence.
Furthermore, as applies to so many problems pertaining to gout, and,
for that matter, to “granular kidney” also, we labour under the grave
disability that both terms are, especially “gout,” very vaguely applied
and when used are often a matter of personal opinion. Consequently, as
Samuel West shrewdly observes, “it is difficult to discuss satisfactorily
the relation of two conditions to each other when neither condition
admits of precise definition, for some authorities are more easily
satisfied in the diagnosis of gout than others; and, while some place all
forms of chronic interstitial nephritis in one and the same category,
others are not so comprehensive, and regard granular kidney as a
definite clinical disease, of which the interstitial nephritis is only a
part.” Under these circumstances, the need for further and more exact
researches in this sphere is but too obvious.
Meanwhile, accepting the general opinion as to the frequency of the
co-existence of gout and granular kidney, is there any explanation
thereof? For myself, I am inclined to believe that the common overlapping
of the two disorders is in large measure due to this, that the factors,
_i.e._, excess in alcohol, overeating, etc., that make for the eruption
of gout, are largely identical with those that promote the development
of _granular kidney_. Hastings Gilford holds “there is very little doubt
that syphilis, lead, and gout do not so much originate Bright’s disease
as excite it into activity when it already exists in a smouldering or
latent condition.”
With this view I feel much in accord, and if to the malign effects
of gout be superadded the effects of alcohol or, haply, lead also,
how incalculably greater the chances of fanning into flame any latent
tendency to nephritis—a legacy, perhaps, of some long bygone infection.
PROGNOSIS IN GOUT
Gout _per se_ rarely, if ever, proves fatal. Certainly, as Sir Thomas
Watson long since said, “_gout in the extremities_ is not a mortal
disease.” When death did occur during or in close relation to an
_acute_ paroxysm, it was by our forefathers attributed either to its
_retrocession_ or to some _misplaced_ or _irregular_ manifestation.
Indeed, their attitude was very much that of the French physician who
observed: “La goutte articulaire est celle dont on est _malade_, et la
goutte interne est celle dont on _meurt_.”
But, as we shall see later in our chapter on _Irregular_ Gout, most,
if not all, of their instances of the assumed translation of the
_materies morbi_ of gout to some vital organ are without foundation. The
demise, often dramatically sudden, was not due to _gout_, but to some
insidious, unguessed-at organic degeneration, or to one of the accidental
intercurrent maladies to which these subjects seem especially liable. To
sum up, the immediate danger to life from regular gout when uncomplicated
is slight.
Not that gout is salutary, lessens the liability to other diseases, or
promotes longevity. Very much the reverse—“a tendency to _recurrence_ is
a law of the disease.” Broadly speaking, the more pronounced the tendency
to recurrence of articular outbreaks, the more protracted the isolated
paroxysms, the worse the outlook, the more sombre, too, the greater
the number of joints involved. Conversely, if the disease, though it
recur, restrict itself to the classic site, the big toe, the longer, as
a rule, the intervals of freedom, the brighter the prospects of long
life. Lastly, the more the subject is crippled, the more pronounced the
tendency to tophaceous deposits, the more likely is the disease to pursue
a downward course, the greater the risk of associated degenerations in
renal and vascular tissues.
While these reflections are in the main, we think, justifiable, we must
recollect that in gout, as in other maladies, the elements of _prognosis_
reside in the _individual_, not the disease. Does he come of a long-lived
stock?—not uncommonly a feature of gouty families. If so, the outlook is
favourable. If he come of a short-lived breed, then in all probability,
no matter how carefully he lives, he will not likely make “old bones,”
this, certainly, if the gout makes its appearance early in life, say
under thirty.
As to the axiom, generally accepted, that the earlier in life gout makes
its _début_, the more unfavourable the outlook, there are exceptions.
Where _longevity_ marks the stock, they usually are true to type. Thus,
even if the first outbreak occurs in the twenties, I have known them
reach the allotted span and over. Nor if their urine show traces of
_albumen_ is this necessarily of grave import, for these gouty veterans
may for many years, even to old age, exhibit traces of albumen without
apparently developing genuine Bright’s disease.
“There dies not above one of a thousand of the gout, although I believe
that more die _gouty_,” wrote Graunt long years since; and this contains
a kernel of truth, for the _prognosis of gout_ rests in the main not on
the _gout_, but the _conditions correlated therewith_—the absence or not
of _complications_. For, be it always remembered, gout, though it may
appear in youth, is chiefly an appanage of the middle and later decades,
in short of the _regressive_ period of life.
This last is, I think, apt to be forgotten, and gout vicariously
saddled with all the infirmities of age. Thus, out of 2,680 examples
of _arterio-sclerosis_ Huchard held _gout_ and lithiasis responsible
for no less than 693. An appalling indictment, but what of the long arm
of _coincidence_? For _age_ unquestionably is the chief factor in the
production of arterio-sclerosis, though many allot gout a dominant _rôle_
in its genesis. This certainly is by no means proven. Still, whatever be
the relationship, _gout_ and _arterio-sclerosis_ are very often found
_in association_. If so, the prognosis will obviously rest, not on the
gout, but on the _vascular_ disease—the pulse tension. If therewith
be correlated _albuminuria_ and a displaced apex beat, the outlook is
unfavourable.
Again, is the subject lean or obese? If the former, so much the better,
for _corpulency_ and _gout_ are a sinister combination. Gout in
itself, as previously observed, favours microbic invasion, and obesity
accentuates the liability. Moreover, the gouty obese are prone to
_arterio-sclerosis_ and _granular kidneys_, with sometimes a superadded
_glycosuria_, or even true diabetes. In such subjects also the presence
or absence of signs of cardiac mural degeneration must enter into our
forecast, which at best is but gloomy.
Apart from arterial degeneration, we have to recollect the tendency to
_phlebitis_ of _recurrent_ type. This when present always carries with
it the risk of _embolism_ and sudden death. Cases therefore displaying
this proclivity to phlebitis must be judged accordingly. The gouty
_glycosuric_, too, is always subject to the risk that the condition may
develop into one of true diabetes. The absence of response to dietetic
restrictions, viz., persistent sugar in the urine, the onset of thirst,
polyuria, or other concomitants of diabetes, will darken the prognosis.
Also I myself believe that the presence of local foci of infection
gravely prejudices the course of gout, accentuates any tendency to
recurrence of the attacks, and incidentally reinforces any latent
proclivity to vascular and visceral degenerations.
Last, but not least, what of the subject’s habits? The “internal
environment” of the tissue cells of the gouty is presumably of itself
none too good; but if to this be added the poison of _alcohol_, lead, or
the toxic products of gluttony, it is incalculably worse. The painter
or the plumber, if he can, would be wise to change his calling. If the
alcoholic be deaf to remonstrance or the glutton continue to gorge, their
chances of life dwindle proportionately, and if given to both vices,
still more so.
In conclusion, the prospects of long life in gout depend in the main
on the presence or absence of associated morbid states. If there be no
complications such as I have indicated, the disease, in my experience, is
not likely to shorten life materially, always provided that the victim is
amenable to what should be the watchword of the gouty,—
“The rule of not too much, by temperance taught
In what thou eat’st and drink’st, seeking from thence
Due nourishment, not gluttonous delight.”
_Milton._