CLINICAL ACCOUNT
ACUTE LOCALISED GOUT
If we would clarify somewhat the obscurity that enshrouds the genesis of
disease, our watchword must here, as in other spheres, be “Despise not
the day of small things.” We know not the proximate cause of gout, it
is true, nor the exact _modus operandi_ of those agents, infective or
other, which bring to fruition the latent morbid potentialities of its
victims. But, even if so handicapped, we should be quick to descry those
portents of the coming storm, those minor backslidings from physiological
righteousness, that doubtless foreshadow the outbreak of the disorder.
For it cannot be doubted that the evil potentialities which make for
gout are for long in operation before their definite installation in its
chosen seat, the joints, ensues. As Trousseau puts it, “The diathesis is
in action before there is time for the local affection to show itself in
a precise form.” In short, given imminence of an attack, the whole system
is charged with gout, or, as Sydenham laconically expressed it, “Totum
corpus est podagra.”
PRODROMAL SYMPTOMS
While we recognise that local inflammatory reaction in the joints is more
particularly characteristic of gout, it is no less necessary that we take
cognisance of the general precursory symptoms that often, if not always,
usher in its onfall. Gout begins in a disorder of _function_.
Uncomfortable sensations may obtain days and weeks before the incidence
of the fit. To old time sufferers they are sufficiently alarming. But
their significance, as heralds of an initial attack, by victim and too
often by physician also, is usually only appreciated when the threatened
fit becomes an actuality. Speaking of premonitory phenomena in gout,
Sydenham remarked, “Its only forerunner is indigestion and crudity of the
stomach, of which the patient labours some weeks before,” and doubtless
this is in the main true.
As Trousseau long since observed, the patient’s appetite often becomes
capricious. He likes his meat strongly spiced, and craves for acids. But
his satisfaction is short-lived. For eating is followed by drowsiness,
feelings of oppression and fulness, with unpleasant eructations, or
more rarely definite retching. The bowels are generally costive, but in
exceptional instances diarrhœa has been noted. The state of the urine is
variable. Generally scanty and high-coloured, it may in some be copious
and pale.
Uneasiness in the right hypochondrium and even slight swelling of the
liver was noted by Trousseau and also by Scudamore. Such congestion
of the portal system and hepatic enlargement may be only fugacious,
but often the same is permanent, a penalty of the same cause—free
living—which leads to the production of gout. For in many instances but
too true is it that “for years together,” as Sydenham said, “a man has
drunk and feasted, has omitted his usual exercise, has grown slow and
sluggish, has been over-studious or anxious, in short, has gone wrong in
some important point of life.”
But more palpable to his friends than to himself are the concomitant
changes in his disposition and character. From being good-natured and
easy-going he becomes morose and irritable. The irascibility of the
gouty is proverbial, and the explosive mental outbursts to Duckworth
appeared at times to be “a metamorphic substitution for a more overt and
regular attack,” or, as Sydenham expressed it, “Non rectius podagræ quam
iracundiæ paroxysmus omnis dici potest.”
Sometimes his mental vagaries are exchanged for or accompanied by
neuralgia, painful cramps in the limbs, etc. In truth, the premonitory
phenomena of gout are protean, inasmuch as, given any prior weakness or
functional derangement of any viscus, the symptoms of oncoming gout are
masked by aggravation of the same, it may be by cardiac irregularities,
vesical irritability, or in an old bronchial subject by increase of
cough, etc.
But it may be objected, there is nothing _specific_ about these various
_functional_ disturbances. They are not more common in the _gouty_ than
in others. Moreover, the habits of life productive of gout favour the
development of gastric and hepatic derangements. The mental irritability,
the gastric disturbances, etc., may be quite as well accounted for by
overeating and overdrinking as by gout.
Now, if there be nothing _specific_ of gout in these so-called
prodromata—“heartburn, acidity, flatulence, etc.”—then what is their
true significance? For, obviously recognition of their true import is
most essential. Now to my mind the said “dyspeptic” symptoms should
be regarded not as symptomatic of gout, but as _etiologically_ related
thereto.
For, though the etiology of gout is still much debated, the same
obscurity will certainly not be clarified, if we merely content ourselves
with dubbing such “dyspeptic” symptoms as “gouty.” On the other hand, if
we, at this early stage, endeavour to elucidate the _true origin_ of the
“dyspeptic” symptoms, who will deny that this is the more rational and
scientific mode of procedure? The timely elimination of _septic foci_
in the mouth, tonsils, and naso-pharynx conjoined with modification
or restriction of food intake and recognition betimes of the signs of
intestinal infection and constipation would perhaps stave off or avert
the threatened articular outbreak.
It has been suggested that there is some statistical evidence that
“acute rheumatism” has declined in frequency since the introduction
of _tonsillectomy_. In the same way, I cannot help thinking that the
growing infrequency and attenuation of gout is in part due to increasing
appreciation by the laity and the profession of the vital importance
of _oral hygiene_ and timely and radical treatment of _local foci of
infection_. The fact that in _children_, victims of so-called _infantile
gout_, the _purin metabolism_ may show those same derangements held
typical of the subjects of gout, is surely an indication that the
disorder begins betimes, and that we too must not tarry if we would
prevent these evil potentialities coming later to fruition.
Now, if there be nothing _specific_ of gout in the “dyspeptic”
derangements held _prodromal_ thereof, the reader may well ask the
pregnant question, Are there any symptoms or signs that will enable one
to identify the victim of these minor discomforts as being “actually” or
“potentially” a “gouty” subject? In attempting to answer this reasonable
query one would emphasise the fact that _tophi in the ears or at other
sites sometimes antedate articular outbreaks_.
Now given that an individual exhibits _auricular tophi_, one or many, can
anyone deny that he is “gouty,” nay more, that he has _gout_, this even
though he never has had, or may never have, an _articular_ outbreak? In
truth, the eruption of a _tophus_ in the _ear_ is as essentially a “fit
of gout” as if it had occurred at the classic site, the _big toe_.
How vivid the light then thrown upon the import, the _etiological_
significance, of otherwise inexplicable _functional_ derangements!
How grim the potentialities of, _e.g._, “dyspeptic” symptoms as
revealed by detection in the subject of a _tophus_! Whether viewed
from the _diagnostic_ or _prognostic_ aspect, its importance cannot
be overestimated. For let us not forget that the _tophus_ is the one
incontrovertible token of the “gouty diathesis.” This morbid localisation
is the sole outward expression of the inward and dominant pathological
trend.
The great Charcot did not despise its aid. He narrates the case of a
man thirty-five years of age, a sufferer for some months from “acid
dyspepsia,” in whom he predicted a fit of _gout_ from noting an _uratic
concretion_ in one _ear_. Is not the moral obvious that in an individual
complaining of gastric or hepatic disturbances, etc., we should, at any
rate, examine the ears for _tophi_?
For, far more often than is currently realised, their eruption
_antedates_ the _articular_ outbreaks.[27] Moreover, they may not be
solitary, but numerous, the _cutaneous gravel_ of older authors. In
truth, these cases of tophi, _uncomplicated_ by _articular_ lesions,
seem to merit some distinguishing term, representing as they do a purely
_ab-articular_ form of gout.[28] They constitute what might be termed
primitive elemental gout, of which the subsequent _articular_ outbreaks
are but an extension, a further manifestation of the “gouty diathesis.”
For it is just this same tendency to _uratosis_ or deposition of sodium
biurate, and this alone, that to our mind constitutes _gout_, this
“primordial vice of nutrition,” not the congeries of distempers that with
the passing ages have clustered around the primitive gout, well-nigh
submerging its identity.
_Premonitory Symptoms of Tophus Formation._—While tophi may _antedate_
articular attacks, we do not always meet with them as _mature_
concretions easily recognisable as such. We must have regard therefore
to the symptoms and signs indicative of their impending eruption.
Consequently in a patient complaining of the various functional
disturbances that so frequently anticipate gout we should never dismiss
as trivial any complaints of _pricking_ or _tenderness_ in the _ears_.
Sometimes the pain in the ears is _acute_, the tenderness such as forbids
their pressure on a pillow. Graves, of Dublin, not only noted that the
pain in some instances was agonising, lasting a few hours, but he himself
suffered also from such attacks of auricular pain, which only disappeared
when gout supervened in his _fingers_. I have myself frequently known the
pain and soreness referred to chilblains, though later their tophaceous
nature was disclosed.
Given such auricular pain and tenderness, we should examine the _pinna
for small red swellings_.[29] These, when definitely localised, should be
punctured and the thick white fluid which exudes examined microscopically
for _urate of soda_ crystals. In some instances the creamy-like exudate
does not yield a crystalline deposit, and Dr. Munro and I are inclined
to believe that there is a _pre-uratic_ stage in the evolution of tophi.
We have observed this absence of crystalline deposits in apparently
unmistakable tophi, as evidenced by the usual pearly white concretions
in the rim of the ear. I recollect that the late Sir William Osler, when
visiting our laboratory, was deeply interested in this possibility,
as suggested by Dr. Munro, of a _pre-uratic_ stage. Needless to say,
all local sources of fallacy—Woolner’s tip, fibroid nodules, sebaceous
cysts—were excluded, while, in the lack of _crystalline_ proof, the
evidence in favour of the associated _arthritis_ being gouty rested
on its being at the classical site, the _great toe_. Moreover, as an
alternative explanation we have the possibility of _reabsorption_. We may
recall Duckworth’s well-known example where a man had two attacks of gout
in the right great toe joint, yet autopsy revealed no speck of uratic
deposit. We know, too, that, following an _acute_ attack, tophi may
diminish in size or even disappear, while coincidently fresh tophi form
at other sites.
_Premonitory Articular Pains._—Again, when, in association with
indigestion or other premonitory symptoms, twinges in the toe recur from
time to time, especially after consuming wines or certain articles of
food, these same are very suggestive of impending gout. Garrod is very
definite on this point: “I have no doubt that many persons experience
extremely slight attacks of gout before the development of the affection
in an acute form, and several of my patients have assured me that for
years before their first severe attack in the great toe they have felt
slight periodic twinges. I am of opinion that when such twinges occur
deposition has already taken place.”
In conclusion, we would urge that, given _gastric_ or _hepatic_
disturbances, etc., in a subject predisposed by _heredity_ or _habits_ to
gout, we should note the presence or absence of the following:—
(1) Pain, pricking, or tenderness in the ears, with or without
small red swellings.
(2) Similar sensations at site of finger joints, with dorsal
swellings over which the skin may be red or unchanged.
(3) The existence or not of pearly white concretions, _i.e._
mature tophi (as tested microscopically), at the above sites or
elsewhere.
Further signs that may be sought for in cases of doubtful nature, _i.e._
_unevidenced by tophi_, would be:—
(4) The presence of _uricæmia_.
(5) A lowered or sub-normal output of uric acid in the urine.
(6) Diminution or retardation of the output of exogenous purin.
To take up the thread of our narrative regarding the _prodromal_ symptoms
which at any moment may give place to an _articular_ outbreak. The
_determinants_ or _exciting_ causes having been already dealt with in
the section on etiology, we shall here only note those symptoms or signs
that portend the _imminence_ of the paroxysm. These are very variable.
But it is suggestive if without any change in the habits the “dyspeptic”
symptoms abate somewhat or disappear.
Indeed, it is well recognised that, whatever the nature of the prodromal
phenomena, they all tend to cease just before the oncoming attack.
Occasionally a pre-existing depression gives way to a feeling of
exuberant health or well-being. We recall the instance of a celebrated
physician whose lectures always just prior to an attack took on an added
brilliance.
Reverting to more definite harbingers, it has been noted that the _urine_
becomes _scanty_, and its content of _uric acid_ much _diminished_, some
three or four days before the paroxysm, though such is not invariable.
Easier of note and widely recognised is the fact that in those exhibiting
tophi _pricking pains or tenderness_ are experienced at their site.
Scudamore, Garrod, and Duckworth are all agreed on this point. Another
sign noted by Sydenham was that the _veins_ of the _part_ about to
be affected become _engorged_—a feature confirmed by Trousseau and
others.[30]
THE ACUTE PAROXYSM
A brief interlude, lasting a few hours or a day, frequently intervenes
between cessation of the prodromal discomforts and the onset of the
attack. This delusive sense of well-being deceives none but the
uninitiated, for to the old time sufferer it is but the truce before the
threatened assault.[31]
Still the subject feels better and more placid than his wont, seeks
his bed, and sinks to sleep (“sanus lecto somnoque committur”). But
suddenly, more commonly an hour or two after midnight, he awakes to a
pain in the foot, usually in the ball of the great toe, though more
rarely in the heel, instep, or ankle. Simultaneously he becomes chilly,
shivers, or has a rigor. But as the pain, at first bearable, grows in
intensity, these feelings lapse, giving way to feverish restlessness.
Posture after posture is renounced, but, toss as he will, he strives in
vain to find a place of ease for the tortured limb. Even the pressure of
the bedclothes is intolerable. But towards morning (“sub galli cantu”)
the pain remits as suddenly as it began. Anon the sufferer breaks into
a gentle sweat, falls asleep, and wakes to find the painful part red,
swollen, tense, and shiny, surrounded with œdema and turgid veins.
The same series of events recurs, though often in mitigated form, for
some days and nights. During the day his pain is lulled, but towards
evening it gathers in intensity to cease or diminish towards morning.
The cycle continues from eight to ten days; then pain ceases, redness
fades, œdema subsides, and the inflamed cuticle peels, with itching.
The temperature meanwhile has sunk to normal, the local tenderness and
stiffness gradually pass off, and health is restored. “Gout is the cure
of the gout,” said Mead long since, and certainly recovery from the
first attack of gout is usually speedy and complete. A renewed sense
of _bien-être_ ensues, free from the discomforts that led up to the
outbreak. Indeed, in exceptionally rare instances the disease seemingly
exhausts itself in a single paroxysm, or decades may pass before
another visitation. Sir William Roberts tells of a Yorkshire squire who
sustained a classical attack in his twenty-seventh year, the next in his
eighty-ninth year. Frequently a second attack may not occur for one, two,
or even three years. But the tendency to recurrence usually becomes more
and more pronounced as the years roll on, and eventually the gouty man
resigns himself to the doleful expectation of an attack once or twice a
year, during spring or fall, with some approach to periodic regularity.
Initial attacks of gout are usually _monarticular_, but consideration
of the polyarticular variety will best be postponed until we come to
consider _acute gouty polyarthritis_. Also we think it will be more
convenient for us to defer discussion of _retrocedent_ gout to the
chapter dealing with the irregular or anomalous types of the disorder.
Meanwhile we will now proceed to detailed description of the individual
phenomena that make up the clinical content of acute gout.
DETAILED CONSIDERATION OF PHENOMENA
_Onset._—From Sydenham’s classical account it might be inferred that the
onfall of gout is always fulminant. But this is far from being the case.
For I find myself in agreement with Hilton Fagge that in many, if not
the majority of instances, even the _initial_ outbreak of the disorder
is installed in a far less dramatic manner. Certainly in not a few cases
its manner of approach is insidious, not to say stealthy. At onset then
the nature of the case is therefore frequently misinterpreted both by
victim and physician. The free liver, fearing that Nemesis has overtaken
him, is fertile in suggestion. He has overwalked, his boot pinched
him, or it is a sprain. Local appearances may be non-committal. There
may be no swelling nor redness, and no access of pain at night. Still
there is discomfort when he walks. The so-called sprain lingers, and one
morning the great toe, instep, or ankle, is swollen, tender, flushed,
and the victim’s fears and the physician’s suspicions are converted into
certainty: it is gout!
Still in this matter of the onset I must not overlook the findings of my
colleague James Lindsay. In 569 cases, the onset was sudden in 458, and
in the remaining 111 examples gradual. It was noted that only 14·5 per
cent. of the male cases were of gradual onset. But no less than 47·1 per
cent. of the female cases developed after this fashion.
Again to resume, it is by no means invariably the case that the onset is
_nocturnal_. For, as Duckworth has pointed out, many attacks begin during
the day, and this is perhaps more often the case after the disorder is
fully established.
_Locality._—Gout in its classical form is _monarticular_ in distribution.
In 375 out of 512 _initial_ seizures, Sir Charles Scudamore found that
the metatarso-phalangeal joint of the great toe of one or other foot was
the joint affected. Garrod, too, noted that, excluding the great toe,
in not more than 5 per cent. were other joints implicated. As to the
frequency of incidence in joints other than the big toe, opinions differ.
For Scudamore it is the ankle, for Garrod the instep, and afterwards the
outer side of the foot and the knee. In contrast, Hilton Fagge holds that
next to the great toe gout vents its initial fury with greatest frequency
upon the _metacarpo-phalangeal_ joint of the index finger, adding,
“certainly not the thumb.” Most authorities however agree that gout in
its early stages rarely attacks the joints of the _upper_ limb, and even
in its most inveterate form the _shoulder_ and _hip_ joints are immune.
Personally, I have never seen a case of gout in the shoulder or hip; such
cases are usually examples of _osteo-arthritis_.
Exceptionally, even in first seizures, more than one joint may be
affected. Thus it may migrate from one big toe to its fellow, or
travelling further afield, may invade ankle, knee, wrist, or elbow, or
small joints of hand. W. Gairdner held that in gout the joints of the
_left_ were more commonly attacked than those of the right limb. But
James Lindsay’s figures would appear to indicate precisely the reverse,
viz. a predilection for the _right_ side of the body.
_Pain._—If we may accept the lurid imagery of its victims, even the
tortures of the Inquisition failed to transcend in agony the—
“... pangs arthritic
that infest the toe of libertine excess.”
_Cowper._
Sydenham said that at its onset the pain was as that of a dislocation
(_ossium dislocatio_). At its zenith it was as if the flesh was being
gnawed, squeezed in a bootscrew, or scalded by molten lead or boiling
water. Sensory perversions are superadded, and, as Ambrose Paré said,
“some patients say they burn, while others complain of icy coldness.”
Its peculiarly exasperating nature is well illustrated by Hosack, an
old time Professor of Medicine of New York, who thus delivered himself:
“Some compare it with the gnawing of a dog, the pressure of a vice, or
the pain of the actual cautery; this probably is not far from the truth,
judging from the anecdote I have heard of a man subject to gout. This man
falling asleep barefooted before a large fire, the fire fell, and a large
coal found its way to his foot; half awake and half asleep, he cried
out: ‘There’s that d——d gout again!’ He at length awoke, when he found
a large coal frying his great toe. The sensation of the two evils was
probably the same.”
The pain is aggravated in that frequent “startings” of the limb prevent
the victim keeping the foot at rest. The slamming of a door, or the
incautious shaking of the bed, so quickens its throbbing intensity as
provokes a literal frenzy of rage. But fortunately it is not always
so. For though the pain of gout is unquestionably severe, at times
excruciating, yet it presents infinite grades of severity. Also one must
recollect that but too many of its victims are already in a high state of
irritability before the outbreak. Moreover, their powers of self-control
are too often sapped by unbridled self-indulgence, and they have but
slight reserves of patience and fortitude to draw upon.[32]
Apart from the personal factor, in _subacute_ cases the pain is notably
less severe than in the _acute sthenic_ form. The pain of gout, as a
rule, is more intense than that of _acute rheumatism_, and, I fancy, than
that of all other varieties of acute arthritis.[33] Sir Thomas Watson in
his fascinating lectures tells of a witty Frenchman who, comparing acute
gout and acute rheumatism in respect of pain intensity, remarked: “Screw
up the vice as tightly as possible, you have rheumatism; give it another
turn, and that is gout.”
Lastly, in respect of the duration of the pain, it is not always
true that it wholly _intermits_ at the approach of dawn. It does so
frequently, it is true, but in some instances pain, more or less severe,
continues during the day as well as the night. Occasionally, on a
_crescendo_ scale, it continues increasing almost up to the crisis.
Generally speaking, too, the shorter the duration of the paroxysm the
more intense the pain, and the more prolonged the less the degree of
suffering.
Following the crisis, the pain gradually becomes less and less, giving
place to a feeling of numbness of the toe, which in older subjects may
endure for some days.
_General Phenomena._—Symptoms, other than those referable to the affected
part, vary widely in different cases. In this respect the acute _sthenic_
forms contrast with the acute _asthenic_ types. In the former the pulse
quickens; the temperature rises, but rarely exceeds 101°-102°, though
Garrod saw it reach 104°. The tongue is furred, the breath foul, with
anorexia and thirst. Though the appetite is frequently impaired or lost,
yet in some instances it is retained. Dyspeptic symptoms, hiccough,
eructations, etc., are sometimes prominent, but often wholly lacking.
The bowels are constipated, as a rule, the stools pale, or dark and
extremely offensive. The urine is generally scanty, high-coloured, with
a lateritious sediment on cooling. It may contain a trace of albumen.
Severe _cramps_ affecting muscles of the leg, thigh, and upper parts of
the body, are more or less prominent symptoms in a considerable number of
instances.
The _pyrexia_ appears to be _symptomatic_, more or less in proportion to
the acuteness of the local phenomena. Comparably the highest temperatures
are usually met with in _sthenic_ forms in relatively young or robust
middle-aged subjects. Duckworth noted the interesting point that “a
preliminary rise is commonly noted for one, two, three or four days
before a joint is actively involved.” With the articular outbreak the
febrile movement becomes more active. The temperature runs up to 100° or
over, but with the morning abatement sinks to normal or nearly so. The
following evening it rises again frequently to a higher level, 102° with
a morning remission, and so it continues for a variable number of days,
it may be only two or eight to ten. It then subsides, and frequently for
a few days remains sub-normal. Lastly, the _acute asthenic_ forms, that
occur often in women (Garrod), may be wholly _afebrile_.
_Changes in the Blood._—Apart from its increased content of uric acid,
further morbid changes take place in the blood in gout.
Neusser in 1894 described what he termed “perinuclear basophilic
granules” over and about the nuclei of the leucocytes in the blood of
gouty patients. He held that the dark granules constituted the mother
substance from which uric acid was derived, and that their presence
in the blood was distinctive of the “gouty diathesis.” Subsequent
researches, however, by Futcher and others appear to have shown the
absence of any interrelationship between the amount of these granules and
uric acid elimination, though Neusser claimed that cases showing them
excreted uric acid in excess.
More significant, however, is it that the blood in acute gout may show a
high grade _leucocytosis_ with _secondary anæmia_.
In a case under my care of _acute gout_ at classic site, though by no
means of unusual severity, the following was the content of the blood
picture:—
BLOOD COUNT.
Red corpuscles, per c. mm. 3,692,000 = 73·8 per cent.
Hæmoglobin 80 ”
Colour index 1·08 ”
Leucocytes, per c. mm. 25,920
DIFFERENTIAL COUNT.
Lymphocytes 8·0 per cent. = 2,074 per c. mm.
Large mononuclears 3·5 ” = 907 ”
Polymorphonuclears 87·0 ” = 22,550 ”
Eosinophiles 0·5 ” = 130 ”
Mast cells 1·0 ” = 260 ”
-----
100·0
The salient feature of the blood picture is the high grade
_leucocytosis_ of leucoid type with moderate anæmia—appearances
quite compatible with, and suggestive of, an _infective_
arthritis. To these interesting blood changes we shall again
refer when dealing with the acute polyarticular variety, the
above case being of monarticular type, _i.e._, the big toe.
_Uric Acid Excretion._—If when on a _purin-free_ diet a gouty subject
develops a paroxysm, the curve of uric acid excretion in the urine is
so characteristic as to be almost pathognomonic of the disorder. As His
pointed out, immediately before the onset of the paroxysm the endogenous
uric acid sinks to a lower level (termed by Umber the _anacritical
stage of depression_). With the onset of the attack the uric acid
content of the urine quickly increases, to reach its zenith on the
second or third day. F. Pfeiffer, who first noted this point, termed
it an _uric acid wave_. Subsequently, with the gradual subsidence of
the paroxysm, it again drops into what Umber termed the _post-critical
stage of depression_. While this curve of endogenous purin excretion
may be modified by oft recurring exacerbations, still Umber holds that
nevertheless it is of decided value in differential diagnosis.
_Local Phenomena._—The site and character of the pain having been dealt
with, we now pass on to consider the objective changes in the affected
part. The local _engorgement_ of veins that _precedes_ the _articular_
outbreak becomes more pronounced, extending from the vicinity of the
painful joint as far as the leg. The overlying skin of the joint
quickly becomes red and tumid. It is not a bright, but a dark red, the
superjacent skin taking on a shining smoothness that has been compared to
the peel of an onion. Indeed, in its more violent form it resembles but
too closely the ordinary appearance of an _abscess_, over which the skin
is becoming thin. The redness is not strictly confined to the surface of
the joint, but spreads a little beyond, and where it ceases _œdema_ is
perceptible.
The redness in its intensity attains its zenith in from twenty-four to
forty-eight hours, and then in hue becomes more violaceous. On the other
hand, the _œdema_ may go on increasing for some days. At first, owing to
tension, the presence of œdema may not readily be elicited. But with the
subsidence of inflammation the swollen parts readily pit on pressure. It
is scarcely possible to detect _intra-articular effusion_ unless it be
the ankle joint that is involved.
According to Duckworth, in the more _sthenic_ forms there may be local
_ecchymoses_. With the crisis the redness, œdema, and venous turgescence
die down. The previously distended skin becomes wrinkled, and with
complete subsidence of inflammation _desquamation_ ensues. This process
is generally attended with troublesome _itching_. It is most noticeable
about the _feet_ and _hands_, but more rare at other sites. Scudamore
said that in seventy-eight out of 234 cases no peeling occurred, but, as
Garrod observed, it may readily be overlooked unless especially sought
for.
The exquisite sensitiveness of the parts, as before noted, gives way to
_numbness_. The diminished sensibility, coupled with _stiffness_ of the
joint, renders walking difficult for some days, and, indeed, a month or
more may elapse before the joint, even in favourable cases, recovers its
customary mobility.
In acute _asthenic_ forms great contrasts appear. Pain and tenderness in
the toe may be moderate, but there may be little local heat or redness
and no _pyrexia_. But _œdema_ is generally in evidence, and the usual
_desquamation_ of skin follows.
_Tophus Formation._—To the local changes that mark their eruption at
ab-articular sites we have already alluded. Here we would only reiterate
that their formation _follows_ the local joint inflammation. Consequently
if a few days after the attack local pain or tenderness, with or without
swelling in the vicinity of the joint, should be complained of, it should
not be dismissed as of no account, but the affected parts should be
scrutinised carefully and, where possible, at short intervals. This in
the interests of diagnosis of a joint affection which may at the time
have been of doubtful nature, more especially if the primary attack occur
elsewhere than at the classical site. Some observations of Trousseau
are well worth quotation: “Physicians who have watched the progress of
the evolution of tophus believe that it is formed during the paroxysm of
gout. They are mistaken: the deposit appears during the interval between
attacks, or at least when the attacks have not been of long duration,
and when they do not recur in such rapid succession as to run into
one another, in which cases their secretion has commenced during the
preceding and continued during the succeeding attack.”