CLINICAL ACCOUNT (_continued_)
ACUTE GENERALISED GOUT
While gout may throughout its life history confine its ravages to the
_foot_, if not solely to the _toe joints_, it may, even in the _initial_
attack, involve many articulations. Such cases usually, if not always,
occur in persons of marked _gouty heredity_. In its simplest forms the
orthodox _monarticular_ seizure is simply exchanged for a sequential
implication of each big toe joint. If so, as Trousseau pointed out,
the joint that is the last to be involved is least affected, and the
soonest to get well again, while the accompanying œdema is of shorter
duration. But in more severe cases not only the big toe, but the _tarsal_
joints, the _knee_ and the _hand_, may be invaded in the _first_ attack.
Occasionally, too, the disorder displays concomitantly its tendency
to involve other structures, _tendons_ and _aponeuroses_, _e.g._, the
_tendo Achillis_, _plantar fascia_. Such _widespread initial involvement_
is usually preceded by _prodromal_ phenomena of unusual severity
and prolonged duration. These _initial_ attacks of _polyarticular_
distribution are extremely rare.
Far more commonly acute gouty polyarthritis supervenes after several
attacks of classic location have been suffered. The gouty inflammation
in these cases invades the joints after a serial fashion. But each joint
as it becomes involved goes through the same painful cycle. Thus, for
five or six days the pain goes on increasing, then abates, and finally
the wished-for crisis comes. So it happens that the gout may be raging
simultaneously in several articulations, though in each at different
stages of evolution. Consequently the symptoms do not pursue an even
tenor, but are made up rather of a series of little attacks—_series et
catena paroxysmulorum_, to invoke Sydenham’s expression.
Frequently periods of apparent recovery take place. The temperature
remains normal for some days, and welcome convalescence seems
established, when, to the victim’s despair, the temperature again rises,
and the same weary cycle, though perhaps shorter, is yet to be endured.
Running this chequered career, the disorder may last for six weeks or two
or three months.
In such attacks not only the _feet_, _knees_, _hands_, and _elbows_,
may be promiscuously involved, but often also the _ligaments_, _bursæ_,
_tendon sheaths_, and _aponeuroses_. The suddenness with which the
disorder shifts its seat from one joint to another, or from joints to
bursæ or muscles, often leads to its confusion with _acute rheumatism_.
In other words, that _fixity_ distinctive of gout in its monarticular
forms is here exchanged for _mobility_, that specific quality of acute
rheumatism.
Naturally, the implication of so many varied structures casts its impress
on the clinical picture, inasmuch as the physical characters vary
with the different textures involved, their capacity for inflammatory
distension, etc. On the _dorsum_ of the _hand_ and _foot redness_ and
_œdema_ will be prominent, and Scudamore noted that the flush might be
widely diffused, simulating _erysipelas_, with here and there small
_ecchymoses_.
When structures more deeply placed, _i.e._, _tendon sheaths_ at ankle,
knee, and wrist, are singled out for attack, swelling is less marked and
redness of the skin more patchy in distribution. The _bursæ_ at the elbow
or back of the knee may swell with extraordinary rapidity. The parts
become exquisitely tender and painful, while the overlying skin takes on
an angry blush. They may subside, but more often continue permanently
enlarged, defiant of reduction.
Involvement of the _olecranon bursa_ is very typical of gout. Pratt,
of Boston (1916), tells of a case in which the subject had during
twenty-seven years suffered from recurring attacks of _acute gouty
polyarthritis_. The eight or ten physicians who had treated him had
all regarded the disease as _rheumatic fever_. Pratt himself observes:
“I did not feel sure of the diagnosis until I saw the swelling on his
elbow, which presented the typical picture of a chronic _gouty olecranon
bursitis_.”[34] Occasionally the bursæ when filled with uratic deposit
undergo _suppuration_ following injuries. The bursa in connection with
the great toe frequently becomes acutely inflamed, and Scudamore in a
gouty hand saw an old ganglion take on the same inflammatory reaction.
The tendon sheaths when involved lead to great disablement, as even the
most tentative attempts at movement give rise to sudden and agonising
cramp. The _tendo Achillis_ is a favourite site, or the tendons of
the wrist, or the ligament of the patella. The same is true of the
_aponeuroses_, the predilection being for the lumbar or gluteal fascia,
in which instance it may extend to the sheath of the sciatic nerve. These
extensions of gout to tendon and nerve sheaths frequently outlast the
articular lesions, and may become the dominant element in the clinical
picture.
Naturally, when not only joints, but _bursæ_ and other structures, are
involved and implicate both upper and lower limbs, the victim presents a
pitiful spectacle, one of almost complete helplessness. Œdema and general
venous turgescence may be very pronounced in one or more members, giving
a subjective sensation of almost overwhelming weight in the limb.
Reverting to the _constitutional_ symptoms, the outstanding feature is
that, notwithstanding the widespread involvement of joints with manifest
local inflammatory reaction, the _pyrexia_ is of _moderate_ grade, and
so frequently, indeed, is it _afebrile_ that this peculiarity is of
diagnostic significance.
_Changes in the Blood._—The findings are extremely interesting in view of
the high grades of _leucocytosis_ to be met with both in _pyrexial_ and
_apyrexial_ examples.
In a case of _acute gouty polyarthritis_ under my care the blood picture
was a very striking one. The patient had suffered from gout for some
eleven years, with recurrent acute exacerbations. There was widespread
involvement of the joints both in upper and lower limbs. On the dorsum of
the mid-phalangeal joints small semi-solid swellings were present, the
exact nature of which was somewhat puzzling. But inasmuch as the pinna
in both ears was studded with _tophi_, this seemed to provide a clue.
The auricular tophi were verified microscopically. The extra-articular
phalangeal swellings were then aspirated with a hypodermic syringe. A
turbid straw-coloured fluid issued, which microscopically was found to
contain _biurate_ crystals. His temperature rose nightly from 101° up to
102° F., with morning remissions. The left knee and wrist were the seat
of _effusion_, and some of the small finger joints were inflamed.
BLOOD COUNT.
Red corpuscles, per c. mm. 4,432,000 = 88·6 per cent.
Hæmoglobin 60 ”
Colour index ·68 ”
Leucocytes, per c. mm. 27,200
DIFFERENTIAL COUNT.
Lymphocytes 9 = 2,450
Large mononuclears 13 = 3,540
Polymorphonuclears 78 = 21,220
Eosinophiles 0 = 0
Mast cells 0 = 0
-----
100·0
The left knee joint was aspirated by Dr. Munro. A clear fluid of straw
yellow tint was withdrawn, which yielded some fibrin on standing. The
cytological examination gave the following results:—
TOTAL COUNT.
44,800 per c. mm. (nearly all leucocytes).
DIFFERENTIAL COUNT.
Polymorphonuclears 92
Lymphocytes 7
Large mononuclears 1
Eosinophiles 0
Basophiles 0
---
100
Attempts at culture on broth and agar proved _sterile_. In addition three
separate blood cultures, taken at intervals of a few days, on agar slopes
and broth, all gave _negative_ results.
In another instance of _polyarticular_ distribution the subject was seen
during the _inter-paroxysmal_ period. He displayed auricular _tophi_, the
crystalline content of which was verified microscopically.
BLOOD COUNT.
Red corpuscles, per c. mm. 5,732,000 = 194·6 per cent.
Hæmoglobin 65 ”
Colour index ·57 ”
Leucocytes, per c. mm. 13,200
DIFFERENTIAL COUNT.
Lymphocytes 34 = 4,490
Large mononuclears 3 = 400
Polymorphonuclears 61·5 = 8,120
Eosinophiles ·1 = 130
Mast cells ·5 = 66
Chalmers Watson some years previously investigated the blood in cases
of _acute gouty polyarthritis_ both during an exacerbation and in the
_inter-paroxysmal_ period. His findings were as follows:—
During the _attack_ the films showed very marked _leucocytosis_. Also
there was present a large number of peculiar myelocyte-like cells, these
more than half as numerous as the ordinary finely granular oxyphil
leucocytes.
“Each of these cells contained a large oval or horse-shaped
nucleus, poor in chromatin. The nucleus occupied about half
of the total area of the cell. It did not stain uniformly,
and it was usually situated to one side, coming right up to
the cell outline, and occupying from a third to a half of the
total circumference. In many of these cells the nucleus was
almost round, with but one slight indentation; in others the
indentation was pronounced. The whole cell stained a pale blue,
presented a degenerated appearance, and contrasted markedly
with the ordinary leucocyte seen in the same film, with its
brilliant blue nucleus and bright red eosinophil granules. The
special cells under description were also remarkable for their
size, measuring about 15 m. in diameter, a few being smaller,
about 10 m. Some of them contained vacuoles in the cytoplasm.
The general appearance of these cells suggested exhaustion
in so far as the cytoplasm did not contain the typical fine
oxyphil granules characteristic of the myelocyte. From the
character of the nucleus and cytoplasm, they were undoubtedly
distinct from lymphocytes. The large lymphocytes were scarce;
small lymphocytes were numerous. True eosinophil cells were
also scarce. The main bulk of the leucocytes consisted of the
ordinary finely granular oxyphil leucocytes and the peculiar
myelocyte cells described.
“_Blood plates._—Some of the blood-plates were large (4 m. in
diameter), and often formed very irregular torn-looking masses.
The red cells were apparently normal.”
Shortly after Chalmers Watson, Bain published his results of blood
examination in _acute gouty polyarthritis_. He also noted the presence
of a distinct _leucocytosis_. A differential count disclosed a marked
increase of the eosinophil cells, and he adds: “There was present a
moderate number of the peculiar myelocyte-like cells originally described
by Chalmers Watson.”
Dr. Munro, though he carefully examined the gouty blood films to this
end, was unable to identify the myelocyte-like cells noted by these
observers.
Recently, through the kindness of my colleague Dr. Waterhouse, Dr. Munro
and I had again an opportunity of examining the blood in a case of this
kind during the _inter-paroxysmal_ period. The subject, a male, had had
repeated attacks at the classic site, with subsequent extension to other
joints. Multiple tophi were present in both ears, and the crystals of
uric acid were demonstrated microscopically.
BLOOD COUNT.
Red corpuscles 7,364,000 = 147 per cent.
Hæmoglobin 74 ”
Coloured index 0·5 ”
Leucocytes 21,400
DIFFERENTIAL COUNT.
Lymphocytes 28·5 per cent. = 6,099 per c. mm.
Large mononuclears 2·5 ” = 535 ”
Polymorphonuclears 64 ” = 13,696 ”
Eosinophiles 3·5 ” = 749 ”
Basophiles 1·5 ” = 321 ”
The blood picture, it will be seen, is one of erythræmia—a marked
leucocytosis, a normal differential percentage count, pronounced
secondary anæmia.
Da Costa also notes, in a case of gout, erythræmia (7,125,000) with a
leucocyte count of 14,000. Ewing, too, records an instance of chronic
gout with huge tophi, seen in an acute exacerbation, in which the blood
gave a leucocyte count of 21,000 with 70 per cent. hæmoglobin. In another
severe instance of subacute type the same observer again met with
leucocytosis (15,000).
In regard to these interesting blood findings, it is to be cordially
hoped that as the somewhat rare opportunities occur they will be taken
full advantage of.
As to the other general clinical features the _nervous_ system, as might
be expected, is often greatly perturbed, and the mental distress and
anxiety in some instances appear to cause even more irritation than the
bodily pain. Febrile movement when present accords with that observed
in _monarticular_ sites, save only in the tendency to _relapses_.
Sweating is not a common feature, as in _acute rheumatism_. Neither does
acute _endocarditis_ occur in gout. On the other hand, as this acute
polyarticular form may recur throughout years, it may in its later stages
be complicated by _nephritis_.
Furthermore, in its differentiation from acute rheumatism the more
advanced age of the sufferer, always over thirty-five and more often
nearer fifty or over, will be of help. The presence of an hereditary
taint, the nature of the occupation and personal habits, and more
pertinently the history of a classical attack in the great toe, may give
a clue.
But in this, as in all other varieties of gouty arthritis, the one and
only unequivocal objective proof of the nature of the disorder is the
_presence of tophi_. Lamentable indeed is the frequency with which this
fact is forgotten, to our confounding and the patient’s detriment. As
Hilton Fagge, discussing the diagnosis of gout, long since observed: “All
those parts which are apt to be the seat of tophi should be examined. If
a single deposit of urate of soda can be found it settles the question.”
In conclusion, before passing to consideration of _chronic articular
gout_, it will be convenient here to discuss certain _concomitant
phenomena_ of the acute types. We refer to the muscular and nerve forms
of fibrositis, which, we hasten to add, are of common occurrence also in
the chronic types of articular gout.
COLLATERAL PHENOMENA OF GOUT
The liability of acute articular gout to be complicated by _muscular_
and _nerve_ disorders has already been briefly alluded to. Also it was
pointed out that in respect of this tendency gout displayed an analogy
with the _specific_ infections, viz., in that these latter too are prone
not only to arthritic, but to muscular and nerve, lesions also.
Our forefathers, greatly exercised by this apparent overlapping of
“gout” and “rheumatism,” in their efforts at discrimination drew fanciful
contrasts between the subjective sensations produced by gout and
rheumatism, but all to no end, for said Heberden, “It must be owned that
there are cases in which the criteria of both are so blended together
that it is not easy to determine whether the pain be gout or rheumatism.”
Gradually, however, a change in attitude made itself felt. It became
no longer customary to regard such examples as blends of gout and
“rheumatism,” but to hold the _muscular_ and _nerve_ disorders as also
attributable to the underlying gout. Thus, so impressed was Garrod
with the frequency of the incidence of _lumbago_ and _sciatica_ in
_gouty_ subjects that he was doubtful as to whether they ought to have
been classed by him as among the “diseases to which gouty persons are
particularly liable.” He thought “they might perhaps have been properly
classed among the forms of _irregular_ gout.”
Duckworth, again, felt sure “that much so-called ‘muscular’ rheumatism
is really gouty,” and forthwith ranked its manifestations among the
_irregular_ forms of gout. Hilton Fagge was likewise convinced that the
muscular types of fibrositis are frequently and obviously related to
gout; while Sir William Gowers, discussing this same muscular fibrositis,
is even more explicit: “It is currently associated with gout, and the
truth of the belief is soon impressed upon the practitioner. But it
is gout with a difference: it may occur in those who are gouty in the
common sense of the word, but some of the most severe cases I have seen,
especially the brachial form, have been in those who have inherited a
tendency to gout, but have not merited its development.”
Turning to the _nerve_ manifestations, Charcot long since pointed out
that gout and sciatica might co-exist, while Gowers is insistent that
“underlying most cases of sciatica is either the state of definite gout,
or that ‘rheumatic diathesis’ in which the fibrous tissues suffer,
especially those that are connected with the muscles, a form closely
connected with common gout by co-existence or descent.”
As to my own opinion, I have, in collaboration with Bassett Jones,
discussed in detail this relationship of gout to fibrositis in our
monograph on the latter disorder, and I shall largely transcribe our
remarks therein on this vexed point.
Of all the conditions reputed to be etiologically related to fibrositis,
in none of them is the connection more obvious or more easily traceable
than between this affection and _gout_. Whether or no the hyperplasia of
the connective tissues be directly due to the gouty toxin must perforce
for the present remain uncertain. But there is no doubt as to the
relatively frequent incidence of fibrositis in “gouty” subjects. It is
as true to-day as when Scudamore wrote it that occasionally “a patient
when he has gout in the regular situations suffers, in consequence of
some partial exposure to cold, a rheumatism in other parts, as in the
muscles of the neck, or in the shoulder joints; and a seizure of lumbago
at the time of the invasion of the gout is also not uncommon.”
Apart from the _simultaneous_ incidence of gout and _fibrositis_ in
the same subject, it is equally certain that the victims of a “gouty”
heritage are unusually prone to develop fibrositis.
Thus, in a series of 1,000 cases hereditary or acquired gout was present
in no less than 281—viz., a percentage incidence of 28·1. While this
taint was more in evidence in fibrositis of the joints, it obtained
appreciably in regard to all muscular types of the affection, more
especially _lumbago_, its influence also being very obvious in the case
of _sciatica_ and other types of nerve sheath involvement.
In light of this, we must admit being somewhat nonplussed by those who
confidently affirm that “gout” plays little or no part in the production
of “fibrositis.” Speaking from an extensive experience, we confidently
believe the reverse is the case, and that the _gouty_ element is but too
frequently overlooked in examples of this affection.
Approaching another aspect of this vexed question of the relationship
of gout, what of the ambiguous attitude of those who, while denying it
any share in the causation of _lumbago_ and other types of _muscular_
fibrositis, yet at the same time attribute to gout an important
etiological _rôle_ in the allied conditions _sciatica_ and _brachialgia_?
Thus, they maintain that the fleeting attacks of lumbar fibrositis or
lumbago which ensue after dietetic indiscretions have no relation to
gout, but are simply indicative of some digestive disability on the part
of the individual for certain articles of diet. Hardly to our mind a
satisfactory mode of differentiation; much less can it be held to put
out of court the influence of _gout_. For are not the gouty precisely
the very persons who display this inability to cope satisfactorily with
unusual or excessive meals? Hence the frequency with which in their
instance attacks of lumbar fibrositis, often transient, almost invariably
ensue when any unwonted excess of purin-containing food has to be
disposed of, and especially when at the same time katabolic changes have
been stimulated in the body by the ingestion of alcohol, not necessarily
excessive in amount.
That the _lumbar_ regions should have been singled out is the more
remarkable, for, if there be one form of fibrositis more than another
prone to be associated with gout, it is precisely _lumbago_.
Our difficulty, moreover, in appreciating the cogency of this plea for
excluding the influence of gout in muscular fibrositis is the more
accentuated in that those who advocate it claim that this very gout is
the salient etiological factor in _sciatica_ and _brachialgia_.
This position is untenable, and for the following reasons: the
pathological lesion in both instances is the same—viz., _fibrositis_; in
lumbago and deltoid rheumatism it implicates the sheaths and interstitial
tissues of the _muscles_, in sciatica and brachialgia the similar
investments of the _nerves_.
Strictly speaking, therefore, any differentiation that we can effect
between muscular and neuralgic types of fibrositis is perforce merely
_topographical_. To draw _etiological_ distinctions is well-nigh
impossible, for the very continuity of the fibrous tissues favours the
passage of one type into the other. Hence clinically we find that the
bulk of our cases of sciatica are preceded by lumbago, and similarly many
cases of brachial neuralgia or neuritis develop by extension out of a
pre-existing deltoid fibrositis.
In light of such transitions of _muscular_ into _neuralgic_ types of
fibrositis, it seems inconsistent to postulate a gouty origin for the
latter and at the same time to deny it any share in the production of
the former. For ourselves, we fully recognise gout as the most potent
predisposing factor in sciatica and brachialgia, and _ergo_ in the
closely associated and often antecedent muscular types of fibrositis.
While insisting on the importance of gout as a _predisposing_ factor in
_fibrositis_, we feel called upon to emphasise the fact that we are not
sheltering ourselves under that nebulous term “latent” gout, for our
contention is based on the ground that in the vast majority of the cases
for which we claim a gouty origin unequivocal proofs of gout, such as
_tophi_, etc., were present.
INCIDENCE OF GOUTY STIGMATA IN VARIOUS TYPES OF FIBROSITIS
Out of 343 instances of fibrositis of the _joints_ such stigmata of gout
were present in 118 males and nine females. Of _muscular_ types, taking
as our example _lumbago_, we find that out of twenty-seven examples no
less than ten displayed definite evidences of a gouty taint. Similarly,
out of thirty-eight cases of lumbago complicated by other manifestations
of fibrositis eleven males and one female were of gouty habit. Also in
twenty-three cases of lumbago associated with arthritic fibrositis six
males, but no females, displayed the same proclivity. Lastly, out of
thirty-eight cases of lumbago complicated by right or left sciatica ten
were of the same diathesis.
Passing in turn to consider this same factor in relation to _sciatica_,
we note that out of 142 examples twenty-four men and three women were
gouty. Occasionally, too, apart from _glycosuria_, it appears to be
responsible for bilateral sciatic pains, for in three examples of this
nature gout was present.
James Taylor is also very definite on this point, that, glycosuria aside,
affections of individual peripheral nerves occur frequently in the gouty.
There is little doubt, he says, that sciatica is “frequently present in
the gouty and is sometimes directly due to that state.” While admitting
that in many, if not most, cases of sciatica there are associated
arthritic changes in the _hip joint_, he yet affirms his belief that
“there are some in which the neuritis is a primary condition.”
With this statement my own experience accords, but with a reservation,
viz., that the _sciatic neuritis_ is apparently _secondary_ to a lumbar
or _gluteal fibrositis_, with sequential involvement of the _sciatic
nerve sheath_ and extension to the nerve trunk.
Taylor holds also that _anterior crural_ and _brachial neuritis_ may be
directly due to _gout_. As to brachial neuritis, he says: “I have known
it occur apart from any recognisable arthritic change in a patient who
was the subject of gout.”
Having regard to the flippant manner in which the term “neuritis” is
but too frequently bandied about, it is refreshing to note that in all
Dr. Taylor’s cases “the existence of the neuritis” was shown “by the
tenderness of the nerve trunks, the spontaneous, often severe, pain, and
atrophic changes both in the skin and the muscles—the glossy skin and
atrophied muscles.”
As for the involvement of other nerves, trigeminal neuralgia is held
to be the most common; but, for myself, I have never felt justified in
claiming any such example as gouty. Nor am I satisfied that persons of
gouty habit are more prone than others to attacks of migraine.
Lastly, I cannot confirm out of my own experience Duckworth’s statement
that “_herpetic_ attacks in all varieties of ‘gout’ are common.” Nor have
I seen _shingles_ co-exist with acute gout, neither have I come across
any examples of so-called _gouty spinal meningitis_!
In conclusion, I would submit that:—
(1) Acute articular gout is not infrequently complicated by
fibrositis.
(2) The same infection that determines the articular outbreak
is responsible for the concomitant muscular and nerve phenomena.
(3) Persons of gouty heritage are especially liable to
fibrositis, notably _lumbago_ and _sciatica_.
(4) Gout predisposes to fibrositis in that the inherent
pathological attributes of gouty tissues favour the incidence
of _infection_.
In regard of this last postulate, it is well known that _gouty_ persons
who contract _gonorrhœa_ are more prone than the _non-gouty_ to develop
_gonorrhœal rheumatism_, in other words, to sustain a widespread
infection involving the fibrous tissues, not only of the joints, but of
the muscles and even of the nerve sheaths. With this concrete example to
hand, is it not reasonable to suppose that such a constitutional taint
will favour the incidence also of other infections or sub-infections,
and that this may explain the relative frequency of fibrositis, not
only in the actually gouty, but in those of gouty heritage, this the
more cogently having regard to the fact that so much exact evidence is
forthcoming in favour of local infection as the cause of all types of
fibrositis?