Chapter XIX: Etiological and Clinical Diagnosis

ARTICULAR GOUT

The intimate cause of gout is unknown—a humiliating reflection, albeit salutary, if it but engender a more catholic attitude on our part when seeking to unravel the nature of this obscure joint affection. For, to secure ideal ends, diagnosis must be, not only clinical, but _etiological_. This is the more likely to be attained if we shed all preconceived ideas and prejudices.

ETIOLOGICAL DIAGNOSIS

Confronted, then, with a suspected case of gout, whether acute or chronic, what shall be our way of approach? Not the easy and hazardous path of lightning diagnosis affected by those who plume themselves on their so-called clinical “instinct,” but the slow, laborious route of clinical “observation,” that leads more surely to the vantage ground of truth, this assuredly in all diseases, but in none more so than in _joint_ disorders, whose outward resemblances so oft hark back to inward disparities.

First, as to the manner of man, while one would not decry the hints obtainable from _physiognomical_ peculiarities, it is often hard, if not impossible, to fit the subject to the so-called “gouty diathesis.” They are not all of the John Bull type; not a few are spare in build. Hence the danger of too ready inference from so-called “gouty” traits, to be regarded rather as ancillary to, but not substitutes for, more exact criteria.

Now, as to heritage, for, despite the fallacies that surround inquiries into family predispositions, they often furnish valuable hints as to the metabolic trend of the stock. True, ancestral stories often prove indefinite, but fortunately less so in the “gouty” than in those of “rheumatic” tendency. For, as Sir Dyce Duckworth points out, even the laity are quick to recognise what they term “chalky” gout, and so “if a history be given of ancestors or relatives thus affected, there need be no hesitation in pronouncing for true gout amongst them, and for the probably gouty nature of such arthritic ailments as may be complained of by the patients under examination.”

Turning to the individual himself—for the subjects of regular gout are rarely women—what is his age? If he is over thirty-five and has never previously had an arthritic disorder, it is much more likely to be _gout_ than rheumatism, this only as a broad generalisation.

What occupation does he follow? What are his habits? Is he of the “idle rich” who “fare sumptuously every day”? Is he a plumber, a painter, or a butler, coachman, or club waiter, these last being men who, as Sir Thomas Watson observes, “often live more luxuriously and more idly a great deal than their masters”? In short, we must search for any evidence of overeating, overdrinking, and indolence. For of this triad of vices is gout too oft begotten.

As to illnesses, his past may tell of classic outbreaks, one or more in the great toe, and if to this be added a visible _tophus_, we stand face to face with a “gouty diathesis.” More eloquent this than a “cloud of witnesses” as to previous attacks of migraine, asthma, eczema, etc. All these and more may emerge during the subject’s recital, and by all means let them be ascertained. But forget not that they often arise in the _non_-gouty. Above all, though, miss not the significance of heightened blood pressure, a cardiac lesion of degenerative type, sugar or albumen in the urine. For these are of the things that will out, but let it not be to our discomfiture!

Even presuming that all facts and observations up to now point to a “gouty” origin of the arthritis, the end is not yet. What has evoked the arthritis? We seek a cause. For to call an arthritis “gouty” is but to restate the problem. How clear the need then for a meticulously careful investigation, in the hope of achieving not a merely nosological, but an _etiological_, diagnosis.

To narrow our field, we should, in the first place, exclude _gonococcal_ infection, and failing this, influenza, syphilis, or any of the zymotic or other disorders prone to be followed by or associated with _joint_ affections.

If none of such be forthcoming, we should search for _local foci of infection_. The mouth and its accessory cavities first claim attention. It should be closely scanned for the presence of oral sepsis, the most fruitful source of which is _pyorrhœa alveolaris_. If _dentures_ are worn it is wise not to take the subject’s word that all his teeth have been extracted. Like others, I have in such found the broken-off stumps still _in situ_. The condition of “bridges” should be noted, fruitful sources of sepsis as they are. Clinical examination of the mouth may prove inadequate, as _buried roots_, _cysts_, or _abscesses_, not to mention _alveolar rarefaction_, etc., demand for their detection _radiographs_.

The _pharynx_ and _tonsils_ should be thoroughly investigated, for disorders of these same are by no means uncommon in “gouty” subjects. Any history of _aural_ or _nasal_ discharges demands the same careful local examination; and, needless to say, the same course must be pursued in regard of any _local infections_ of the _genito-urinary passages_. In short, in _gouty_, as in _non-gouty_, forms of _arthritis_, thorough and routine examination of every patient by modern _bacteriological_ methods is imperative.

Ignorant of the precise _etiology_ of _gouty_ arthritis, we can ill afford to overlook any associated _infective_ foci which may prejudice the well-being of the victim, as, for aught we know to the contrary, we may be overlooking the very _fons et origo mali_. Compare our attitude towards other arthritides of cryptic origin, how systematic our search for _infective_ foci, and what a light has thereby been shed on their intimate etiology!

Here may we lodge a plea for routine examination of the blood in all cases of _gout_? For, as shown, the findings, _leucocytosis_, etc., have doubtless some profound significance. Apart from this, the routine employment of _complement-fixation_ tests for the organisms responsible for local infections might illumine the obscurity that overhangs this complex problem of their relationship to remote pathological lesions.

If up to now our search for local foci prove futile, it remains for us to note the presence or absence of _functional derangements_ of the _alimentary tract_, or its _accessory glands_. We must not, because we think perhaps that the patient “looks gouty,” assume that his _dyspeptic_ symptoms are of like origin. It is our duty to ascertain, if possible, the precise nature and origin of the dyspepsia.

We know that, given _oral sepsis_, sequential infections of the _appendix_ and _gall bladder_ are not uncommon. Recently it has been remarked that many _gouty_ patients suffer with attacks of pain in the region of the appendix, and simultaneously tenderness over the gall bladder. That the subjects of gout enjoy no immunity from appendix or gall bladder disorders is certain, and at this we need not be surprised, seeing the frequency with which they suffer from alleged causes thereof, _i.e._, dental sepsis, etc.

But what we would insist upon is that we should not be content merely with dubbing these symptoms “gouty,” as they are much more likely to be, not symptomatic of gout, but _etiologically_ related thereto. If then we are to arrive at the exact nature of the underlying lesion, the probable site of infection or toxic absorption, we must invoke all modern methods of investigation. Thus, how valuable the existence of an X-ray barium or bismuth meal in furnishing positive evidence of gastric or duodenal ulcer on the one hand or of _gall bladder_ or _appendix_ disease on the other. What an aid to the location of adhesions the demonstration of _ileal_ and _cæcal_ stasis, etc.!

In obscure cases the _fæces_ may have to be scrutinised for evidences of _pancreatic_ inefficiency, viz., bulky pale stools, undigested meat fibres, and excess of neutral fat. Their _bacterial_ content, too, if abnormally high, should be noted. As in other arthritides of unknown origin, the results following the administration of _vaccines_ prepared from the predominant organisms have been such as to suggest a causal connection.

The urine should be subjected to _chemical_ and _bacteriological_ examination. As to _uric acid_, the delusion still widely prevails that gouty subjects excrete large amounts thereof. How frequently is “the degree of acidity” of the urine or “its content of uric acid” held to justify a diagnosis of gout. The deduction is quite unjustifiable. Equally so the assumption that the reverse, a defective excretion of uric acid, is an invariable feature of the gouty diathesis. For though when on a _purin-free_ diet the output of uric acid in the gouty is low, it rarely, if ever, falls below the level of normal. The truth is that we cannot _on the mere basis of the variations in uric acid excretion in the urine_ presume to diagnose gout.

To have any semblance of diagnostic value, the patient should be on a _purin-free_ diet, and a long series of exact quantitative examinations made. C. v. Noorden, to gauge the limit of tolerance of his patients, gives them increasing amounts of purin, and so determines the quantity the subject can deal with without showing retention. But, as Von Fürth satirically observes, “when a physician allows a quantitative analysis to be made of any arbitrarily collected specimen of urine of his patient and then makes a diagnosis of the presence or absence of a ‘gouty diathesis’ after a glance at the list of data of the analysis, he is really not proving by his actions his possession of diagnostic acumen as much as he is laying bare his total ignorance of bio-chemical matters.”

So much for the diagnostic valency of uric acid estimates in chronic gout, but if the patient be on purin-free diet, and an acute attack ensue, the curve of uric acid excretion is fairly characteristic. In other words, for a day or two preceding the outbreak, the uric acid output falls below the usual level, but early in the attack rises markedly, to be followed by a secondary fall.

Some aid in diagnosis has been afforded by the fact that after ingestion of purin-containing food the gouty individual does not, like a normal person, eliminate the excess of uric acid, but the excretion is “spread out over a number of days.” But this retardation and diminution in the excretion of exogenous purins has been seen in non-gouty forms of arthritis, not to mention some cases of nephritis and chronic alcoholism. Hence delayed nuclein exchange, though highly suggestive of gout, is not infallibly diagnostic thereof.

_As to uric acid in the blood_, it will, I fear, not for long, if ever, be easy to prevail on patients to submit to withdrawal of the amount of blood necessary, even by modern methods, for its estimation. Fortunately, our American _confrères_ appear to be more successful in securing such opportunities. Pratt states that in his twenty-one cases of genuine gout the uric acid content of the blood, irrespective of diet, was 3·7 mg. per 100 grams, as opposed to 1·7 mg., the average amount in 156 non-gouty cases studied by Adler and Ragle. Still Pratt noted that in a few cases of undoubted gout the uric acid content of the blood was within normal limits, though it never fell, even on a purin-free diet, below 1·4 mg. Nevertheless he holds that there is conclusive evidence that the uric acid content of the blood is in gouty individuals notably increased both in the intervals and during attacks.

He has found the sweetbread meal an aid in diagnosis, and the following is his method of procedure: “The patient is placed on a purin-free diet, and the daily output of uric acid in the urine determined. After having been on this diet for at least four days the blood is analysed for uric acid, and 150 to 300 grams of sweetbread (weighed raw) are fed. The purin-free diet is then resumed. The blood of gouty subjects forty-eight to seventy-two hours after the sweetbread meal has shown in every case examined an abnormally high amount of uric acid, while in control subjects this was not found. It is not improbable that this rise in the uric acid content of the blood may occur in certain cases of nephritis and other pathological conditions.”

A _bacteriological_ examination of the _urine_ should be undertaken. Trautner held _mucous colitis_ as one of the initial manifestations of gout, and believes that the _bacillus coli communis_ is the primary agent in gouty affections. He suggests that it produces a reducing substance which during its passage through the body is transmuted into xanthin and uric acid. Be this as it may, there is increasing evidence that an etiological potency may attach to coliform bacilli, streptococci, and other organisms. Dr. Munro in his researches at the Royal Mineral Water Hospital, Bath, noted that the blood serum in one of my cases of acute gout agglutinated _B. coli_. He has also found streptococci in the urine in acute gout, and these subjects certainly enjoy no immunity from other forms of bacteriuria.

It is beyond the scope of this volume to outline the methods of differentiating and determining the exact organisms which may be responsible for gouty arthritis. But if we aim at rational as opposed to purely haphazard serum or vaccine therapy, we must effect a differential specific diagnosis in a bacteriological sense. How searching our investigations must be in these cases we learn from Adami’s brilliant address on _sub-infection_ when he laid down the axiom that in all cases “there ought to be routine blood cultures, routine examination and reports on the stools and their predominant bacterial types, blood counts, hæmoglobin examination, in fact the full clinical study of each case, so that nothing is neglected.”

No apology is needed for our insistence on the imperative necessity of routine systematic investigation from all sides of these cases of gouty arthritis. For its origin still remains hidden, and who can doubt that, to remove this long-standing reproach, we must approach our study of these cases in a more catholic attitude of mind, one bent on _etiological_, not merely nosological, diagnosis?

CLINICAL DIAGNOSIS

_Introductory Remarks_

The word gout itself is void of offence, innocent of scientific pretensions, neither expressing nor violating any article of pathological belief. But let us not forget that the term is neither self-explanatory nor final. Derived through the French _goutte_ from the Latin _gutta_, it but expresses laconically the fanciful doctrine of those who so christened it.

What the old humoralists saw was the _tophus_, and would that they had clung more steadfastly to this as their sheet anchor in diagnosis! but casting their moorings, they launched forth on the uncharted seas of abstract philosophy. Even in the writings of the nineteenth century physicians we trace the influence of their disquisitions, and we are tempted to think that some even of our day still bide beneath their thrall.

But, with the advance of pathology to the dignity of a natural science, we must assert our independence of misty hypotheses, rendering obeisance only to facts. What then, may we ask, is the outstanding fact of the “gouty diathesis”? It is, in a word, the _tophus_! Even as the vague and shadowy constitutional warp known as the “rheumatic diathesis” finds expression, or rather becomes incarnate, in fibrous _nodule_ and _induration_, so also does the equally nebulous “gouty diathesis” become objective, crystallised in the _tophus_.

THE DIAGNOSTIC STATUS OF TOPHI

This problem calls for more critical consideration than is usually accorded thereto. The tophus is, in truth, the touchstone of gout, yet not a little controversy obtains as to the frequency of its incidence in “gouty” subjects.

At one extreme we find Sir Charles Scudamore maintaining that tophi have occurred in only a few individuals “of particular ‘gouty’ idiosyncrasy,” in, according to him, less than 10 per cent. of the victims. At the other Sir Alfred Garrod, discussing these figures, observes: “From my own experience I consider these numbers far below the real proportion, from their being deposited in parts of the body scarcely to be expected.”

Now as to these distinguished physicians, who shall doubt that of the twain Garrod stood on firmer ground than his predecessor? In arriving at their diagnoses of gout, Scudamore rested on clinical “instinct,” Garrod on clinical “observation.” To the more scientific mind of the latter the tophus appealed with all the insistence of a fact, while the former was yet in bondage to abstract philosophy, dominated too much by crude and unproven hypotheses.

_Given the presence of tophi, the diagnosis of a “gouty diathesis” is assured; in their absence it is but speculative._

It is upon this dictum that we would take our stand, and this without depreciating in any way the pioneer researches of Garrod. For it must be recognised that the increasing differentiation of joint diseases has proceeded apace. How many are now affiliated to specific germs, not to mention the undreamt-of light thrown on their inward characters by X-rays! Scudamore’s work appeared exactly a century ago, Garrod’s in 1876. The conclusion then seems inevitable that many of their alleged cases of _gout_—at any rate, those _unattested by tophi_—would now be relegated to widely different categories.

But this zeal for infinite cleavage and subdivision, so characteristic of the modern school, far from diminishing, does but _accentuate_, the _diagnostic_ valency of the tophus. It still remains _the_ infallible criterion of diagnosis, and, for myself, I feel convinced that infinitely more good than harm would ensue if we refuse to recognise any individual as being of the “gouty diathesis” unless he exhibit these objective stigmata thereof.

Of course to some such a rigid attitude will spell anathema. I hear them say in oracular tones: “Never forget gout, or awful indeed will be your awakening.” More harm, say they, is wrought by failure to recognise gout than by diagnosing gout where none is. Doubtless they are right in counselling us not to forget gout, but not to the exclusion of all else. For, at issue with them, I hold it better to miss gout than to miss _syphilitic_, _gonorrhœal_, and other forms of arthritis.

“A name being so readily found for an obscure disease, the practitioner considers himself as excused from the difficult task of nicer discrimination.” Thus wrote Scudamore a century since, a rebuke and a warning for all time.

TOPHI IN RELATION TO ARTHRITIS

How elated we are, and rightly, when in an obscure form of arthritis we pounce on these objective criteria of gout, how apt to deem our diagnostic quest as ended, and with what fatal glibness the time-worn “gout” slips from our lips, sure, alas, of ready and almost complaisant acceptance. Fallacious inference, all too prevalent, that the presence of _tophi_ stamps any _concomitant arthritis_ as “gouty.”

True, tophi are pathognomonic of gout, but their existence does not confer on their host _immunity from all other forms of arthritis_. In view of the increasing light shed upon joint disorders, who can doubt that (and this not only for our forefathers) the _tophus_ has too often proved a veritable snare, allaying all diagnostic doubts, lulling us into false security? For an individual may, for example, exhibit _auricular tophi_ and be the victim also of an _arthritis_, but the latter is not inevitably “gouty.” All that can be assumed at sight is merely that the joint disorder, whatever its nature, has ensued in a subject of “gouty diathesis.”

For it may be of specific infective origin, _gonococcal_, syphilitic, pneumococcal, etc. _Quâ_ a concomitant arthritis, then, the diagnostic significance of tophi, at any rate when of _ab-articular_ site, must not be overrated. It is at once a beacon and a warning. In other words, the diagnosis of a co-existent arthritis as “gouty” should not be entertained pending the exclusion of all other forms of arthritis.

_Conversely, in the absence of tophi, the diagnosis of an arthritis as “gouty” is not absolute, but presumptive._

For in the lack of these objective stigmata how can the authenticity of our diagnosis be established? Is it not when achieved a _nosological_ rather than a diagnostic feat? Put otherwise, is not our diagnosis, especially in _initial_ attacks, largely _topographical_? Not that we would for one moment decry the advantage of realising the predilection of certain organisms for this or that particular joint: of the gonococcus for the sterno-clavicular, of typhoid for the hip, post-scarlatinal rheumatism for the phalangeal joints, etc. But we would drive home the fact that our diagnosis in _initial_ attacks of “gout” is very largely _topographical_. Let but inflammatory trouble ensue in the _big toe_, and forthwith we assume it gout, as if, forsooth, this particular joint were immune from all other forms of disease, this, too, while in the same breath we comment on its extreme liability to injury. So, indeed, we maintain, is the marked predilection of gout for the toe joint explained. Is not this a little crude? Does not the same circumstance increase its liability to _infection_ and, we may add, not less important, its proneness to _static deformities_? But to this we shall recur when discussing _differential_ diagnosis.

To return, how often, apart from the above pitfalls, is the diagnosis “gout” arrived at without any search for tophi wherewith to support the assumption. Our contention is that even in primary attacks of gout our search for _tophi_ should be exhaustive. If undiscoverable, why not be honest with ourselves and recognise that our diagnosis is _presumptive_ pending their development?

Sir William Roberts on this point observes: “As a rule, diagnosis of acute articular gout is easy, but exceptional cases of difficulty occur. The _gouty_ character of the inflammation is _affirmed by the discovery of uratic concretions_ in the rim of the ear or elsewhere.”

Again, Sir William Osier, discussing the diagnosis of acute gouty polyarthritis, remarks: “We have had of late years several cases admitted for the third or fourth time with involvement of three or four of the larger joints. The _presence of tophi_ has settled the nature of a trouble which in previous attacks has been regarded as ‘rheumatic.’”

One may, we think, gather from these two statements the inference that both these distinguished authorities hold _tophi_ to be the _only infallible criterion_ upon which to base a diagnosis of _gouty arthritis_. In my own practice I must affirm that I never feel justified in christening any arthritis as _gouty_ unless I have discovered _tophi_, and then only when to the best of my ability _all other known causes of arthritis_ have been excluded.

FREQUENCY OF TOPHI IN TRUE GOUTY ARTHRITIS UNDERESTIMATED

In reviewing the statistics of authors as to the frequency of the incidence of tophi in their cases of assumed gouty arthritis I am inclined to think their relative infrequency is apparent rather than real, in other words that many of their cases of alleged “gouty” arthritis which _lack tophi_ would, if investigated by modern methods, have been shown to be due to other causes of arthritis, this especially as regards their assumed cases of _chronic_ gout. For who can doubt that prior to the discovery of X-rays many cases of _osteoarthritis_, etc., were thus erroneously labelled? Nor indeed, as we hope to show later, is it improbable that similar fallacies obtained even in regard to _acute_ types of gout, particularly when of _polyarticular_ distribution.

It will be noted that we confine our criticisms to those examples of “gouty” arthritis _unassociated with tophi_. But if, as we maintain, our scepticism be justifiable, then it follows that it _diminishes_ to an unknown extent the _percentage of cases of genuine “gouty” or uratic arthritis which lack tophi_.

DIFFICULTY OF DETECTING TOPHI

Apart from the probability of such erroneous relegation to the “gouty” category of _non-gouty_ arthritides, there remains this further consideration, the ease with which tophi, even when superficial, may be overlooked. We look for pearly white concretions, and if none are seen we straightway assume that _tophi_ are _absent_. This, I am sure, is a very common pitfall. At their inception tophi are neither white nor hard. They are largely fluid and soft to touch. The skin over them may be unchanged in colour or reddened. Only when mature, and the overlying skin is thin, do they assume the ordinary aspects of a tophus. These observations apply not only to tophi in the ears, but to those in the vicinity of the small joints of the hands and feet or elsewhere. I would urge that in the case of all soft localised swellings of dubious nature in the neighbourhood of the phalangeal joints aspiration with a hypodermic syringe will often prove very helpful. If fluid can be withdrawn and the same microscopically examined, it will more often than is supposed reveal the presence of biurate crystals.

More information is badly needed as to the relationship of their formation to acute attacks of gout. Garrod on this point remarks: “The deposits are probably formed during an attack of gout, but occasionally they appear shortly afterwards. In one case, of which I have notes, the ears were carefully examined without result when the patient left the hospital, but within ten days, on re-examination, a deposit was found. Perhaps some fluid was effused during the fit, but being at first transparent, could not be easily distinguished.” Sir Dyce Duckworth, too, observes: “After acute attacks of gout have passed off there may follow renewed pain in the neighbourhood of the joint, and later there is discovered a nodular or soft swelling. In the latter case there may be fluctuation, indicating a liquid collection of urates. This should never be opened. In a few weeks this tumour tends to indurate, grow more compact, and a so-called ‘chalky’ concretion is established.”

Reflection upon the foregoing considerations leads me to the conclusion that not only was Garrod right in his affirmation that “_gouty inflammation is invariably attended with the deposition of urate of soda_,” but more that _examples of true uratic arthritis which lack tophi are exceptional_, and that _in their absence their diagnosis as such cannot be with certitude established_.

We have now, we trust, sufficiently defined our attitude towards the tophus, the salient objective stigma of a “gouty diathesis,” and the indispensable _rôle_ it plays in enabling us to establish the diagnosis of articular gout.