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?