XXV. OCULAR DISEASE IN THE GOUTY
BY W. M. BEAUMONT
With the passing of Jonathan Hutchinson disappeared the premier British exponent of l’arthritisme, that generic term so attractive to our French confrères. Whether gout and rheumatism are branches of one common stem need not detain us, for it is an abstraction more suitable to the philosophic age of medicine before pathology emerged as an exact science. Be this as it may, there has been in the past, and there still remains in the present, as a bond of union, a universal belief that both are subtle causes of disease of the eye. But the age of hypothesis is giving place to the era of facts, and we find in recent writings a more cautious expression of individual opinion, a less dogmatic positivism regarding the relationship of gout and rheumatism to ocular disease.
In referring to modern text-books we find Parsons[44] describes gout as one of the “alleged causes” of iritis. In rheumatic iritis he states that the patients “are often gouty.” The gouty nature of iritis is indicated by the similarity of onset of some cases of iritis with that of gout. “Iritis in an elderly patient is likely to be gouty, often starting suddenly in the night and sometimes ushering in an attack of gouty arthritis.” In episcleritis “rheumatism and gout are commonly indicated as the chief causes.”
Werner[45] includes gout in a list of disorders of metabolism which produce iritis “by means of toxins of a chemical nature.”
Sim[46] considers that iritis occurs in gout “as the result of some toxic influence”; and in addition he says, “Iritis is to be met with in gout.”
These authors express accurately, I think, the present views with regard to gout as it affects the eye; with each there is a tone of restraint and suggestion rather than of boldness and assertion, and the contrast to Hutchinson’s emphasis is noteworthy: “I believe,” he tells us, “that iritis due to the arthritic diathesis is a common malady.”
Among the many and indiscriminate diseases of the eye which have been considered to be due to gout are included blepharitis, conjunctivitis, episcleritis, scleritis, orbital cellulitis, neuro-retinitis, retro-bulbar neuritis, optic neuritis, optic atrophy, iritis, cyclitis, choroiditis, glaucoma and retinal hæmorrhage. Truly an all-embracing rather than an eclectic list, a medley of diseases without any melody.
Evidence of Gout in the Eye.—When we inquire what is the evidence which justifies the belief that gout causes ocular disease we find little more than a traditional hypothesis inherited in a long line of succession from the Fathers of Medicine. Nevertheless the opinion that there is a connection is widespread, not only in Europe, but also in America.
In considering this relationship we cannot overlook the effects of the diathesis on other viscera. How in these is a diagnosis of gouty origin arrived at? It would appear that the assumption of an irregular form of gout is based upon the following observations:—
(i.) That it sometimes happens that an undoubted attack of articular gout aborts and is followed by symptoms referable to a grave visceral disorder, e.g., gout in the stomach (retrocedent gout);
(ii.) That sometimes the converse occurs, viz., that an attack of visceral disorder may suddenly be replaced by an acute articular manifestation;
(iii.) That such visceral derangements may alternate, not only with articular, but also with other, such as cutaneous, outbreaks;
(iv.) That eye disease has been known to wax and wane in unison with concurrent arthritic gouty manifestations;
(v.) That occasionally in gouty people an attack of iritis of sudden onset in the night has been followed by remission of the symptoms in the day[47];
(vi.) That visceral symptoms in the gouty are anomalous and inexplicable on any other basis;
(vii.) That the treatment usually advocated for gout has a favourable influence.
Deposition of Urates.—Two cases are recorded by Garrod in which there was a deposit of urates in the sclera. These instances do not appear to have been confirmed by other observers, and they may be regarded as exceptional cases, occurring, it should be noted, in the outer envelope of the eye. But though these tophaceous deposits may occur in the sclera and in the eyelid, they have never been known to invade the intrinsic structures, such as the iris or ocular media. The eye, in fact, is on all fours with the sites of urates elsewhere—deposition occurs in parts of relatively low vitality.
Although urates are not found within the eye, there is in other morbid ocular conditions quite frequently a deposition of foreign matter, such as alien crystals, of varied description. For instance:—
In the sclera on rare occasions we find osteomatous degeneration.
In the choroid there may be true bone which forms a cup so extensive that it can be felt by the finger, or, again, there may be calcareous plaques.
The retina may undergo colloidal changes or be the site of carbonate of lime or of cholesterin.
The vitreous may sparkle with showers of cholesterin.
The lens may contain both tyrosine and cholesterin.
The aqueous shows similar crystals.
In the iris degenerative calcareous or osseous deposits are occasionally seen.
The cornea may be affected by hyaline degeneration with deposition of lime salts.
The conjunctiva may be calcareous.
In all these cases the foreign particles, whether crystals or otherwise, are usually the retrogressive changes of senescence proclaiming that the forces which make for degeneration are more potent than those which make for regeneration.
But urates are not found in the eye, even though the patient is gouty. On the other hand, both in gouty joints and in other similarly affected parts of the body we find a deposition of urate of soda.
Gouty Diathesis.—From the days of Sydenham—himself a martyr to gout—diathesis has been a name to conjure with, and an all-sufficient diagnosis. In the podagrous patient any intercurrent disorder, any inexplicable ache or pain, was ascribed to gout, and patient and doctor were alike satisfied. “Tempora mutantur,” but still we are prone to call morbid conditions gouty when they occur in gouty people.
If we accept the theory that gout is due to an excess of uric acid in the blood, the view which I have expressed elsewhere[48] that gout does not cause iritis is directly challenged. For if it be granted that a sudden outpouring of so non-toxic an acid causes an acute inflammation—for instance, in the synovia of the great toe—why should not our faith incline us to go further and find in this malevolent, though bland, acid a source of inflammation affecting the fibro-muscular meshwork of the iris?
If, however, we adopt the infective theory, then the association of the uratic deposits no longer dominates our creed—we view them as mere clinkers and by-products erupted from the furnace.
The infective theory of gout also lends plausibility to an association with iritis, for this latter is a disease of infective origin. For the intimate relationship of all forms of asthenic arthritis with iritis is of very frequent occurrence, but is practically never seen in the more sthenic arthritides: rheumatic fever, acute gout and traumatic arthritis.
Nearly fifty years ago Jonathan Hutchinson drew up a “Report on the Forms of Eye Disease which occur in connection with Rheumatism and Gout.”[49]
At the present day it is not easy to differentiate his 117 cases according to modern classification, but he includes gout, rheumatism, rheumatic arthritis, etc. The differential diagnosis between gout and rheumatism was simplified by the creation of a mule—“rheumatic gout”—and upon its back were packed the doubtful cases.
Hutchinson’s views regarding the essential difference between gout and rheumatism are crystallised in his statement that in rheumatism there is an arthritic susceptibility to weather, in gout an arthritic susceptibility to diet.
Osteoarthritis also seems to have been included as one of the gouty diseases, probably because post-mortem examination revealed uratic deposits in the disorganised cartilage. This, however, would appear to be an epi-phenomenon, and must not be allowed to obscure the essential distinction between true gout and osteoarthritis. It is a sign of articular disorganisation of long standing, and is the homologue of the similar deposition of crystals, etc., already referred to as occurring in the eye as the result of chronic disease therein.
The significance of tophi, as the touch-marks of gout, is undoubted, but even if they are detected in the eyelids or elsewhere, we are skating on thin ice if we rashly declare that a coexisting intra-ocular disorder is gouty. Most forms of iritis betray the same clinical facies, although the etiological causes are diverse. But in none do we find any appearances pathognomonic of gout.
The argument that because a patient has tophi therefore the iritis is also gouty does not hold good, for gout does not confer immunity from other diseases, and even though we cannot prove an alibi for the diathesis, we can often in these cases also indict gonorrhœa, pyorrhœa or some other pathogenic agent.
The favourite site for tophi is one in which blood-vessels are sparse; but, although the cornea is void, imbibition of blood from the marginal looped plexus of capillaries and an abundant lymph supply provide amply for nutrition, and tophi are not found in this locality. The sclerotic, however, has a meagre supply of vessels, and for some unexplained reason tophi rarely invade it. In the eyelids, on the other hand, possibly from the cartilage being rich in sodium, tophi are occasionally seen. If we accept the tophus as the one unequivocal criterion of gout, we are not justified in labelling an iritis as gouty in its absence. If we do, our diagnosis is presumptuous and not absolute. Strictly speaking, the diagnosis cannot be made. We may the more readily admit our limitations, inasmuch as they are a blessing in disguise, and suggest a further etiological search.
In Hutchinson’s list of eye diseases which occur in association with rheumatism and gout there is a history of gonorrhœa in twenty-six cases, syphilis in seventeen, of both gonorrhœa and syphilis in six. Herpes occurred in two, pustular acne in one, eczema in one, albuminuria in one, ague in one. Bad teeth are reported in two. In all the total was fifty-seven cases out of 117 (48·7 per cent.) in which there was a possible source of infection. It is probable that this percentage would have been materially increased if at that time it had been recognised how great is the influence of pyorrhœa and other sources of infection in the etiology of irido-cyclitis.
With regard to all infections it is only in the present day that full advantage is taken of bio-chemical and bacteriological methods of differentiation. How frequently the true origin of disease must have been overlooked when the pallid spirochæte was unknown, when the Wassermann test was not applied, and when the complement fixation test for gonorrhœa was not recognised.
With regard to a combined cause it has been maintained that gonorrhœa is always more severe in the gouty than in other people, and it may be that the more intense the gonorrhœa the more likely may it be to produce constitutional symptoms, of which iritis is one. In all such the combination of gout and iritis would indelibly impress upon the mind of the surgeon the intimate association of joint and eye. It was long ago recognised that many forms of joint disorder were associated with iritis, and, as the cause of the arthritis was not always gout, Mackenzie introduced the generalisation “arthritic iritis.” “Not being able,” he tells us,[50] “to determine the diathesis which predisposes to this ophthalmia” (iritis), “I use arthritic as a conventional term, without adopting it in the strict sense of gouty.” The expression is well worthy of retention for the reason that it warns us to be prepared for an attack of iritis in many forms of arthritis and arthralgia.
In the following articular diseases the triad joint, muscle and nerve disorders is not uncommonly linked with iritis:—
Tuberculous arthritis; Syphilitic arthritis; Gonococcal arthritis; Certain forms of specific arthritis: malarial, dysenteric, etc.; Infective arthritis of undifferentiated type, as yet unaffiliated to specific germs.
In the following forms of arthritis iritis is less common:—
Acute articular rheumatism; Acute gout; Osteoarthritis (hypertrophic); Rheumatoid arthritis (atrophic).
Iritis occurring in these last suggests the possibility of error in the diagnosis of the putative parent disease. Especially is the clinical similarity of gonorrhœal (polyarticular) rheumatism to rheumatoid arthritis to be borne in mind.
The Relative Incidence of Iritis.—In the text-books it is often stated that the syphilitic form of iritis is the one most frequently met with, and that gouty iritis, if it is met with at all, is much more rare. But in these comparative statements we have no clue to the frequency of iritis with syphilis, nor of iritis with gout. For a true analogy we do not want the syphilographer to tell us the aggregate number of cases of iritis that he has seen, but what is the percentage of cases of syphilis in which iritis occurs, and we want the gout physician to state his percentage of iritides in gout, or, negatively, what is the percentage of cases in which iritis does not occur.
If gout is a more prevalent disease than syphilis, it does not follow that “gouty” cases of iritis will be more numerous than those due to syphilis. Let us suppose, for the sake of clearness, that 1 per cent. of people suffering from gout get iritis, and that also 1 per cent. of people infected by syphilis get iritis, and that in a certain town there are two hundred people who are gouty and one hundred people who are syphilitic. It is probable that there will be two persons suffering from gouty iritis (always supposing there is such a disease), but only one from syphilitic iritis. The absolute totals will differ, but the relative will be identical. It is clear, then, that infectivity cannot be gauged by the statistical enumeration of the consulting-room. Gout is a rarer disease than our patients would have us believe, but accepting their views, even then we should expect to see more cases of iritis caused by it, if such existed; we should expect to find more definite proof of a causal connection, and less frequently a history of gonorrhœa, of pyorrhœa, and of syphilis.
No Uratosis, no Gout.—If we pin our faith to the equation
Hyperuricæmia + Uratosis = Gout,
we can at once exclude all cases of ocular disease as gouty in the absence of either factor. According to Garrod, “true gouty inflammation is always accompanied with a deposit of urate of soda in the inflamed part.” We should therefore expect that uratosis would occur in situ if an iritis were gouty. But it does not: the touch-mark is absent, and there are no chemical, pathological or clinical signs of urates in the iris after the inflammation has subsided. What then is the alternative? Either Garrod’s aphorism is inaccurate or iritis is never gouty. In other words, we must postulate that an iritis may be regarded as gouty without uratic deposits. If this be the case, the so-called gouty iritis may well rank with the occult migraines, flatulencies and acidities which are termed irregular, suppressed or latent gout. Strictly then it would be a latent gouty iritis fit to rank with that last refuge of the uric acid enthusiasts, the “latent nephritis” which they worship as the fons et origo mali of gout.
Metastasis.—The predilection of the gonococcus for synovial membranes is seen not only secondarily to urethral infections, but also in ophthalmia neonatorum, in which the joints of infants are affected sequentially to the eyes.[51]
The gonococcus also has been found in cases of peritonitis, pleurisy, pericarditis, etc., but it is said to have only once been isolated in the eye in iritis.[52]
It is not only the gonococcus which can initiate a metastasis from the eye to the joints, to the peritoneum, or elsewhere. The same process may be started by the bacillus typhosus, by the streptococcus of erysipelas, and by that of puerperal septicæmia.
De Grandmont[53] records the case of a young man recovering from typhoid, complicated with jaundice and nephritis, who was attacked by iritis with posterior synechiæ and hypopyon. Paracentesis was done, and the pus of the anterior chamber was transferred to agar-agar. Two days later a pure culture was obtained presenting all the reactions and characteristics of the bacillus of Eberth. Of this culture a small quantity was injected into the vitreous of a rabbit. A month later the rabbit was killed, when the liver and intestines were found to be infiltrated with the same bacillus of Eberth.
In erysipelas de Grandmont has seen a hyalitis from which a culture was grown on gelatine that presented all the morphological characteristics of erysipelas.
He has also met with a case of hyalitis associated with puerperal septicæmia, and he has no doubt that it was the result of a similar microbic invasion of the vitreous.
Gout does not render patients immune from tuberculous, syphilitic or gonococcal disease, and when in such so-called diathetic stocks an iritis occurs, especially in gonorrhœa, years after the primary disease, it is probable that gout, rather than lues, will be assigned as the cause.
The local appearances of iritis are identical in gonococcal and other infective iritides; they resemble clinically those seen in syphilis and tubercle except that in these there are sometimes condylomata of the iris in the one and tuberculous nodules in the other. To be comparable a gouty iritis should be characterised by iritic tophi.
“Arthritic” Iritis.—Forty-eight is a large percentage in Hutchinson’s cases of ocular disease associated with gout and rheumatism, and it is justifiable to assume that there was something more than coincidence in the triple entente of diathesis, arthritis and iritis. But the fact that the poisons of syphilis and gonorrhœa, etc., are potent causes of iritis is indisputable, and therefore the patients might have suffered from it even if they had never had either gout or “rheumatism.” Consequently these articular diseases are both superabundant and superfluous, and they may have no etiological status. A patient afflicted with arthritis is very susceptible to an associated attack of iritis provided that there is a septic focus anywhere in the body.
A practical point to remember, especially in gonorrhœa, is that the onset of joint trouble should warn us to anticipate the possibility of an associated iritis and should prompt us to instil atropine at an early stage. We should forestall the disease by treating the suspicion. The frequency with which gonorrhœa is followed sooner or later by iritis entitles this ocular phenomenon to be considered a secondary symptom of gonorrhœa, as it is of syphilis.
Before the potency of distant infective foci (for example, in nasal disorders, pyorrhœa, sinusitis, etc.) to produce ocular disease was recognised, there was justification for the inclusion of a so-called idiopathic iritis, but it is seldom now that we have to be satisfied with this negative diagnosis. Nevertheless the assignment of a toxæmic etiology must be based on a definitely ascertained focus of toxic absorption, or failing this, at least on symptoms of general malaise which render such a focus highly probable.
Frequency a Factor in Diagnosis.—It was known a century before the birth of bacteriology that gonorrhœa caused iritis. It was also noted that certain constitutional symptoms occurred in syphilis, and that among them not infrequently iritis was one. Observation and deduction was the process with our forefathers, and it seldom led them astray.
If in any sequence of events cause and effect are to be established when there is no obvious proof of connection, we may have to be content with an empirical diagnosis, and this was the position before the discoveries of bacteriology enabled us to place the etiology of iritis on a firm basis. How then did our ancestors know that syphilis and gonorrhœa caused iritis? Was it not—
(1) That the frequency of the association was the essence of the diagnosis,
(2) That there was absence of any other recognised cause, and
(3) In the former disease the effect of anti-syphilitic therapy?
Applying these rules to gout, we find—
(1) No marked frequency of association of ocular disease and gout,
(2) That when iritis does occur there is often some other possible source of origin, and
(3) That anti-gout treatment has only a doubtfully beneficial effect.
“Gouty” Iritis is not a Clinical Entity.—Before a symptom or affection can be classed as secondary to a primary disease there must be evidence of a connection stronger than post hoc, ergo propter hoc. For instance, in syphilis an iritis frequently follows which may be of the specific condylomatous type, and a laboratory examination of the inflamed iris may demonstrate the presence of the spirochæte. On the other hand, an iritis occurring in a gouty patient is indistinguishable from that form which results from infections of undifferentiated type. Moreover, iritis so seldom occurs associated with gout, and when it does there are so often present other well-recognised possible causes, such as pyorrhœa or gonorrhœa, that the doubt about the paternal relationship of gout to the iritis is overwhelmingly strong.
In the following table a comparison is made between types of iritis:—
IRITIS.
-----------------+-------+--------------+------------------+--------- | Gout. | Syphilis. | Tubercle. |Toxæmia. -----------------+-------+--------------+------------------+--------- Pathognomonic | 0 |Gumma of iris.|Tubercles of iris.| 0 symptoms. | | | | -----------------+-------+--------------+------------------+---------
If pathognomonic symptoms were always present the differentiation of the various causes of iritis would be less difficult. But this is not the case, and consequently, whatever the primary cause, the appearances of the iritis, in spite of the pathogenesis, objectively resemble each other in very many instances.[54]
Medical authorities call certain cases (not varieties) of iritis gouty; they are content to rest the diagnosis on the ground that they occur in gouty people. Yet there is not a single ocular symptom which differentiates the disease from a similar one in non-gouty subjects. Before the dogma can be accepted that because a gouty man has iritis it is therefore a gouty iritis and, like the poet’s primrose, nothing more, it must be shown that irido-cyclitis is proportionately more frequent in people who are gouty than in those who are not. Even then it is suggestive, but not conclusive, for it is conceivable that, although gout is not strictly the cause, yet it may so reduce the resisting power of the iris that it becomes a readier prey to some lurking organism.
It is commonly reported that the existence of a gouty diathesis gives to any inflammatory condition of traumatic origin—synovitis, for instance—a special tendency to chronicity, and I would not deny that it may have the same influence in the case of iritis of traumatic endogenous origin.
If then a gouty man is not immune from other possible causes of iritis, one of these, and not gout, may be responsible for it. Especially is a gouty diagnosis doubtful when there is a focus of suppuration in the tonsils, teeth or elsewhere. Also the prolonged hibernation of the gonococcus, for many years after the attack of gonorrhœa, is apt to be overlooked. The presence of excess of uric acid in the blood, which sometimes occurs in these patients, may mislead us into the belief that we have a true gouty iritis to deal with. But even although it is ascertained that a hyperuricæmia of 4-8 mg. of uric acid is present, it is no proof that the co-existing iritis is necessarily gouty. We might have an even higher content of uric acid in the blood in leukæmia, and yet no iritis be present. It may be admitted that on rare occasions iritis occurs in leukæmia, but no one suggests that the leukæmia or the associated iritis is due to uric acid toxæmia. We should be on infinitely surer ground if not uricæmia, but uratosis, were present. We could then, at any rate, confidently assert that, whatever the origin of the iritis, it had supervened in a subject of gouty habit. I do not think that we, as clinical observers of iritis, should go further than to say: “The man is gouty; his iris is inflamed.” Here in Bath, among hecatombs of gouty people, irido-cyclitis is one of the rarer associated diseases requiring treatment. When it does occur it is usually of obviously septic genesis rather than of gouty origin.
Contrasting gonorrhœa with gout, we find in the former when there is systemic infection, as shown by arthritic complications, there may be also iritis, so often, in fact, that it is legitimate to bracket it as a related symptom. It is a toxæmic condition in which we rely on the frequency of the combination to diagnose the cause.
In writing on iritis in 1908,[55] I referred to the rarity of the association of gout and iritis. In an analysis of 17,197 cases of “rheumatism” and rheumatoid arthritis occurring at the Royal Mineral Water Hospital, Bath, in twenty years, there were twenty patients who suffered from acute or subacute iritis. During the same period there were 2,159 gouty patients not one of whom had iritis. In a special hospital it is possible that the diagnosis of gout might be limited by a stricter nosological differentiation than occurs in private practice. It is, moreover, not uncommon for ophthalmic surgeons to see patients who call themselves gouty, or who say that their doctors have told them that they are, and yet on examination no corroboration is found, no clinical outbreak, or, more pertinent, no tophi. They come to us with an attribution of iritis to gout without the filmiest shadow of evidence.
In considering the correlation of cause and effect it not infrequently happens that we find no obvious connection between the one and the other. In syphilis, for instance, alopecia is a usual secondary symptom, and we rely on the frequency of the sequence to satisfy ourselves that it is no mere coincidence. If it could be shown that alopecia did not occur more frequently in syphilitic people than in non-syphilitic we might justly doubt the connection. The same reasoning may be applied to iritis and gout: the association is so rare that it is negligible. To justify a causal connection between diseases the possibility of a fortuitous concurrence must be excluded, for when the double event occurs only very exceptionally, it is difficult to exclude the long arm of coincidence.
A man has iritis and tophi; ergo we say he has gouty iritis. But why? They co-exist, it is true, but where is the link of attachment of cause and effect? How different is our attitude if we know in another case that our tophaceous iritic patient has gonorrhœa. We then say, gonorrhœal iritis in a gouty subject. Would it not also in the first case be more scientific if we frankly confessed that it was an infective iritis of undifferentiated type occurring in a person of gouty diathesis?
In considering the iritides in relation to gout there are two types which demand our attention. With the possible exception of traumatic iritis, this grouping embraces all the etiological varieties of the affection. In the first are those cases which are due to specific infection, such as syphilis, gonorrhœa and tuberculosis. In the second are those infections of undifferentiated type in which the causal germ has not yet been isolated. Now clearly we must read the latter in the light of their analogues, the specific iritides. In them the modes of onset, the clinical course, are duplicated, presenting similar variations, and they are doubtless the reflexes of the varying grades of intensity of the causal organism.
Concussion iritis would fall into line, for it is possible in this case that the iris is rendered a pars minoris resistentiæ by the blow, and that the iritis which follows is due to a cryptic focus, it may be in the gastro-intestinal tract or elsewhere. The chief sources of iritis are syphilis, gonorrhœa, tubercle and infections from undifferentiated organisms of low grade. If these said iritides occur in a person of gouty diathesis they are unmodified by it clinically or pathologically, macroscopically or microscopically, save possibly in the direction of chronicity—a result, it may be, of those inherent peculiarities of tissue metabolism ingrained in a gouty subject, and in which presumably the iris shares.
And that which has been said of iritis in the gouty applies equally to other forms of so-called gouty ocular manifestations. There are no statistics available to show that there is any differential frequency in those who are gouty compared with those who are not. Authors have laboriously recorded cases of eye diseases which have waxed and waned in unison with podagrous toes, but the publication of these cases is in itself a confession of the rarity of the coincidence, a rarity which destroys the authenticity of any communal kinship. Coincidence is merely another name for the rigid and immutable law of chance, for a cycle of events which occurs with irregular regularity. If it could be shown that a diet rich in purins brought on an attack of ocular disease in gouty people, and if the experiment could be repeated with a similar result and sufficiently often to exclude all probability of coincidence, scepticism would no longer be justified. But until more definite evidence is forthcoming “gout” in the eye is nebulous.
In attempting to define the relationship of gout to ocular disease, there is one author to whose opinion we turn with the respect due to a master. Garrod’s judicial summing up supports the view that there is a connection between gout and ocular disease, but his cautious statement seems to imply that the affection of the eye is modified by rather than due to gout. His statement is as follows[56]:—
“Gout of the Eye.—A form of ophthalmia connected with gout has long been recognised, and appears to be tolerably well established, but as rheumatic inflammation of the eyes is equally allowed to exist, difficulties may at once arise in the diagnosis. I have witnessed many cases in which conjunctivitis and sclerotitis appeared to be distinctly connected with the gouty diathesis, and in two cases there existed deposits of urates on the surface; gouty iritis also occasionally occurs. I once saw a case of acute inflammation of the sclerotic coat and iris which supervened a few days after the operation for cataract in a gouty subject. By active treatment the disease was arrested, but distinct articular gout soon manifested itself.
“Our information on this subject may be thus summed up: patients having a well-marked gouty diathesis now and then experience attacks of inflammation of the different structures of the eye; and it is important to bear in mind the fact that the state of the habit considerably modifies and keeps up such affections, and also that treatment directed to the gouty condition of the system proves very effectual in curing the local mischief.”
It will be observed that Garrod tells us that his two important cases of sclerotitis “appeared to be distinctly connected with the gouty diathesis.” With the reticence of the careful and accurate observer, he does not say they were due to it even though there were deposits of urates on the surface. He would seem to recognise that cases of sclerotitis with uratic deposits were unusual events, and that generalisations cannot be based upon exceptional cases. A gouty man is gouty to his innermost cells, and the eye, like every other part of the body, is a potential uratic site. We must grant therefore that the course of an iritis, however caused, may be influenced, though not necessarily dominated, by the diathesis. Consequently it may be necessary that cases of iritis of undoubted gonococcal or other infective source occurring in gouty people should be treated by iodides, salicylates, atophan or colchicum.
From the academic point of view ocular gout may exist, but from the practical point we should invariably seek, and we shall probably find, some still more important source of infection requiring treatment.
Ocular Symptoms in Hyperuricæmia.—The popular view that gout depends upon uricæmia is so generally accepted that the expressions “uric acid diathesis” and “gouty diathesis” are tantamount to tautology. Nevertheless they are different, the first postulating the supposed cause, the second the inferred result. There is a commingling of cause and effect. Uricæmia is a normal condition of the blood, but in certain diseases—gout, leukæmia, plumbism, pneumonia, etc.—a considerable excess of urates is found. No form of ocular disease is included as an associate of hyperuricæmia unless one or other of the ancillary diseases is also present.
In leukæmia when severe there is an extremely pale fundus, with a yellowish tint; hæmorrhages, when they occur, are often pale; the choroidal vessels also, if they can be seen, are pallid; the veins in the retina are full and tortuous. There may also be yellow foci, and occasionally retinitis with white spots. In a word, the leaking vessels tell of vascular disease.
In lead-poisoning we find paralysis of ocular muscles, amblyopia, contracted fields of vision, papillitis and retro-bulbar neuritis. It is the nervous system upon which the stress principally falls.
In pneumonia we do not expect to find any ocular complications; in spite of the uricæmia, the eyes are scatheless.
It seems unlikely that hyperuricæmia can produce such widely different signs in the eyes. Rather, on the other hand, the ocular symptoms conform to the type we should expect to find associated with leukæmic blood in the first and with lead-poisoned nerves in the second.
In this congeries of ocular symptoms, marked by hyperuricæmia, we do not find iritis included, and yet this is a commonly accepted gouty affection of the eye.
False Gout.—It often happens that patients tell us that they are gouty although they do not claim to suffer from attacks in the old-fashioned way. With them there is a wide difference between the substantive “gout” and the adjective “gouty,” the latter apparently implying an attenuated form of the former. Such patients are seen at health resorts and are very frequently those in whom obesity and plethora are present to a marked extent. The full-blooded appearance involves the head, body and limbs, but the eyelids, for some unexplained reason, may escape. The patients have lived not wisely, but too well. On examination an increased quantity of uric acid in the urine is found, and is supposed to justify the diagnosis of gout. Sometimes the malassimilation, is associated with arterio-sclerosis, with diabetes, or with albuminuria. But the patient is almost invariably convinced that he has gout, that it is hereditary, that it has been handed down to him through a long line of ancestry from primeval days, and that an ascetic life would not have prevented it in his case.
Should such a one be attacked by iritis, the circularity of the argument is complete: he has iritis, therefore he is gouty; he is gouty, therefore he has iritis. But usually in the early days of this so-called gout we see no ocular changes; the time for organic disease (inflammatory and hæmorrhagic) has not yet arrived; auto-intoxication has not yet begun. But sooner or later with the maturation of disease come ocular degenerative signs, retinal hæmorrhages, and so on. The sequence is malassimilation, “goutiness,” sub-infection, ocular disease. Thus in diabetes melitus (omitting toxic and traumatic forms) we find pancreatic disease, nutritional changes, and not usually until late retinitis, cataract, iritis, etc. In renal disease retinitis is also late and often ushers in the final scene.
If in these cases of so-called gout we implicitly accept the patient’s nomenclature of disease, we shall find plenty of gouty iritis, but we may overlook the fundamental condition of his arteries, of his kidneys, and of other organs.
The sins of repletion in such patients may be relieved by the virtue of abstinence, not by colchicum.
Retinal Hæmorrhage.—That retinal hæmorrhage may be caused by gout was firmly maintained by Jonathan Hutchinson.[57] This opinion was shared by Gowers, who states that the “influence seems well-established.”[58]
Hutchinson pointed out that in cases of retinal hæmorrhage of renal origin, stellate white deposits occurred, whereas in gouty cases they were absent. By this criterion he classified his cases. In his first patient Hutchinson relates that he can only state from memory that there was no albumen, but that “he seemed in good health and that there was reason to suspect gout, although he had not had a definite attack.” In his second case, a woman who had suffered from rheumatic gout and true gout, there were numerous hyaline casts in the urine, but no albumen. In both cases the hæmorrhages were flame-shaped, and Hutchinson lays stress on the shape in gouty retinitis hæmorrhagica. The group consisted of fifteen patients, eleven men and four women. “Gout had been positively present in six, and was strongly probable in four or five others. In one the gout was complicated, and probably in part produced, by lead poisoning, and this is the only instance in which the urine contained much albumen. In another in which no history of gout was obtained, the patient, a man æt. 67, had diabetes, which was the probable cause of the retinitis.... In about a third of the cases albumen was found in the urine, but it was usually a mere trace and only present occasionally.... In four, including the case of diabetes, white deposits characteristic of renal retinitis were present in small quantity, and in all these albumen was found in the urine.”
Hutchinson sums up his cases with the catholic observation that retinitis hæmorrhagica is a malady the boundaries of which are very indefinite. And when we bear in mind the changes of modern medical opinion with regard to the influence of arterio-sclerosis on the retinal circulation and the effects of vascular hypertension the etiological difficulties regarding retinal hæmorrhages are hardly less illimitable than they were when Hutchinson penned his valuable contribution. In all his cases (as in those which we see now forty-two years later) there are many factors which may have been responsible for the hæmorrhages apart from gout.
In renal disease gout is widely recognised as a possible precursor. So we are again in the same quandary that we experience in considering the relationship of gout to iritis. Are the retinal hæmorrhages due to gout or to the resulting renal disease? The claim of gout to be the deus ex machina once more seems to be superfluous, for retinal hæmorrhages are an end result which may be reached by a variety of pathological routes. Gout may be one, but if so it acts viâ interstitial nephritis. In other words, hæmorrhagic retinitis is the apanage of nephritis and the appendix of gout.
It is impossible to affirm that a retinitis is gouty, for there are no distinctive features, but it occurs in gout when vascular disease has supervened, not gouty retinitis, therefore, but retinitis in the gouty. This is all that can be affirmed when we find albumen in the urine and tophi in the ears, eyelids, etc. Moreover, it is wiser in the interest of the patient to take this broad view. There may be a link between the kidney and the diathesis, but it is invisible.
Neither are we absolved from searching for some other cause of renal disease. The case may be fundamentally one of arterio-sclerosis with a secondarily induced sclerotic kidney, or, on the other hand, the hæmorrhages may be symptomatic of pernicious anæmia and due to toxins. With regard to prognosis it is helpful to remember that retinal hæmorrhages, especially when they are isolated, suggest the possibility of death ensuing suddenly from cerebral hæmorrhage; but albuminuric retinitis is itself frequently a terminal stage of chronic renal disease. We have not sufficient proof to call retinitis gouty, and we should adhere to the more catholic appellation “nephritic retinitis.”
James Taylor, writing on neuro-retinitis in the gouty,[59] states that—
“Commonly, of course, it occurs in association with albuminuria, yet it is met with apart from this even in cases where no very obvious cardio-vascular changes can be demonstrated in other regions. And thromboses in retinal veins, apart from cardiac hypertrophy and demonstrable changes in the arteries or in the blood pressure, are of frequent occurrence. In such cases gout is possibly—in many cases demonstrably—a very important factor in the etiology.”
The opinion that cases of neuro-retinitis may be gouty is based upon (a) the fact of the apparent absence of cardio-vascular disease elsewhere, (b) the lack of any other ostensible cause. Doubtless many cases of retinal hæmorrhage are seen for which we are unable to assign a cause; in some of these there is no suggestion of gout and nothing to support a postulation of a latent form of that diathesis. Taylor’s statement that gout in many cases is demonstrably a very important factor in the etiology cannot be lightly set aside, but as the appearances of neuro-retinitis are similar whether gout is present or absent, it is legitimate to question if the diathesis is really necessary.
Glaucoma.—Brudenell Carter, Hutchinson and Nettleship have claimed that gouty people are more apt than others to suffer from glaucoma, but no convincing argument has been brought forward in proof of any definite nexus.
The conclusion I would arrive at is that it is unwarrantable to speak of “gouty” ocular disease, for there is nothing in the character of the inflammation specific of gout. We renounce the prefix in order—
(1) That we may not be lulled into false etiological security, and
(2) That we may approach the elucidation of the case and the treatment thereof free from preconceptions. The mouth and its accessory cavities are the primary sphere of our investigation. This is no mean task, including as it does the radiography of the teeth, even though these are apparently healthy. In the tortuous route of elimination we look for concealed dental roots, rarefying osteitis, buried tonsils, post-nasal infections, antral disorders.
The view that non-traumatic iritis is only a symptom imposes upon us a wide outlook in our search for a diagnosis. In this no viscus can be overlooked, no organ forgotten. All are members one of another, and the wise physician takes cognisance of their interdependence. The recognition of an inflamed iris is only the first stage in the diagnosis, for iritis is the sequel of a story written elsewhere. It is a question, not an answer.
But we know not what the future has in store, and though, with our present knowledge, I affirm that I can find no evidence that the eye is a locus signi for gout, the day may come when, either from bacteriological or other sources of progress, it may be shown that there is a mystic source of intercommunity. In other words, it may yet happen that the mysterious materies morbi of gout, whether microbic or chemical, may be demonstrated experimentally as capable of inducing, not only the arthritic phenomena, but also those inflammatory lesions in the eyes which provisionally are sometimes called “gouty.”
Lastly, I would enter a plea for more systematic, more scientific, investigation of the true link, if any, between iritis and arthritis. The war has taught us the value of “team-work”; it has taught us that the clinician must be reinforced by the bio-chemist, the bacteriologist and the pathologist. The work and the workers must be co-ordinated in our daily struggle with disease as we meet with it in our individual patients. The realm of medicine, with ever widening borders, is too vast for single control. In the foregoing pages I have said much about iritis, and it is a good example of what I mean. In justice to our patient, we may call for a Wassermann or a complement fixation test; we may require the teeth-roots made visible by an X-ray expert, or, it may be, the passage of a bismuth meal radiographed, hidden tonsils explored by the laryngologist, or the antrum illuminated; the fæces may need bacteriological examination. A gynæcologist may help us regarding a leucorrhœa or a possible ovarian abscess.
With many of our patients, alas! considerations of expense compel us to forego our aspirations.
What is the remedy? Is it not State help, central clinics staffed by highly trained experts engaged in research work? Here the poor could be examined and reports supplied to the attendant doctors free, and less impecunious patients at an inclusive fee. Centres such as these would do much to advance the science of medicine and thereby raise the standard of health and make the sick and ailing healthy citizens of a great empire.
Salus populi suprema lex.
XXVI. TREATMENT OF GOUT
Adaptation is the keynote to progress in therapy—adaptation of our therapeutic measures to the ceaseless advances of pathology. In the history of gout it has ever been so, the changing, oftentimes contradictory, vogues in treatment, always the reflex of equally mutable and conflicting views as to its pathogeny. For who can doubt that the facts of pathology supply the indices of rational as opposed to empirical methods of therapy?
Albeit, much remains to be done before we can claim to fulfil the demands of ideal treatment of gout. For we are still ignorant of its exact etiology, cannot yet boast of our control of the morbid potentialities that constitute the pathological groundwork of the malady. We cannot obliterate the diathesis, and must still deplore with Sydenham that “as for a radical cure, one altogether perfect, and one whereby the patient might be freed from even the disposition to the disease, this lies, like truth, at the bottom of a well; and so deep is it in the innermost recesses of nature that I know not when or by whom it will be brought forward into light of day.”
But although we cannot dissipate the inherent proclivities to the disorder, we can, I think, claim to fulfil the humbler rôle, viz., obviate their coming to fruition. Haply in the fulness of time we may be able to influence the endogenous factors that make for gout, may through the labours of the bio-chemist be able to translate or assess them in terms of functional inefficiency of this or that particular viscus. But meanwhile we must perforce content ourselves with the eradication or control of the exogenous factors of gout—the excitants whereby or through whose agency the malady from being latent becomes manifest and overt.
RADICAL TREATMENT OF LOCAL FOCI OF INFECTION OR TOXIC ABSORPTION
When discussing the etiology of gout we emphasised the probability of the intrusion of an infective element in its genesis. We commented, too, on the extreme frequency with which local infective foci are encountered in gouty subjects and the imperative necessity of their early recognition and radical treatment. In doing so, we but conform to what should be regarded as the salient canon in the treatment of any form of arthritis, viz., a diligent search for a focus of infection. A monarticular arthritis, such as gout in its initial outbreaks almost invariably is, calls for the same painstaking investigation as a polyarticular, for one never knows when the former may merge into the latter. Nor, if we find one focus, should we rest content, assuming that this is the only one of significance. For in many instances there are probably several foci. Thus, how frequently are septic teeth conjoined with tonsillar and aural troubles, and, as modern investigation shows, these, again, may be associated with remote foci in gall bladder, appendix, etc.
To begin with, a thorough examination of the mouth and nasopharynx is essential. During the inspection any artificial dentures must be removed, lest we overlook concealed and septic stumps. “Bridges,” again, are a notable source of sepsis. The roots upon which they are fixed or the related gums may be infected. Phlebitis, as we know, is a common associate of gout, and C. A. Clark, emphasising the septic potentialities of bridges, cites an obstinate case of phlebitis which only cleared up after removal of a filthy device of this nature.
Again, devitalised teeth that have been “crowned” should always be suspect. Infection at the root is common, with abscess formation. Such are not necessarily painful, and may give no indication of their presence until they find an exit of discharge, maybe by a gumboil or viâ the antrum, etc. These abscesses around the apices of non-vital teeth are difficult of diagnosis in their early stages. Even the X-rays may fail to detect them when minute, this owing to the small amount of pus, or because abstraction of the lime salts from the bone has not proceeded to an extent that may be appreciable by skiagraphy. The first indication of their presence is a small area of rarefaction in the bone around the apex of the root.
It is important to recognise that teeth that appear sound upon external examination are not necessarily so. In short, ordinary clinical examination may be quite inadequate. Not only must the condition of the “crowns” of the teeth, but that of their roots also, be ascertained. For when we reflect that, in addition to abscesses, cysts, buried roots, inflamed and impacted molars may be present, we see, if we are to achieve a full and accurate diagnosis, radiographs of the jaws are essential. A single-plate negative is practically of no value. A series of films taken all round the mouth is the only satisfactory procedure. Such give finer detail, and show up the interstices of the teeth—the sites of predilection for periodontal disease or pyorrhœa alveolaris.
Passing to pyorrhœa alveolaris, which has been defined as the twentieth century scourge, it cannot be denied that if all the evils attributed thereto are to be nipped in the bud, then X-ray examination of the teeth must be resorted to at a much earlier stage than it commonly is. Clean as well as unclean mouths fall a prey thereto, and, as a rule, investigation of the teeth is an after-thought, this particularly in the subjects of gouty arthritis. Usually the gout has been in full swing for years. The patient’s dyspeptic symptoms have been dismissed as “gouty,” and “alkaline stomachics,” etc., have been his lot, though his teeth may be in a foul condition—one which would not have been tolerated probably in any form of arthritis other than “gouty.”
But if to diagnose pyorrhœa alveolaris in its early stages we must needs invoke radiography, on the other hand we should be careful not to overlook its presence when advanced. The gums may be pale and shrunken, at other times red and swollen and very prone to bleed. When pockets form round the teeth, pus and blood may be expressed. Probing may not reveal their true depth, whereas X-rays do.
Sometimes only one or two teeth are affected, at other times many, and these not necessarily adjacent to each other. Thus it happens that the disease is more advanced at one part of the mouth than at another. Exacerbations frequently occur—a blessing in disguise. The affected teeth become tender to bite on and loose in their sockets, but often pain lessens, and the tooth again tightens up, and the all-necessary visit to the dentist is again and again postponed. Sometimes abscesses form, which discharge into the peridental pockets. Eventually the teeth may drop out almost painlessly. Herein resides the danger of the condition, its relative painlessness. Hence the ease with which secondary infections may ensue, e.g., in the tonsils, the gastrointestinal tract, etc., while the original source may be altogether overlooked.
The subjects of gout are often middle-aged or old. We should recollect then that chronic periodontitis may in their instance ensue in sequence to senile atrophy of the alveolus. Recently in a patient of mine nearly eighty, a sufferer from gout and sciatica, a persistent pyrexia, of apparently cryptic origin, forthwith ceased after extraction of his teeth. He lived some considerable time afterwards, but I often regret that his septic teeth had not been drawn long before.
Unfortunately no specific germ can as yet be saddled with the responsibility for pyorrhœa alveolaris, though some would convict the endamœba buccalis. Spirillæ and staphylococci form a large proportion of the bacterial flora met with in oral sepsis, but the results of vaccine treatment would seem to indicate that streptococci, diplococci, and staphylococci are the most frequent causes of complications. Still it must not be forgotten that the streptococcus viridans is by some held to be specially related to arthritis. Hartzell (1915) invariably found it in the teeth and peridental tissues in 220 patients suffering from arthritis. This streptococcus hæmolyticus frequently leads to secondary tonsillar sepsis, and, as previously noticed, to subsequent gall bladder infection, etc.
Passing to local treatment, if oral sepsis or pyorrhœa alveolaris exists, carious teeth when present should be extracted, or their cavities cleansed and filled. Accumulations of tartar should be removed, and unhealthy gums attended to. Thus “pockets” should be swabbed, syringed, or subjected to ionisation. Exacerbations frequently follow the extraction of teeth. Acute paroxysms of gout have followed this simple operation. In cases where the extraction of many teeth is called for, it should be preceded by as thorough a cleansing of the mouth as can be assured. It is a matter of common experience that severe exacerbations of arthritis follow neglect of this precaution, owing to the enhanced toxic absorption from the extensive raw surface.
Unquestionably, whether it be a matter of curettage, of “pockets,” alveolar abscesses, or extraction of teeth, it is wiser to proceed gradatim. Hartzell, when many septic foci exist in the gums and teeth, allows three to six days to intervene between “treatments,” this in order to gain full advantage of what may be called surgical auto-inoculation. For, as he contends, any local measures, curettage, etc., necessarily involve inoculation of the subject with a large number of organisms, thus producing an effect similar to that of an efficient vaccine, “with the added advantage that the constant supply is shut off from the focus disturbed.”
Recurring attacks of tonsillitis—well-recognised determinants of gouty outbreaks—demand thorough local treatment. If this fail, the propriety of removing the tonsils will call for consideration. But, as tonsils may be very misleading in appearance, the aid of an expert is often indispensable. Thus the worst types of tonsillar sepsis may exist in the small “buried” tonsil. In such cases the indications for enucleation are the more emphatic when we note the increasing evidence that tonsillar sepsis may be etiologically related to appendicitis or cholecystitis.
Again, as before pointed out, Wynn Wirgman noted that some cases of gout are associated with nasal disorder, and certainly in non-gouty forms of arthritis expert treatment has reacted very beneficially on the joint condition. Watson Williams has recently drawn attention to “latent sinusitis” as a cause of systemic infections. He cites two cases of chronic rheumatoid arthritis which, previously resistant to treatment, were greatly improved by operation on the sphenoidal sinuses. The washings from the sinuses were free from pus, but on culture showed growths, in the one case of streptococcus albus and in the other of streptococcus aureus and streptococcus brevis.
Needless to say, the genito-urinary tract should be carefully investigated, especially in polyarticular gout, or monarticular when located in unusual articular sites, this if only to eliminate the possibility of a latent gonococcal infection. Apart from this, we should recollect that cystitis is common in gouty subjects, and, according to older authors, might occur as a result of “metastasis,” not to mention the cases of so-called “gouty” urethritis, which, it is claimed, not uncommonly supervenes at the end of an articular attack of gout. Nor should we forget the rectum, for hæmorrhoids are not uncommon in these subjects. Years ago Garrod noted that the cessation of a habitual hæmorrhoidal discharge frequently proved the signal for an outbreak of gout. Moreover, there is increasing evidence that rectal ulcerations may be causally related to some forms of arthritis.
When all the foregoing regions have been thoroughly investigated the lower levels of the gastro-intestinal tract must be thoroughly examined by all modern methods. Diminution, absence, or excess of free HCL may call for determination, while X-ray studies may afford us an explanation of dyspeptic symptoms. Lastly, the urine and fæces may call for exhaustive investigation.
In conclusion, however, if there be any local focus of infection so situated as to admit of radical measures, these should be undertaken prior to resorting to vaccine therapy.
But, obviously for the success of vaccine therapy, it is essential that an accurate bacteriological diagnosis of the case under consideration be accomplished, which of course is comparatively easy if we are able to isolate the particular organism by direct cultural experiment. To this end cultures should be made from the roots of extracted teeth, the gums, tonsils, or nasal or other discharges. Albeit, we must never be content to select haphazard any organism that we may isolate from the patient’s mouth, nose, urine, fæces, or elsewhere. Doubtless the true clue will lie in the institution of complement fixation tests for the organisms responsible for local infections. Research to this end is now in course of progress at the Royal Mineral Water Hospital, Bath, for it is becoming increasingly clear that nothing short of “team-” work will suffice for the full elucidation of the “gouty” and the non-gouty arthritides.
DIET
Truly in respect of diet the gouty have “suffered much of many physicians,” have been the butt, so to speak, of all the fads and frailties of medical opinion. Should that chemical outcast “uric acid” but appear in excess in the urine, it was, and still is for many, an infallible index, not only of gout, but of gout maintained and nurtured by improper feeding. The inference seemed obvious: the ideal diet for the gouty was a diet free from any uric acid-forming material. This achieved, the gouty “will be free from his leprosy, and henceforward, if he abide by the prescribed regime, all will be well with him.” But, as Sir James Goodhart, from whom we take this last passage, pertinently asks, “is this so?” The answer is, I fear, in the negative. For who has not met with gouty veterans who, having run the gamut of endless dietetic experiments, still remain “gouty,” though, mirabile dictu, still avid for fresh ventures?
For myself, I know of no stereotyped diet for the “gouty,” for in this respect every man is a law unto himself. “Get the acid out of your system,” is the watchword of many, and, I fear, often to the undoing of their victims. Bent on the annihilation of the disease, they overlook the individual. But, weary of futile chasing of uric acid out of the economy, most students of gout now agree that the aim of all dietetic measures should be to secure, as far as possible, gastro-intestinal asepsis. For, as experimental studies have shown, it is possible, by means of a judiciously selected and varied diet, to modify the character and even to inhibit the growth of the intestinal flora. The far-reaching nature of such an influence is clear when we reflect that all abnormal fermentative and putrefactive processes in the alimentary canal appear to be referable to the action of microbial agents.
Diet in Acute Paroxysms.—The initial outbreak of gout may occur at any age, and respect must be had to this as well as to other individual peculiarities. If the subject be young, say in the forties, and a free liver, he may at the onset experience distaste for food, if not actual nausea. If so, let him follow his bent, and confine himself to hot water, barley-water, or hot weak tea. Such a modified process of starvation is beneficial rather than harmful. Drinking freely of bland diluents promotes the elimination of toxic or waste materials, while the intake of hot water stimulates the hepatic cells and promotes the excretion of bile.
Milk, easy of digestion and rapid absorption by a febrile patient, is the ideal form of nourishment. Moreover, a milk diet constitutes the most effectual means of attaining a comparative degree of intestinal asepsis. From two and a half to three pints may be taken in the twenty-four hours. While some will find no difficulty in assimilating it, others soon experience nausea, vomiting, and even diarrhœa, from the passage of undigested curds. It is therefore advisable to begin with small amounts given at regular intervals. If ill digested, it may be diluted with some alkaline water, or three to five grains of citrate of soda added to each tumblerful.
To obviate monotony the intake may be varied by oatmeal or barley gruel, veal, mutton, chicken, or vegetable broth, but strong soups and animal extracts must be avoided. There is no objection, however, to bread and milk, tapioca, semolina, or sago puddings.
With the disappearance of fever and the decline of acute symptoms fish may be introduced into the dietary, with later on a little white meat or chicken. This may be safely done when local pain and tenderness decline, and alike the tension of the parts, as shown by pitting. Moreover, at this stage the appetite usually asserts itself. Still the return to regular diet must be made slowly and cautiously, if we wish to combat the very common tendency in these patients to functional gastro-intestinal and hepatic derangements. Lastly, in acute sthenic gout occurring in a robust subject there is no need whatever for alcohol in the febrile stage. Also, it may be added, the younger and the stronger the patient, the better will he thrive on a pure milk or a lacto-farinaceous diet, and the less urgent the necessity for relinquishing the same until all fear of a relapse has passed.
On the other hand, in acute asthenic gout in an elderly and perhaps somewhat debilitated subject one must more than ever have regard to the individual, especially if he be an old time sufferer, perhaps with multiple joint involvement. Such a man “has not so much the gout as the gout has him.” He has to be helped to support his burden. In short, the diet for the young and plethoric differs from that suitable for the old and asthenic.
Restriction of such to a milk diet is sometimes positively harmful. The mischief is, that, once begun, every attempt at a more varied diet immediately provokes a relapse.[60] As Sir Thomas Watson wisely observed: “They must be allowed a certain quantity of their accustomed good cheer, or they become an easier prey to the disease. In such cases you must ‘trim’ as well as you can between opposite dangers, between the Scylla of excess and the Charybdis of debility.” In short, you must maintain their vigour and their strength. For this a pure milk diet will not suffice. In addition thereto, pounded or minced chicken, a little fish, sole or whiting, may be given. When also, as often happens, they have been wont to take alcohol, two ounces of mature brandy or whisky, well diluted with Salutaris or other mineral water, may be allowed them every twenty-four hours.
Indeed, if the subject be old and broken down, it may be necessary to increase the amount of stimulant. In such cases to go on treating the disease, heedless of long-established habits, is bad policy. Wholly to withhold alcohol may well precipitate disaster. Homilies on abstinence or temperance are best postponed pending convalescence.
Moreover, these cases of acute gouty polyarthritis, whether in the middle-aged or old, very commonly run an afebrile course. If then, as not infrequently happens in these distressing cases, the patient’s progress is slow and unsatisfactory, there need be no hesitation in renouncing a strictly lacto-farinaceous regimen in favour of a more mixed diet: clear vegetable soups, well-made Julienne, mutton, veal, and chicken broths, lightly boiled fish of the digestible kinds, pounded and minced chicken, etc.
Even when in these cases pyrexia is present, it is rarely continuous, but is diversified by afebrile intervals. If then, while the paroxysm is in full flare, it be deemed advantageous to adopt a milk diet, it is all the more important that in the inter-paroxysmal stages we take full advantage of these periods of enhanced digestive capacity.
Diet in Chronic Gout.—Sydney Smith, writing to the Countess of Carlisle in his seventy-first year, humorously apostrophises his gout: “What a very singular disease it is! It seems as if the stomach fell down into the feet. The smallest deviation from right diet is immediately punished by limping and lameness, and the innocent ankle and blameless instep are tortured for the vices of the nobler organs.”
Precisely so, but what constitutes the “right” diet? We are told that this is good and that is bad for gout. Some would have us eschew red meat and cleave unto white; for others common salt is the devil that must be cast out. Some speak ill of all the fruits of the earth. Strawberries especially, they say, are the bane of gout, yet in these same Linnæus found salvation. For many, again, sugar is anathema, tea and coffee but uric acid solutions, and alcohol in all forms rank poison!
What a trial the gouty subject who, obsessed by his “acidity,” has passed through the furnace of many spas! “Everything I eat turns to acid” is his plaint. He has been all things by turns—a fruitarian, a vegetarian, no meat or all meat, etc. Such persons, in truth, are “uric acid” maniacs. But—forget it not—they are of our making, and often in their multitude of counsellors have found, not wisdom, but starvation! Well would it be if the evil done ceased with themselves, but unfortunately they seek converts to whatever cult they affect.
The Fallacy of Fixed Dietaries.—As Bacon in his “Regimen of Health” (1597) wisely observes: “Some physicians are so regular in proceeding according to art for the disease as they respect not sufficiently the condition of the patient.” The wisdom of this has, I fear, been overlooked by those who hold that the ideal diet for the “gouty” is one destitute of the precursors of uric acid. Its acceptance makes not for flexibility in dieting, but rigid, undiscriminating routine.
Apart from the violation of principle, the direct result is, that the victim runs amok among the carbohydrates, with as a frequent penalty an acute outbreak, this although uric acid is not a direct product of carbohydrate metabolism; nor, as far as is known, does the carbohydrate intake influence the rate of formation of uric acid. Thus do theory and practice come into conflict, and, as usual, the patient pays. How pernicious this obsession that uric acid is a morbid agent! Uric acid is not an etiological entity, and, as Walker Hall rightly observes, “it is high time that every practitioner made a point of fully educating the public in this respect.”
Any attempt to formulate a set dietary proves but a snare and a delusion. No regime is applicable to the “gouty” as a class, nor even to the individual “gouty” subject at all periods of his life history. His disease persists for an indefinite period, and, like most chronic maladies, undergoes variations. Pari passu his digestive capacity rises and wanes. The regime therefore must be adapted and readapted to his varying necessities. For it is the patient, and not the “gout,” dictates the diet. But only too commonly the disease is dieted, the victim ignored—hinc illæ lachrymæ!
Our dietetic ventures must obviously rest on a sounder basis. This we do know, viz., that functional disturbances of digestion generally precede a “gouty” paroxysm, and that their amelioration is followed by relief of symptoms. The aim of our dietetic measures then is the prevention of digestive disturbances, not the routine withdrawal or reduction of uric acid precursors.
The dietetic treatment of the “gouty” is that of the “dyspeptic,” with, if anything, an added discrimination, for an unknown factor intrudes—the “gouty diathesis”—which has also to be reckoned with, but of this later. Now “dyspeptics” cannot be dieted by rule of thumb. Whether they be “gouty” or “non-gouty” matters not. A careful study of the phenomena of digestion, if not essential in every case, is certainly called for in the more obstinate and obscure forms. In short, an attempt should be made to determine the special form of “indigestion.” Is the derangement of function a disorder of motility or secretion? Is it catarrhal or nervous in origin?
That such is the proper mode of procedure is undeniable. For are we not too prone to assume that the “dyspepsias” of the “gouty” are sui generis, all due to one cause, the materies morbi of gout, instead of being merely “excitants” of gout and due to a variety of digestive functional disabilities, and these of equally diverse origin?
Thorough Physical Examination a Necessary Prelude to Dieting.—When we recall that the “dyspepsias” of the “gouty” endure through long years, the suggestion that every effort should be made to localise and establish the exact nature of the underlying derangement seems almost superfluous. Yet how often is the question dealt with offhand, though, ideally speaking, I cannot help thinking that the primary outbreak of gout should be the signal for an exhaustive examination by all modern methods. The consequences of dyspepsia in the “non-gouty” are bad enough, but infinitely more so in the “gouty” subject. But it is the former group, not the latter, that has been the favoured object of study by experts, which is, I think, somewhat unfair.
There is need of a searching investigation, a more common invoking of the tests whereby the functional efficiency of the stomach may be gauged. We know that there may exist on the one hand hyperchlorhydria and on the other hypochlorhydria. But we need to know more as to disturbances in gastric motility, delay or hurry in digestion, not to mention abnormalities in shape, position, size, tone, pyloric end rhythm, etc. In view of the almost general admission that gastro-intestinal derangements are causally related to outbreaks of gouty arthritis, surely our remissness in this matter is somewhat surprising, the more so in light of the heroic procedures, viz., ileocolostomy and colectomy, advocated in rheumatoid arthritis, a condition by many deemed related to gout.
Leaving such aside, none will, I think, deny not only the value of test meals for free HCL variations and experimentation with all kinds of foodstuffs, but also of X-ray examination of the alimentary tract. How subversive of all preconceptions the revelations of radiography in gastric and intestinal conditions, of what infinite value in disentangling the ambiguous significance of purely subjective sensations! Thus, alterations in gastric tone, motility, and peristalsis may hark back to remote lesions in gall bladder or appendix, and these also account for variations in free HCL.
“Great eaters,” said Sydenham, “are liable to gout, and of these the costive more especially”—an observation the truth of which all will confirm. It may be taken as a maxim that nothing for the gouty is more prejudicial than constipation. Here it is obviously of importance that we know the site of delay, whether in the lower coils of the ileum, the colon, or merely the rectum, i.e., dyschezia. How else obtain this information, save through X-ray examination?
Any departure from normal in consistency, colour or content of the fæces should be noted so as to identify hepatic or pancreatic derangements. An analysis of the urine should always be undertaken, its reaction noted, the presence of albumen or casts ascertained. It is important, too, that we do not overlook glycosuria or oxaluria, or substances indicative of excessive intestinal putrefaction. All these bear far more pertinently on diet than estimates of uric acid.
The behaviour of the skin, whether inactive or not, must also be taken into consideration. Moreover, as the subjects of gout are usually middle-aged or old, it is highly important to note the general drift of metabolism, whether in the direction of obesity or undue leanness. Herewith we must take an inventory, as it were, of the subject’s general mode of living. What are his habits in respect of food and drink? Is his diet excessive or improper in quality? Are his meals taken at irregular times? Does he masticate his food properly?
In the matter of exercise, his occupation or pursuits require thought. Do they involve excessive exertion or favour a sedentary habit? For both these factors bear narrowly on his power or not of disposing of ingested material. Indeed, all the foregoing reflections stand in close relationship to the complex processes of digestion and metabolism, and the efficacy of our prescribed regime will depend on how far our suggested innovations meet the particular needs of the subject under review.
Need for Collaboration of Clinician and Bio-chemist.—Before we shall be able to lay down a diet for the “gouty” on truly scientific grounds much remains to be done. Our clinical examinations, in no way to be despised, must nevertheless be supplemented by the more subtle tests of the bio-chemist. Consider the complexity of the problem. We have to diet not only the “gouty,” but the “potentially” gouty.
They shade the one into the other. Even the man who has had gout has his periods of respite, of apparent unblemished health. If seen at such a juncture, he may display the relics of his gouty attacks, i.e., tophi. But can we say of him that he actually now has gout? He has crossed the Rubicon, disclosed his morbid trend, but meanwhile he has apparently recrossed to the vantage ground of normal metabolism. He stands again with those who are about to, but have not yet developed the disorder, i.e., the “potentially” gouty.
Who will deny that it is when a man is, so to speak, gravid with, but not yet delivered of, gout that dietetic measures will avail him most? But this, alas! carries with it as its postulate the diagnosis of latent gout. Now, Walker Hall suggests that “the nuclein metabolism of the gouty patient is run at high pressure or full capacity, instead of the usual normal quarter or at half-pressure capacity, in order to cope with the ordinary processes of assimilation, and that there is very little reserve energy.” Does not this seem to indicate that a fruitful sphere of research might be the invoking of “endurance” tests and other methods of determining the functional capacity or efficiency of the various viscera?
At present we content ourselves with blaming the stomach, the liver, the kidneys, etc., and often on very inadequate grounds. It would be a great step forward if we could determine betimes which particular viscus is functionally deficient. There are signs that this boon will not be long withheld, signs that not only can the functional efficiency of the stomach be tested, but also of the liver, kidneys, and even the spleen.
Thus Labbe and Daughin study the colloidal nitrogen in the urine, and find the ratio to the total nitrogen much augmented when the functional efficiency of the liver is depressed. Again, Bauer and Spiegel use the bilirubin content of the blood to the same end. They maintain that there is a bilirubin threshold, the assessment of which denotes the functional capacity of the liver. In health the blood content thereof is surprisingly uniform. But in passive congestion of the liver it rises very markedly, and the same after administration of cholagogues.
In like fashion the value of blood urea concentration is extolled by Kast and Wardell as a satisfactory index of the functional power of the kidney. The uric acid content of the blood is by Baumann, Hansmann, Davis, and Stevens regarded as a very delicate index of renal function, though unreliable in the presence of œdema, cardiac decompensation, or when the urine is highly concentrated in hot weather. These are but a few of the methods available, and in the same way Frey has devised tests for the functional efficiency of the spleen, while Barton invokes the administration of urea, chlorides, adrenalin, creatine, etc., to assess the functional capacity of the liver, kidney or spleen.
Such is the trend of modern medicine—to link up clinical with laboratory findings—and in gout perhaps more than in any other disease is this collaboration urgently called for. For who can doubt that gout is a malady of mixed intrinsic (endogenetic) and extrinsic (ectogenetic) origin?
We need to know more about the endogenous factor, the basal perversion of cell structure or function, that differentiates the tissues of the “gouty” from those of their fellows. For it is these inherent peculiarities—structural, physical, or chemical—that give to the disease its sui generis character. How then in the “living” subject shall these hidden morbid potentialities be identified? How save through the medium of function, the outward expression of metabolic activities, in other words by appraisement of the functional capacity of the various viscera? For gout primarily is a disorder of function, or, as Rendu phrased it, a primordial “vice of nutrition.” Hence our insistence on the invoking of the various laboratory methods for elucidating the functional powers, the efficiency or not of the liver, kidneys, etc.
This satisfactorily achieved, we may, through their reflected functional disability or disabilities, divine somewhat the nature of the innate tissue peculiarities of the “gouty,” may hope at long last to translate the misty “gouty diathesis” in terms of functional deficiency, deficiency of the working capacities of the stomach, liver, or kidneys, and perhaps find that the basal flaw in some lies in the liver, in others in the kidney, and thus the older clinicians be justified of their claims for “hepatic” or “renal” varieties of gout.
That exogenous factors, i.e., infections, bring to fruition these latent morbid tissue potentialities of the gouty, is my belief. Hence my contention that dietaries for the “gouty” should be such as promote gastro-intestinal asepsis. Albeit, infections are but the “seeds,” and who can doubt that the ideal diet for the “gouty” should also take cognisance of the “soil”—the pathological groundwork of gout?
The “soil” in gout is, I believe, one peculiarly favourable to microbic invasion, and here again recent studies of the cytology of the blood bid fair to yield us some criterion whereby the “degree of body resistance” to infections may be gauged.
But until the bio-chemist reveals to us the why and the wherefore of their peculiar tissue vulnerability our dieting of the “gouty” must perforce consist largely in diminishing the exogenous excitants of the malady. Ultimately, when researches now in progress have fructified, we may be able to influence the endogenous factors, may correct the functional defect of this or that viscus, stabilise the nuclein exchanges, and heighten the resistance of the tissues. In short, as Sir Archibald Garrod puts it, “we must consider the soil as well as the seed which falls upon it, and that he is the best exponent of the healing art who treats the individual patient rather than his disease.”
“The Accessory Food Factors.”—“Due nourishment, not gluttonous delight,” is the true clue to the rational dietetic treatment of the “gouty.” But this question of “due nourishment,” how complex it grows in light of recent revelations. Thus, it is now generally agreed that to satisfy the animal needs for growth and the maintenance of nutrition something more than a due admixture of proteins, fats, carbohydrates, and inorganic salts is essential.
We must, of course, ensure that the caloric value of the food intake be adequate, and the supply of protein sufficient to maintain the nitrogen balance, also that the intake of protein suffice for the exigencies of tissue waste, not forgetting that for this is required a sufficient quota of the individual primary fractions of the protein molecule.
But this, we now know, is not all, for there are other and indispensable dietetic components. In the food we eat are substances of hitherto unguessed-at potency—the “vitamines,” or, as they are now more properly termed, “accessory factors of diet.”
Of these elusive bodies but three as yet have been isolated: fat-soluble A, water-soluble B, and water-soluble C. In infancy absence of the first-named “vitamine” leads to rickets. Lack of the second engenders scurvy, of the third beri-beri.
But, apart from these well-defined “deficiency diseases,” McCarrison has pointed out that the absence of these “accessory food factors” leads to grave functional derangements, especially of the organs of digestion and assimilation and those subserving endocrine functions, not to mention malnutrition of the nervous system and the induction of hyperadrenalinæmia and chronic inanition.
A heavy indictment, but, more pertinently to our subject, McCarrison inclines to think that bilious vomiting, cyclical acidosis, mucous disease, and other metabolic disorders met with in children are very probably due to deficiency of certain “accessory food factors.” In light of this it is interesting to recall that these same symptom complexes are by Comby and others regarded as manifestations of infantile gout.
More arresting still is McCarrison’s observation that all the clinical phenomena distinctive of “deficiency diseases” as a whole are apparently the result of nuclear starvation of all tissue cells. In short, these “accessory food factors” are essential to due nutrition of the nuclear substance. How interesting this in light of the generally accepted view that “gouty” individuals are victimised by some inherent defect or alteration of nuclein metabolism. Does not this seem to indicate that one of the clues to successful dieting of the “gouty” must be adaptation of the nuclein intake to the needs of the individual, in short that we must strive for the stable maintenance or conservation of nuclein metabolism?
Again, as before stated, one of the results attaching to deficiency of “vitamines” is functional derangement of the organs of digestion and assimilation. Such disturbances are prominent in gout, and that “errors of diet” play an important rôle in the genesis of the disorder can scarcely be denied. At the same time there is no proof as yet that the absence of some mysterious “accessory factor” makes for the development of the disorder.
Nevertheless reflection on these findings is, I think, wholly apposite. It should, at any rate, chasten those who affect extreme dietaries on insufficient grounds. They are not justified of results, for, with Sir Archibald Garrod, I venture to doubt “whether by dieting our ‘gouty’ patients we achieve nearly as much as we think we do.”
Such good, moreover, as we do compass, is, I think, exerted indirectly. Even in the inter-paroxysmal periods of the disorder, despite good or perhaps exuberant health, gout is there. Its morbid tissue potentialities are latent, though functionally inactive. To maintain this state of passivity is the aim of all dietetic measures, viz., to diminish or withdraw the dietetic factors that are provocative of gout.
The diet most void of offence is one the least calculated to excite digestive disturbance—one that makes more surely for gastro-intestinal asepsis. At this juncture it is interesting to note McCarrison’s observation that although the absence of certain “accessory food factors” is the essential etiological agent in the genesis of “deficiency diseases,” yet he holds that infections and parasitic agencies are often important causes in determining the onset of symptoms.
Similarly in the causation of gout, “errors of diet” are not the only agencies at work. They are in truth but contributory factors in that such indiscretions favour the incidence of catarrhal states. These again promote increased toxicity of the intestinal flora with sequential disturbance of general nuclein metabolism and associated specific local reactions in certain tissues.
I make no apology for this somewhat lengthy digression. In the sphere of dietetics, as elsewhere, “a little knowledge is a dangerous thing.” We need to walk more circumspectly in this matter of dieting; and to this end reflection on the disabilities that still beset us cannot fail to be salutary, and will form, I think, a fitting prelude to our suggested mode of procedure.
XXVII. TREATMENT OF GOUT (continued)
REGULATION OF DIET IN THE GOUTY
The victim of gout is easier led than driven. Show no “bowels of compassion” for his failings, talk to him in the spirit of a dehumanised disciplinarian, and your tenure of his confidence will likely be short. You deal with a man more often wise than foolish, not merely a digestive tube.
The physician must be authoritative and yet tactful. Thus if the victim be a hearty eater, and you think he eats too much, try and get him to eat less. But do not bid him straightway live as an anchorite. Be a little more diplomatic. A good appetite is not a sin. An appetite over-stimulated by condiments or endless varieties of courses is. He should eat to satisfy his hunger, not to gratify his palate.
Do not irritate the patient with a strict dietary if avoidable. Far more often than not it is the quantity, not the quality, of the food that is at fault. Frequently mere reduction in bulk of the pabulum of all kinds taken will suffice. In short, restriction, not elimination, is the wiser maxim, especially so in indolent or sedentary persons in whom we may with advantage limit the food intake to the minimum consistent with the due maintenance of nutrition.
On the other hand, there is a widely prevalent idea among “gouty” subjects that if they take enough exercise they can eat and drink what they please and as much as they please. That active habits do counteract to some extent the evil effects of overeating and overdrinking is certainly true. Nevertheless, as Sir Thomas Watson reminds us, gout was extremely common in the old time squire, who not only “rode hard,” but “lived hard” also. It is so, though to a less extent, even to-day, and often such subjects prove very refractory. Often a reference to their “weight” will appeal more than any hygienic considerations. Make use, therefore, of their sensitiveness on this point, and so by diplomacy attain your end.
Overeating often goes with overdrinking at meals. I well recall a gouty old sportsman of bucolic type who was accustomed to swill his food down with several whiskies and sodas. Very conservative in all ways, it was not easy to break him of the habit. Fortunately it occurred to me to ask him, “Did you ever see a horse eat and drink at the same time?” Reflecting solemnly, with obvious reluctance came the reply, “Damme, I never did, now that I come to think of it.” That settled the question. I had no more trouble, neither had he. Not often is one so lucky. But “Eat your meals dry” is not a bad rule in cases of sheer overeating. The appetite is sooner blunted.
As to the quality of the food, always recollect that “gouty” people are very prone to idiosyncrasies; but the idiosyncrasy is purely personal, not applicable to the “gouty” as a class. With them it is very much a case of “What’s one man’s meat is another man’s poison.” The physician who rides rough-shod over idiosyncrasies in the matter of foods rides for a fall. Let him rely on his own experience and knowledge in the matter of general dietetic principles; but when it comes to details—the eschewing or not of this or that—let him trust, not in his own, but in his patient’s, experience.
Many of these subjects know perfectly well what suits them and what does not. Their experience is your best guide. Having elicited this information, an appeal to their common sense rarely fails. Of the “gouty” it is especially true that “every man at forty is either a fool or his own physician.” For the fool there is but one corrective—dolor acerrimum naturæ pharmacum. The wise has only to be reminded of his own experience, viz., that certain articles of diet infallibly disagree with him—verbum sapienti satis.
In dieting the “gouty” we should never forget that the main groups of foodstuffs must be duly represented. We may reduce this or that, but never for long will they do well if one or other of the essential ingredients of human food be wholly eliminated. It is, as Sir Archibald Garrod remarks, doubtful whether even a minor constituent, such as the purins, can be continuously withheld with impunity.
Still, even from the more extreme dietaries advocated by some one may glean this useful lesson, that the temporary benefit that often accrues points the moral that simplicity of meals is best for these subjects. If they crowd soup, fish, meat, game, sweets, etc., all into one meal, they always pay the penalty. As Burney Yeo wisely says: “We should not mix up albuminates, fats, and carbohydrates, or flesh, vegetables, fat, and fruit in the same meal. One meal should be composed almost exclusively of nitrogenous food, another of fats and carbohydrates, and another of fruit, at proper intervals, and they will all agree and be suitable, but the contrary will be the case if they are mixed together in the same meal, one hindering the digestion of the other.”
I have often found the old rule, “One meal of meat, one meal of fish, and one of neither,” an excellent way of impressing on these patients the importance in their instance of simple, as opposed to elaborate, meals. Arrangement of their daily bill of fare along these or similar lines is well worth the trouble.
If the food of the “gouty” needs to be carefully selected, it is no less necessary that the cooking be simple and appropriate. For the manner of the cooking is, I am sure, in many instances, more responsible for “gouty” outbreaks than the nature or the quantity of protein or other intake. Twice-cooked food, made-up dishes rich in extractives, are unquestionably pernicious. Nor are pickled or salted meats desirable. Similarly, strong meat consommés, hare soup, and beef extracts are best avoided. The same applies to rich gravies, sauces, spices, etc., all obviously likely to upset the digestion. Again, as to fish, it is better boiled or grilled than fried, and still better not fried in fat. In short, it is the “trimmings” more often than not that do the mischief, these strongly abetted by “second helpings.”
The physician may well insist upon a sufficient interval elapsing between meals. To attain due space between lunch and dinner, I invariably forbid “gouty” subjects to eat anything with their tea. The repasts should be taken in a leisurely fashion, if possible in a cheerful atmosphere. “Unquiet meals make ill digestions.” The nerve element in these cases is so pronounced that caution is anything but superfluous, viewing the inhibitory effects of worry and mental excitement on the secretory mechanisms of the alimentary tract.
The importance, too, of thorough mastication and regularity in meal-times should be impressed upon them. The desirability, too, of postponing the drinking of fluids to the end of the meal, and then only in small amounts, should be emphasised.
Strenuous exercise, mental or bodily, immediately after a meal is undesirable, and if, as is so often the case, there be any gastric disorder, the subject should rest both before and after meals. This is best taken lying down, especially if there be any tendency to gastric dilatation or visceroptosis. The same in hyperacidity, but in this latter sleep is contra-indicated. For it has been shown experimentally that the acidity of the stomach content is greater during rest than movement. But this is just one of those points on which authorities differ, and decision may have to be left to the patient’s own experience.
Lastly, we should always endeavour to ascertain as nearly as possible the actual amount of the food intake per diem. This then must be weighed in light of the subject’s age, body weight, and mode of life. The middle-aged “gouty” person tends more often than not to obesity, and it will fall to the physician to decide whether the food intake be excessive or his habits too sedentary. Far more often than not it will be found that it is not that he walks too little, but that he eats too much. The appetite of youth goes ill with the inactivity of middle age. With these general considerations we will now pass to a discussion of the main elements of diet.
THE INDIVIDUAL FOODSTUFFS
Proteins.—Ruthless cutting off of protein foods, though not so usual as of yore, is still far too commonly practised. The number of unfortunate wretches who are docked of their red meats is still astonishing. The “uric acid” bugbear dies hard. Unless red meat is known to disagree, I never advise a “gouty” subject to abstain wholly therefrom. I feel sure that it is rarely, if ever, called for, and when enjoined has frequently wrought much harm. As far as I know, there is no scientific reason for the very prevalent idea that for the “gouty” white meat is preferable to red. It is certain that both contain an equal quantity of extractives, and equally certain that for some, mirabile dictu, white meat, e.g., rabbit, is more indigestible than red.
Accordingly let your “gouty” patient eat animal food, at any rate at one meal, but let it be of one sort only. Let his appetite be his only sauce, his meat plainly cooked and well masticated. It matters not if it be red or white. What does matter is whether for him it be digestible. Mutton or lamb are more likely to prove so than beef or pork, and chicken, turkey, or fresh game more easily assimilable than duck or goose.
From Walker Hall’s experiments Luff thinks “it would appear reasonable to administer sweetbread to gouty patients, since its nuclein portion is only slightly absorbed, for thymus sweetbread contains principally adenin, which is rapidly excreted, and pancreas sweetbread contains mainly guanin, an amino-purin incapable of increasing the urinary purin output and of exerting any injurious effects upon the tissues.”
Nevertheless I still think that “gouty” subjects are better without thymus, pancreas, and other highly nucleated substances. Despite our ignorance of the true nature of gout, we do know that there is generally an excess of uric acid in the blood, and that to increase the content thereof is undesirable. Again, we know that in normal men, after ingestion of pancreas and thymus gland, the uric acid output in the urine is markedly increased. But, on the other hand, many observers—Magnus-Levy, Vogt, etc.—have noted that after the eating of thymus by gouty individuals they found far less uric acid in the urine than in the case of normal persons. In short, such purin-rich foods in their instance is followed by uric acid retention.
More pointed still is the fact that acute outbreaks of gout have been repeatedly brought on by administering thymus to the subjects of chronic gout. Surely, in light of this, it is impolitic to approve of sweetbreads as desirable ingredients of a “gouty” dietary, this even if only on empirical as opposed to scientific grounds. That some “gouty” persons eat sweetbreads with impunity is undeniable. But certainly if on inquiry a subject overtly gouty admits a penchant for these foods, we should at any rate advise their restriction or elimination.
Fish.—This pre-eminently, with certain exceptions, is very desirable food for the “gouty,” especially those whose digestive powers seem unequal to coping with the stronger kinds of animal food. The white-flesh fishes, i.e., sole, whiting, turbot, brill, cod, plaice, flounder, are the preferable. On the other hand, the red-flesh fish, i.e., salmon, mackerel, herring, sprat, pilchard, eel, etc., contain much fat, and are more likely to upset the “queasy” stomachs of the “gouty.”
But fish, it must be recollected, is less stimulating and satisfying than the flesh of birds and mammals. If wholly denied butcher’s meat and restricted to white fish, the subjects soon tire of it. It is best to prescribe fish for one meal, say lunch, and in addition one type of meat for dinner. Also it is important even in white fish to choose those most easy of digestion, viz., sole, whiting, or flounder, in preference to cod and haddock. Above all, let the fish be fresh, and not “out of season.” Again, fish which is dried, salted, smoked or pickled, is much less digestible than when fresh. If, even when taken in moderation and only occasionally, it has been found to upset digestion, then abstinence is the better course. Caviare is, I think, best abstained from, and hard or soft roes generally only taken in strict moderation.
As to shell-fish, they have the reputation of being most unfriendly to the “gouty.” Toxic symptoms after lobster and crab are held to be more common in their instance than others. But many are, I fear, ready to extend a personal idiosyncrasy on the part of some particular “gouty” subject into a law for all “gouty” subjects. I myself have seen no harm follow them when taken in moderation, this as regards the fleshy parts, more digestible in the lobster than the crab. It is, I think, wise to abstain from the spawn of the female lobster, still more from the sauces for which it is so largely used. As to oysters, I do not think there is any objection to a “gouty” individual eating them raw, and when “in season,” but in moderation.
In conclusion, there is, in the matter of flesh or fish, no rule applicable to all “gouty” persons. Far from being harmful, it is both necessary and beneficial if taken in moderation. No small part of the objections raised to red meat is referable to the other rich foods that often accompany it rather than to the meat itself.
Carbohydrates.—If it be wrong to withdraw recklessly all proteins, it is no less inadvisable, in the absence of special indications, wholly to eliminate sugar or starchy foods. Nevertheless far more often than not “gouty” subjects get the impression that if they wholly eschew sugar all will be well. Latterly, too, I have noticed that the ban is being extended to starchy foods also.
Surely this as a routine procedure is wrong, the more so if, as too often happens, the unhappy subject is left without any guidance as to how long he is to suffer this deprivation. As a temporary measure it is often beneficial. But “gouty” subjects form no exception to the ordinary law that if nutrition is to be maintained, their diet must contain a due proportion of the main groups of foodstuffs. A “due” proportion, not excess, for though quâ uric acid carbohydrates may appear ideally suitable, yet the “gouty” are unfortunately no more immune than others from the dyspeptic disturbances that almost infallibly ensue when sweet foods are taken immoderately.
It is this tendency in some “gouty” subjects to amylaceous dyspepsia that has been wrongly extended into a law for all gouty subjects, whether they exhibit any carbohydrate intolerance or not. The only law is that for the “gouty,” as well as for the non-gouty, carbohydrates, whether taken as starch or sugar, are harmful if eaten to excess.
With this reservation, bread may be given as crisp toast, or rusks, or in the form of Zwiebach. Nor is there any objection to milk puddings—sago, tapioca, etc.—always provided that they are found digestible when taken in moderate quantity. Similarly in regard to sugar there is, as Sir Archibald Garrod says, “no reason to believe that to a gouty man a lump of sugar is poison, and provided that it is digestible it must surely be immaterial whether the allowance of carbohydrates be taken in the form of sugar or starch.”
Fats.—Apart from obesity, there does not seem to be any scientific reason why fats should be denied to the “gouty.” All depends on their digestibility, and in this they display variations. The fat of ducks and geese is well dispensed with in favour of bacon fat and pork fat, which are much more digestible. The fats of meat, when roasted or browned, are best avoided.
Similarly there is no harm in a moderate amount of butter or cream, but fatty sauces and soups are, I think, best refrained from. Ebstein considered the best form of fat for the gouty was good fresh butter. As to cream, Sir James Goodhart, discussing the treatment of uric acid, observes: “In strict moderation it is seldom hurtful, for there is very little in the common objection that it makes one bilious. Those who avoid it are commonly ‘bilious’ because all their organs are starved.” But he makes this further observation for our guidance, that “after middle age cream taken in any excess may associate itself in some with the output of uric acid.”
Vegetables.—The various green vegetables are eminently suitable for the “gout,” not so much on account of their nutritious qualities, but because of the important inorganic salts they supply, notably salts of potash. They give a wholesome variety and relish to food, render the urine more alkaline, and do not favour the deposit of fat. Their indigestible residue, too, stimulates the intestinal coat, and so promotes regular action of the bowels.
Cabbages, greens, savoys, Brussels sprouts, cauliflower and broccoli are familiar examples. These, provided they are fresh and well cooked, are preferable to root vegetables, with the exception of potatoes. Nor must we overlook the fact that green leaves are rich in fat-soluble vitamine. Fortunately, too, in the case of this particular vitamine, the loss involved by ordinary cooking is not serious. Spinach, too, is rich in vitamines, and is laxative, but, being rich in oxalates, is contra-indicated in oxaluria. Sorrel, by reason of its acid oxalates, is also undesirable under such conditions, and the same is true of rhubarb. Tomatoes also in former days were forbidden in gout under the erroneous idea that their content of oxalic acid was high. Cucumbers, I think, when eaten raw, are apt to upset “gouty” people. Asparagus and onions should be taken sparingly, as they are rich in purins.
For “gouty” subjects, of all vegetables, the cruciferous or cabbage tribe is the most suitable, provided they are young, fresh, well cooked, and taken in moderation. In addition to its rich vitamine content, cabbage, like cauliflower and lettuce, is almost purin-free. The excessive intake of meat may often to some extent be counteracted by encouraging such gluttons to eat freely of green vegetables. In this way we obviate that sinking sensation which habitual overeaters suffer on limitation of their pabulum. Lastly, vegetable soups are most suitable, preferably those easily digestible, relatively poor in purins, or rich in potassium salts.
Of the roots and tubers even of potatoes the “gouty,” I think, should eat sparingly. The large percentage of starch in potatoes is apt to upset those of feeble digestion. Much depends on whether they are “mealy” or “floury,” and not “waxy” and “watery.” Steaming is the best method of cooking them. Turnips are best abstained from, and also carrots, parsnips, beetroot and radishes, save at any rate in minimal quantities.
Lastly, the legumes—peas, beans, lentils—because of their high purin content, should always be partaken of sparingly, though perhaps it may yet be found that their purin content may be more than compensated for by their contained vitamines. The edible fungi, mushrooms and truffles are best dispensed with.
Fruits are a valuable food for the “gouty.” They impart alkalinity to the urine, and promote intestinal action, always provided they are not partaken of immoderately or when unripe or overripe, when they are apt to set up gastro-intestinal irritation.
Most fresh ripe fruits are wholesome. Their content, too, of vitamines cannot be overlooked, especially that of oranges. Moreover, the fact that vitamines, as a rule, are destroyed at cooking temperatures seems to indicate that some uncooked food should on principle be taken daily by the “gouty” as well as others. Raw ripe fruits in this respect, like salads, have an advantage over cooked fruits or vegetables.
In my own experience I do not know that there is any fruit, even strawberries, that will infallibly disagree with the “gouty.” One meets now and again with gouty subjects who are unable to eat certain fruits with impunity, but one meets with quite as many of the same idiosyncrasies in the non-gouty. The objections to certain fruits, e.g., strawberries, as to certain vegetables, e.g., asparagus, are largely theoretical rather than practical. Let the subject’s own experience be your guide in this matter, or if he be unobservant, teach him to observe for himself what fruits, if any, disagree with him.
With this reservation I am of opinion that, taken in moderate quantity, fruits are most useful constituents of diet for the “gouty.” In some cases it will be found that they cannot take fruit when mixed up with other food, but both enjoy and derive benefit from it when taken by itself. It is well, again, in others to restrain their immoderate indulgence in lemons, as these frequently, as Sir James Goodhart pointed out, upset gastric or intestinal digestion. It is advisable also to warn them that plums, currants, gooseberries, and other fruits containing large quantities of free acids are apt to have the same effect, while the melon, too, is prone to give rise to gastric disturbance. Peaches and nectarines, on the other hand, are eminently suitable for the “gouty,” also apples, pears, oranges, grapes, cherries, etc.
Condiments.—These substances give a flavour and relish to food, while their carminative properties stimulate appetite and favour digestion. On the other hand, their excessive use is a potent source of gastric irritation. Thus, for example, they are valuable in atonic dyspepsia, though liable to aggravate a condition of chronic gastritis.
The most important and most extensively used is common salt. Some incline to think that its use by persons of the “uric acid diathesis” is prejudicial. But unquestionably it is a necessary and wholesome article for the “gouty” when taken in moderation. In cases of gout complicated by hyperchlorhydria strict moderation in or abstinence from salt seems indicated, this because, the HCL of the gastric juice being wholly derived from the chlorides of the blood, it seems irrational to increase the supply. Some therefore forbid its use both as a condiment or in the cooking of food, making the subject depend on the salts naturally present in foodstuffs.
Vinegar, I am sure, upsets some “gouty” persons’ digestion, and I think Sir Dyce Duckworth is right when he counsels abstinence therefrom. Thus some “gouty” subjects can digest raw cucumber, but not with vinegar. Others find salmon if combined with the same condiment upsets them, but not without. As to the various other condiments—mustard, pepper, horseradish, etc.—there is no objection whatever to their use by the “gouty” in moderation and in the absence of any definite gastric disorder.
So much for our consideration of the individual foodstuffs—their suitability or not—for the subjects of gout. That such a general survey is advisable may perhaps be conceded, but in so far as it may approximate to fixed rules it savours of evil, this at any rate as far as the dieting of dyspeptic derangements of the “gouty” is concerned. To bring into prominence my point, I would lay down the postulate that there is no specific form of “gouty” dyspepsia.
The gastric derangements met with in gout are in no sense peculiar thereto. In other words, they present no symptoms specific of gout, despite the term “gouty dyspepsia.” The term “hyperacidity” as commonly invoked is far too laxly used in regard to “gouty dyspepsia.” The “acid risings” of the “gouty” are of two kinds. Hyperacidity may be due to organic acids, butyric, lactic, or acetic, the outcome of fermentation, or the condition may be one of hyperchlorhydria, or excessive secretion of HCL.
Hyperacidity due to organic acids is met with in some cases of atonic dyspepsia, chronic gastritis, and dilatation of the stomach. The free HCL is either diminished or absent. Differentiation of this type from hyperchlorhydria may be impossible without examination of the stomach contents.
Hyperchlorhydria per se sometimes occasions pyloric spasm, and minor degrees of dilatation follow, this the more commonly as the subjects of gout are middle-aged or elderly. In others the dilatation is part of a general neurasthenia from which the “gouty” no more than others are immune.
Again, gout of long standing is often associated with chronic gastric catarrh. Such is very common in beer-drinkers or men employed in breweries. A state of atonic dilatation of the stomach is a common sequel. In these cases of chronic gastritis in the “gouty” the free HCL may be normal, diminished or absent. Eventually, as the result of oft-repeated gastritis, the parts involved undergo widespread fibrotic degeneration. Also we have to recollect that the “gouty” are very subject to obstinate gastralgias.
We see therefore that the “dyspepsias” of the “gouty” may be not only of varied nature, but may also demand differential dieting at different phases of their evolution. The subject in the early stages of his gout may suffer from hyperchlorhydria, while later chronic gastritis may ensue, with the reverse condition, hypochlorhydria. The protein dietary suitable for the former has in the presence of the latter to be replaced by carbohydrates, despite their tendency to fermentation. Again, if either condition be complicated by dilatation other exigencies must be met. The meal content must be light, not bulky, and the fluid intake restricted.
Again, the foregoing gastric disorders may be complicated by glycosuria or albuminuria, each with separate dietetic indications. How inevitably futile then must be any attempt at stereotyped diet for the “gouty.” In short, the dyspepsias and other morbid states of the “gouty” call for eclectic, not routine, dieting, and to this end I append a few suggestions.
SPECIAL DIETARIES
Amylaceous Dyspepsia.—Not a few “gouty” subjects suffer from atonic dyspepsia, with acidity due to organic acids arising from fermentation. Frequently it appears to be the outcome of some previously prescribed regimen forbidding all flesh food, or of too frequent or irregular meals or habitual overfeeding, food-bolting, excessive smoking, etc. Correction of such faulty habits is an essential prelude to any dietetic rules.
In such cases it is advisable to reduce the intake of starchy and saccharine foodstuffs, such as bread, potatoes, pastry, sugar, milk puddings, and the like. Bread should be stale, or dextrinised by dry heat, as in thin toast and rusks. Potatoes, if taken, should be in the form of purées. Sweet dishes should be partaken of sparingly, if at all. They should be encouraged to take the more digestible forms of meat and the lighter kinds of fish. Green vegetables and fresh ripe fruit, raw or cooked, are valuable. Fats of the more digestible sorts are also desirable. Grilled but not fried fat bacon is easily digested.
As to beverages, light China tea is more suitable than strong Indian kinds. Frequently I have found substitution of cocoa most beneficial. But in any case the amount of fluid at meal-times should be restricted.
As a guide to the formulation of a dietary in such cases the following may be suggested:—
On awaking in the morning a tumbler of hot water should be slowly sipped. A squeeze of lemon may be added if liked.
Breakfast.—Boiled or plainly grilled sole, whiting, or flounder, or a slice of crisp grilled bacon or lean cold tongue, or a soft-boiled egg. A slice or two of crisp dry toast or stale bread and a little butter. At close of meal sip slowly one cup of weak China tea, or the same of cocoa or milk and water.
Lunch.—Chicken or game, or lamb, mutton, or beef, hot or cold, roast or boiled. Gravy to be free from fat. One only of the former kinds of meat to be taken with a reasonable quantity of tender, well-boiled vegetables. Spinach, kidney or French beans, sea or Scotch kale, vegetable marrow, or salad may be taken, but without oil, vinegar, or beetroot. Dry toast or rusks. Half a tumbler of water sipped after eating.
Afternoon Tea.—One or two cups of weak tea with milk or one cup of cocoa.
Dinner (two courses only).—Fish of the kinds allowed for breakfast without potatoes, or a slice of any tender meat, e.g., saddle or loin of mutton or thick part of an underdone chop, or small portion of fresh game, without bread sauce or crumbs. One or two slices of stale bread or dry toast. A little well-stewed fruit or custard, junket, or jelly. Half a tumbler of water with from one to two tablespoonfuls of spirit if desired.
If there be any suspicion of chronic gastritis, condiments and stimulants must be renounced, but not in purely atonic dyspepsia, in which they are of value. In either disorder the patient should abstain from salted and cured meats, tinned foods, pastry, sweets, raw vegetables, and cheese. Before retiring a tumbler of hot water with a squeeze of lemon may be sipped slowly.
Hyperchlorhydria.—This, the true “acid gouty dyspepsia,” is the most troublesome type of dyspepsia met with in the “gouty.” Regulation of the diet is the best means whereby to combat the excess of HCL in the stomach. All irritating spices or condiments, mustard, vinegar, etc., should be avoided. Salt especially should be used sparingly or wholly abstained from. As a rule, alcoholic stimulants are not well borne, and may, in the absence of special indications, be prohibited. In a limited number of instances a light wine may be allowed as a stomachic. To avoid irritation, hard substances, such as nuts, should be interdicted, and food thoroughly masticated, and taken neither too hot nor too cold. Bolting large morsels of food may readily excite pyloric spasm.
In these cases of superacidity the most suitable foods are proteins, which combine and neutralise the excess of acid. A liberal meat diet consisting in the main of chicken, beef, mutton or ham, is indicated. Also fish, eggs, hard or soft boiled, are permissible. Farinaceous foods are not well tolerated, and if given must be of the most digestible kind. Vegetables should be mashed and strained to rid them of cellulose, and only the more digestible kinds taken, and in the form of purées. Fats tend to lessen acidity, and are therefore indicated in the form of butter, cream, olive oil, and such like. Of beverages alkaline and mineral waters, Apollinaris, Seltzer, and Vichy, prove very beneficial. Their contained carbonic acid exerts a sedative effect and diminishes the secretion of acid. Milk or stimulants may be profitably diluted therewith.
Coffee is best abstained from, and cocoa and tea freshly made with half milk substituted. Soups are best avoided. If with the hyperacidity there be associated any degree of atonic dilatation, the fluid taken at meals should be restricted. Also in this instance the food should be taken in small quantities and at frequent intervals. Otherwise these cases of hyperacidity do well on three meals per diem provided they are separated by an adequate interval.
If the foregoing measures prove ineffectual the carbohydrate content of the food should be withdrawn, and the patient limited to a strictly meat diet, taken either raw or very slightly cooked. It goes best when finely minced or grated on stale bread. According to Osler, an ample dietary is afforded if three and a quarter ounces of meat and two medium slices of stale bread be taken three times a day, with a glass of Apollinaris water or soda-water, or what in this authority’s opinion is just as satisfactory—spring water. For the bread a little dry toast or twice baked (Zwiebach) bread may be substituted. Some advocate the meals being taken wholly dry, or with two ounces of fluid only; but two hours later a half to two pints of hot water should be slowly sipped. A month or six weeks of such a diet will usually suffice, after which a gradual return may be made to a mixed dietary.
Apart from the binding of excess of acid by the protein substances and consequent relief of discomfort, the so-called Salisbury diet has other advantages. Abstraction of the carbohydrates obviates intestinal fermentation and flatulence. Also, the food administered being small in bulk, and taken more or less dry, a dilated or atonic stomach tends to revert to its normal size.
In conclusion, in regard to these cases of hyperchlorhydria it must be realised that not only their diet and the manner of their eating, but their general habits of living, must also be revised. They must be warned of the great tendency to recurrence and the necessity of orderly and regular habits and of strict abstemiousness in regard to not only alcohol, but tobacco. The nerve element in some of these cases is very pronounced, and sometimes nothing short of a rest cure will suffice.
Hypochlorhydria.—Chronic gastric catarrh due to overeating and overdrinking is not an infrequent complication of gout in its later stages. Such subjects suffer with daily or periodical vomiting of stringy mucus. In such cases the HCL of the gastric juice is deficient or absent. Consequently protein foods are digested with difficulty, and carbohydrates are more easily disposed of. The lighter forms of meat, such as chicken or fish or raw scraped beef, are indicated. Nor, in view of the chronic nature of the derangement and the necessity of maintaining nutrition, should we hesitate to allow such “gouty” subjects other digestible forms of meat, such as sweetbreads, brains, etc. Fats also and carbohydrates up to the limit of tolerance should be allowed. Ingestion, however, of fluid at meals should be reduced as far as possible. Of beverages milk, and especially buttermilk, is particularly suitable.
Despite the deficiency of HCL, they may suffer much with acid eructations or flatulency owing to organic acids arising through fermentation. If so, farinaceous foods must be restricted, particularly potatoes and the coarser vegetables, while of course pastry and sweet foods should be prohibited. Bread should be taken in the form of dry toast or rusks.
Hyperuricæmia.—As far as is known, the endogenous moiety of urinary uric acid is uninfluenced by diet. On the other hand, as has been shown in previous chapters, the exogenous fraction can be reduced by suitable dieting. To this end, in order to prevent the intake of food containing uric acid precursors, the purin-free dietary was devised. Under such a regime both red and white meats must be proscribed, also fish and the legumes—peas, beans, lentils, asparagus, onions and oats—as these last are all rich in purins. Tea, coffee, and chocolate must also be eschewed.
In lieu of these substances more or less poor in purin bodies must be exclusively taken: milk sour or curdled, buttermilk and whey, white bread, butter, cheese, eggs, rice, tapioca, macaroni, sago, cereal foods, nuts and fruit. Even strawberries are permissible, for Weiss noted that the addition to an ordinary diet of 1 lb. of strawberries, 1½ lb. cherries, or 2 lb. of grapes, diminishes the amount of uric acid excreted by almost 50 per cent. With the exception of those interdicted above, all vegetables are allowable, cabbage, cauliflower and lettuce being almost purin-free.
Personally I am not enamoured of purin-free diets for the “gouty,” any more than I am of the purely vegetarian regime, so extolled by some as the means of averting gout. The purin-free diet, if I may say so, smacks too much of the laboratory, its raison d’être the baseless assumption that uric acid is the fons et origo mali.
I am very doubtful of the intrinsic merits claimed for it. I do not think it exerts a direct or specific anti-gouty influence. Such advantages as do accrue are referable, in my opinion, to the greater measure of intestinal asepsis that such a regimen promotes. It is suitable, therefore, in cases in which there are evidences of intestinal putrefaction. Distinctly unappetising, it is useful, too, as a disciplinary measure for those prone to overeating.
Its advocates claim that it tends to diminish the excess of uric acid in the blood. But, as was pointed out when dealing with uricæmia, variations may occur in the uric acid content of the blood independently of diet. Moreover, acute attacks have been observed even when the uric acid blood content was at a sub-normal level.
To place all “gouty” subjects on a purin-free diet as a routine procedure is to my mind wholly impermissible. The fact that prolonged adherence thereto is usually found impracticable is surely an indication that we are violating nature’s laws. It may prove beneficial in a few isolated cases, and then only for a time; but in the vast majority of instances it is frankly prejudicial. Given a carefully revised mixed diet, it will, in my experience, be rarely, if ever, necessary to subject “gouty” individuals to this dietetic penance.
The Reduction of Obesity.—Unfortunately obesity is a common associate of gout, and with it not infrequently comes glycosuria. Middle-aged “gouty” subjects have in their youth often been given to strenuous exercise. But notwithstanding that with advancing years their capacity and disposition for exercise lessens, they nevertheless take the same amount of food as of yore.
It is most difficult to make them realise that, with the alteration of their habits, the amount of food which at one time was but adequate is now excessive. I have found it useful to remind such of Ebstein’s dictum, “The gouty who have grown old in spite of their disease are almost always those who have been able to avoid obesity.” Still it is only fair to add that in some of the gouty obese no accusation of overeating or overdrinking can be lodged, and their aptitude for fattening seems often hereditary.
Reduction of the body weight when excessive in gouty subjects is hardly, I think, sufficiently emphasised. The victim himself is but too often convinced, however, that he ought not to be “lowered,” and sometimes, I think, infects the physician with his apprehensiveness on this score. But, as Harry Campbell rightly observes, “people do not die of starvation so easily as is generally thought, and it is very difficult for the physician to kill his patients in this way.” Yes, and, on the contrary, how often do gouty people “dig their graves with their teeth.”
Again, there is the static element to be considered in these cases. The articular manifestations of gout are by preference located in the lower extremities. It is clear then that excessive stoutness, particularly if of recent development, must inevitably throw increased strain on the already-hampered articulations. The feet of the “gouty” are their most vulnerable point, and the number who are flat-footed is noteworthy. In the presence of this static fault, “strains” or “sprains”—those fertile excitants of gouty outbreaks—are much more liable to occur, and I myself feel sure that in this way the frequency of attacks in the feet and, for that matter, in the knees also, is favoured.
Lastly, the gouty obese is frequently elderly, his vessels somewhat the worse for wear. Also he may show signs of cardiac weakness or a trace of albumen or sugar in his urine. Even so his weight should be reduced if possible. His watchword should, like Falstaff’s, be:—
“Make less thy body hence, and more thy grace; Leave gormandising; know the grave doth gape For thee thrice wider than for other men.”
There are so many dietetic methods of treating obesity that they cannot all be outlined here. The Banting method, like the Salisbury, is too severe for the average patient, while the Weir-Mitchell method has one cogent objection to general adoption, viz., the expense entailed. Nevertheless as regards the last-named, or skim milk, method, it certainly achieves marvellous results in those cases in which there is a mere accumulation of fat without any other complication.
Generally speaking, however, one has to be content with the following suggestions: All varieties of lean meat may be taken, as well as poultry, game, and fish, subject to idiosyncrasies and digestibility. Meat may be taken twice daily, not exceeding six ounces at one time. All starchy and farinaceous food is to be reduced to a minimum or wholly forbidden. Leaf vegetables may be taken freely, but the roots and tubers, such as potatoes, abstained from. Bread should be largely reduced in quantity and thoroughly torrified. Sugar must be prohibited, and saccharine or saxin substituted. Fresh fruits may be eaten, but milk should be avoided, also cream, or very strictly limited. Where feasible, it is often a good plan if the subject can for one day a week content himself with a diet of skim milk.
Alcohol, as far as possible, should be rigidly excluded, or only a very moderate quantity of good whisky or a light wine, such as hock or Moselle, permitted. As a rule, only a little hot water should be sipped at meals. But I think in these subjects of so-called “uric acid diathesis” it is well not to restrict their fluid too markedly. A pint of hot water may be drunk one and a half hours before each of the three meals, and one pint more half an hour before bedtime. Weak hot tea may be substituted, as many subjects find a difficulty in drinking so much plain hot water at one time. If while on this regime the subject lose weight and pari passu gain strength, all is well. If he lose weight and therewith lose strength, further reduction or its continuance is contra-indicated. It should be recollected that the reducing effects of dieting may be markedly enforced by an open-air life, with riding or other outdoor exercise.
Glycosuria.—This condition conjoined with obesity is not uncommon in middle-aged “gouty” subjects. It is of benign type, and the amount of sugar excreted is usually reduced to a mere trace by extraction of the carbohydrates in the food. Thus, we should forbid, e.g., sugar, pastry, sweet wines, and dishes made with flour, rice, or sugar. In these cases von Noorden considers that it is better after reduction of the amount of sugar by dieting to a mere trace to be content rather than to get rid of it wholly by a rigid elimination of all carbohydrates. To this end the patient may be allowed to eat a limited amount of bread, potatoes, and other vegetables, while he may eat freely of butter, bacon, and other fats.
One should recollect also that these “gouty” glycosurics have periods of enhanced carbohydrate tolerance, this, as Burney Yeo pointed out, quite “independently of any therapeutic interference.” In short, at times they can take quite a considerable amount of carbohydrates without passing sugar in their water.
Needless to say, the regime must be adapted to each individual case. The urine should be examined frequently, and the influence on the sugar content of different articles of food noted; also the weight should be frequently taken. It is certainly unnecessary in gouty glycosurics to wholly banish the carbohydrates. By such a plan we are more likely to do material injury than by exceeding by a little their limits of tolerance. Our remarks of course apply strictly to alimentary glycosuria. But we should also remember that exceptionally a case of gouty glycosuria may emerge into one of true diabetes.
Albuminuria.—In the so-called “gouty” contracted kidney, if the amount of albumen in the urine be very large, or when there are symptoms of nephritis, a milk diet for a few days or a week at a time may be given. More often it is unnecessary, or it is frequently badly borne or rejected. Consequently a modified milk diet has to be adopted, and a gradual return to a mixed diet permitted, provided no increase in the quantity of albumen ensues.
But at the same time it must be realised that no rigid rule can be laid down for “gouty” albuminurics. As a guide to the suitability of a diet it is better to rely on the general condition than on variations in the amount of albumen. For, as Professor H. Andrew Smith, of New York, long since said, “if on changing from a non-nitrogenous diet to a nitrogenous one we find a general improvement in the patient’s condition, it is an evidence that the change is beneficial, no matter if the albumen fills a larger portion of the test tube. On the other hand, if we cut off a large proportion of animal food from the diet, and our patient grows more dyspeptic, weaker, more anæmic, more dropsical, it is nothing to the point that only one half or one-third of the former quantity of albumen is found in the urine; the change has done harm, and the sooner we change back again the better. We should, above all things, seek that diet for the patient which he can best digest and assimilate, for we may rest assured that the products of faulty digestion and assimilation will irritate the kidneys more than any amount of normal material they may be called upon to eliminate, while, at the same time, the general system will suffer from lack of support.”
Lastly, up to this juncture all our suggested dietetic modifications have been in the direction of reduction or abstinence. But we must recollect that in practice we find that not a few gouty persons are most careful and prudent in diet. They commit no indiscretions, but nevertheless their gout is still with them. They are of the asthenic type, thin, pale, sallow, and given to neuralgic forms of fibrositis. They do not want “lowering”; to curtail their food is harmful. In their instance, with due respect to digestive idiosyncrasies, a more or less generous diet should be prescribed. Let them forsake dietetic schedules and follow their instincts. Let your advice be that of Sir William Temple: “Simple diet, limited by every man’s experience to his own easy digestion, and thereby proportioning as near as can be the daily repairs to the daily decays of our wasting system.”
BEVERAGES IN GOUT
It cannot be gainsaid that the beneficial effects of so-called “water cures” are in great measure referable to the increased amount of water ingested during their progress. Absorbed in the main in the small intestine, it passes into the general blood stream, whence it is excreted viâ the skin, kidneys, lungs, and fæces. Its elimination through these various channels sufficiently accounts for its value as a means of flushing the bodily tissues and hastening the excretion of retrograde and toxic products. Indeed, its efficiency as a depurative agent cannot be over-estimated, and nothing is more beneficial for the subjects of a “gouty” diathesis than regular consumption of an adequate quantity of this admirable solvent.
By general consent, the water ingested should be preferably hot. Water of a higher temperature than that of the blood stimulates the hepatic cells, and promotes biliary excretion. It has been shown, moreover, by Glax that while draughts of cold water raise vascular tension and diminish pulse frequency, on the other hand hot water diminishes arterial tension and accelerates the pulse rate.
It is also claimed that the increased elimination of water viâ the kidneys is correlated with an augmented output of the solid constituents of the urine; that the phosphates, sulphates, sodium chloride, and likewise urea are for the time excreted in greater amounts.
The point at issue, however, is whether or no this increase in the amount of urea excreted can be held to indicate enhanced tissue change in the nitrogenous elements in the body fabric.
Winternitz claims that it does, in contrast to Von Noorden, who holds that nitrogenous tissue change and the formation of urea and uric acid are uninfluenced by the amount of water imbibed. In further contradistinction some contend that following the ingestion of water the excretion of uric acid is diminished.
Fortunately for “gouty” subjects, the beneficial effects of water flushing of their systems occur independently of any coincident increase in their uric acid output. This is true even of mineral waters. Thus Bain and Edgecombe noted that following the ingestion of the old sulphur water of Harrogate the excretion of uric acid was diminished. Nevertheless cases of “gout, especially of the asthenic type, derived the most marked benefit from its use.” “This fact is mentioned,” they say, “because some writers attach the greatest importance to an augmented excretion of uric acid in the urine as a necessary concomitant of successful treatment. This we firmly believe to be an erroneous view.”
Indeed, ignorant as we are of the exact etiology of gout, we must at any rate provisionally attribute the proved efficacy of water-drinking in gout to its flushing action on the tissues, its furtherance of the excretion of waste products. Nor can we doubt that the ingestion of hot water, involving as it does equalisation of its temperature with that of the body, must exert a profound and intimate effect upon processes of cell nutrition. Moreover, through its solvent and penetrative quality, its mineral or chemical constituents are enabled to penetrate freely the interstices of the tissues throughout the economy.
It is, therefore, well to advise “gouty” subjects to drink daily on rising from eight to ten ounces of hot water, repeating the same half an hour before lunch and dinner, and finally the last thing at night. For in my experience “gouty” subjects on the whole do better if they drink some time before their meals than during their progress. It is an old belief that hard waters are unsuitable for the “gouty.” Sir Dyce Duckworth believed so, and Sir Charles Scudamore in 1823 delivered himself as follows: “The kind of water denominated hard has always been considered as unfriendly to health, and especially injurious to persons afflicted with gravel or stone. Many probably imagine that the earthy salts which it contains assist in making up the mass of the calcareous concretion.”
But more probably, as Sir Archibald Garrod suggests, the old view that tophi were composed of chalk had probably something to do with the origin of the tradition. That hard waters may be noxious in so far as they favour constipation may be granted. But, on the other hand, we have to reconcile with this the awkward fact that earthy or calcareous waters, e.g., those of Bath, etc., are among those whose efficacy in gout is beyond question.
Again, how can we reconcile with this view the prevalent practice of placing “gouty” subjects, temporarily at any rate, on a milk diet, this although milk is especially rich in lime? That a regime of milk in the young and robust “gouty” subject is often extremely beneficial is beyond question. On the other hand, it is equally certain that others do not thrive thereon. In prescribing it, therefore, we must be guided largely by personal idiosyncrasy.
Lastly, as to tea and coffee, there is a theoretical objection that both contain methyl purins. Albeit, it must be seldom indeed that gout is met with in pure tea-drinkers who at the same time abstain wholly from alcohol. Either tea or coffee, if taken apart from food, usually agrees well with the “gouty,” always provided that they be well made and not over-strong. Of the twain tea is, I think, more generally suitable than coffee, and where both disagree cocoa is an excellent substitute.
ALCOHOL IN GOUT
Said Sir Thomas Watson: “I am sure it is worth any young man’s while who has had the gout to become a teetotaler.” Few will gainsay the wisdom of this advice. But I would fain go further and impress on gouty parents the incumbent duty of bringing up their children as total abstainers. For gout, once avowed, has a vicious tendency to recurrence. The illustrious Sydenham, I think, would have approved of such advice: “Water alone is bad and dangerous, as I know from personal experience. When taken as the regular drink from youth upwards it is beneficial.”
When, however, gout attacks a man for the first time in middle or late life, most authorities agree that an abrupt change of habit in respect of stimulants is of questionable wisdom. In saying this, I do not for one moment mean that excess should be approved, but that I do not believe that the enforcement of total abstinence is prudent. In such cases restriction, not total elimination, is the better course. One must recollect, too, that total abstainers are by no means exempt from gout, while, on the other hand, many, if not the majority, of drunkards are. The latter have their penalties, cirrhosis, etc., but not inevitably gout.
I agree that gout is infinitely more common in those who take alcohol than in those who abstain therefrom. But nowadays, at any rate, the “gouty” as a class cannot with fairness be ranked as among the confessedly intemperate. With relatively few exceptions, they belong rather to those given to what may be termed the legitimate use of alcoholic beverages. My conclusions then are that:—
(1) The children of “gouty” parents should be brought up as total abstainers.
(2) The incidence of a first attack in a young man should be the signal for abstinence from alcohol in all forms.
(3) Given its occurrence in an older subject who has used alcohol but sparingly and stands in no need of it as a stimulant, the same total abstinence should be inculcated.
(4) In middle-aged or old subjects habituated to the use or abuse of alcohol abstemiousness, not abstinence, is the safer course.
THE VARIOUS ALCOHOLIC BEVERAGES
Malt Liquors.—I think we should distinguish between the “strong” and the “mild” varieties, even as we do between “heavy” and “light” wines. “Strong” malt liquors unquestionably are most provocative of gout, and it is not without significance that most “gouty” subjects have, frequently on their own initiative, abandoned their use. So much importance, indeed, do I attach to this, that if I were called to formulate any rule in the matter of alcohol for “gouty” subjects it would be the unsuitability of “strong” malt liquors, which not only increase the tendency to recurrence of the paroxysms, but appreciably lengthen their duration.
The prefix “strong” I use advisedly, as the volume of alcohol contained in different beers may vary by as much as from 1 to 10 per cent. Thus Scotch ale contains as much as 8·5 per cent., and, generally speaking, all “old” ales are usually “strong” ales. Albeit, to condemn malt liquors unreservedly is, I am sure, inadvisable. The truth is that in respect of their gout-inducing power malt liquors, like wines, display great variations.
Thus “strong” malt liquors, like “heavy” wines, are markedly provocative of gout, whereas the “milder” ales, like the “lighter” wines, are relatively impotent in this respect. Said the elder Garrod on this point: “The lighter wines, as claret, hock, and Moselle, although capable of acting as the exciting cause of an attack in gouty subjects, have when taken in moderation but comparatively little inducing power, and in this respect rank with the weaker kinds of malt liquors.” In this connection is it not significant that gout is extremely rare among agricultural labourers, who drink freely of that popular and ancient beverage mild beer? Sydenham on this point is very definite: “This is a rule for the gouty: they may take those liquors which neither chill the stomach nor intoxicate in any moderate quantity. Such is the small beer in our own country, which in foreign countries may be replaced by weak wine-and-water.”
I hold no brief for alcohol, but of the twain I am sure it is wiser to advise a poor man, even though “gouty,” to stick to “mild beer” rather than urge him to betake himself instead to “ardent spirits.” For the rich man, too, while in his prime and still capable of vigorous exercise, I am firmly of opinion that, with due deference to idiosyncrasy, a mild beer not containing more than from 3 to 6 per cent. of alcohol will do him not more, but less, harm than whisky.
I have yet to learn that the working man who has gout and sticks to mild, sound beer in moderation gets attacks more often or more severely than the rich man who affects whisky. “It must,” as Sir Archibald Garrod observes, “be confessed that among hospital patients who could not, if they would, follow out any strict rules of dietary, who seldom pay heed to our advice that they should give up beer, and who, as soon as an acute attack is over, revert to their previous habits of life, the course of gout does not seem to differ materially as regards the character, frequency, and severity of the attacks from that followed in people who are able to adjust their living according to the best advice to be obtained.”
I think then in this matter of malt liquors, their suitability or not for “gouty” subjects, we should be well advised to reconsider our attitude. In other words, I would urge that we draw a distinction between “strong” and “mild” malt liquors. By all means let us continue to condemn the “heavy” varieties, while not extending the ban to the “lighter” forms. I would, however, make the following reservations: that—
(1) It be a “light” beer, in which the “bitter” principles predominate, and the extractives are small in amount[61];
(2) It be “sound” and not “turned” beer, and of course free from any possibility of lead impregnation;
(3) It be taken in moderation, not exceeding one to two pints per diem;
(4) The “gouty” subjects by whom it is taken be physically active;
(5) Due respect be paid to personal idiosyncrasy, reserving its use for those in whom its effects are definitely stomachic and tonic, while discountenancing its use when followed by heaviness, drowsiness, and biliousness.
As to cider, there is no doubt that the partially fermented or sweet variety is more harmful than “dry” or “rough” cider. Still there is no room for dogmatism even here, for a “gouty” man, if he be unaccustomed to cider, may find that, whether “dry” or not, it may provoke an attack. Sir Archibald Garrod tells us that he has known not a few gouty patients who alleged that cider suited them admirably, but he adds: “An experience of some months has usually modified their opinion on this point.”
Wines.—When we come to consider wines, we are on very uncertain ground, this especially if we base our opinion too much on the chemical analysis of this or that variety. The current belief is that the most unsuitable wines are those that contain large amounts of alcohol, sugar, or free acid. Then we discover it is not the amount of alcohol in the fluid that determines the incidence of gout and, in witness to our perspicuity, call to note the rarity of gout in Scotland, where whisky is the favourite beverage; ergo whisky par excellence is the drink for the “gouty,” and so we find ourselves in this impasse: we fulminate against alcohol as the cause of gout, and in the same breath advise our “gouty” patients to drink precisely those fluids containing the highest percentage thereof.
True, when we turn to wines we find that it is precisely those that are richest in alcohol that most potently predispose to gout, e.g., port. But seeing that whisky contains infinitely more alcohol than port, and yet is little gout-provoking, we search round for some other constituent in wine on which to lay the blame. So we decline on the varying degrees of acidity in different wines. But this again on reflection, it is decided, is of little moment. For, on the one hand, port and sherry are among the least acid wines, and yet, like the even less acid malt liquors, most productive of gout, while, on the other hand, the more acid clarets and hocks are deemed relatively harmless. Then the varying quantities of sugar in the different wines come under the ban. But here again no definite line can be drawn. For some wines most provocative of gout have a high sugar content, while others equally potent in this direction contain but small amounts.
Now the most salient deduction from the foregoing considerations is our inability at present on chemical grounds to determine why certain wines are productive, and others are relatively nonproductive, of gout. We can impeach neither the alcohol content, the acidity, nor the sweetness. For on all these points startling exceptions preclude dogmatism. Does not the clue to these varying reactions quâ gout reside in the individual, not in the character of the wine? We are far too prone to say that this or that wine is “gouty,” to say that this wine gives you gout, and that not.
The evil potentialities that make for gout reside not in this or that particular wine, but in the individual. This or that wine does not give him gout, but evokes or brings to fruition a morbid tendency already latent in him. In the absence of this inherent proclivity, it would not have elicited those specific local reactions typical of gout. But for those who would interpret this statement as approval on my part of alcohol or an absolving thereof from any part in the genesis of gout I would issue this caveat: Alcohol will not originate gout in a non-gouty subject, but it will almost infallibly in those in whom there exists by heredity an inborn tendency to gout. In short, the “gouty” are hypersensitive to the evils of alcohol; the greater the need then for abstemiousness and self-restraint.
But, to resume the thread, in the absence of any absolute chemical criterion as to the relative suitability of this or that wine for the “gouty,” what shall be our advice to the “gouty” individual on this point? In a word, his “palate” and his “stomach” are the best criteria of the wholesomeness of this or that particular wine in his particular instance. If he is in the habit of taking wine do not forthwith, as is so often done, forbid him wine in all forms and order him whisky. This is done so light-heartedly that I do not wonder that the subject goes away frequently with the idea that whisky is not only innocuous, but desirable.
The whisky-drinker is not immune from gout, and I have no hesitation in affirming that “light” wines when fine, mature, and of a good quality are, subject to individual idiosyncrasy, quite as suitable for the “gouty” as whisky. Of the many wise warnings given us by Sir James Goodhart none is more apt for the present day than the following. Discussing the “treatment of uric acid,” he observes: “I am as much as ever an opponent of the prevalent dictum, ‘You must not touch wine; you must drink whisky,’ which too often means to the patient, ‘A glass of good wine is poison; I may take as much whisky as I like, and it is harmless,’ one of the most mistaken and mischievous beliefs that ever plagued a world.”
Again, if a “gouty” man takes wine, there is always one special variety that agrees with him, and as certainly one other or more that infallibly upset him. Putting aside all preconceived ideas, find out his personal idiosyncrasies in this respect. In this way you elicit and utilise for your ends the individual’s own experience, the only experience that counts.
A man of a certain age, he generally by the time he develops overt gout has arrived at definite conclusions as to what does and what does not suit him. He will frequently tell you he has had to give up malt liquors, perhaps port and champagne, and now finds that whisky, gin, or the lighter wines agree with him better. Or, as like as not, he may upset all your preconceived ideas. He may be of those gouty subjects—and they are not so few—who can drink champagne in moderation, or even a glass or two of port, daily with apparent impunity. On the other hand, a glass of claret or hock plays the mischief with him. He may, like some individuals cited by Burney Yeo, be one of those exceptional gouty subjects in whom even stout is well borne, Yeo thought largely because they habitually took daily large quantities of alkaline salts.
The sum of these erratic findings is that you must respect idiosyncrasy. It is said that the best wine for a “gouty” subject is the one that causes most diuresis. For myself, I am equally positive that the worst wine for a gouty man is that which upsets his stomach, which gives him some hours afterwards “acidity” or a feeling of “liver.” Often, too, it is not the wine, but the stomach into which it is put, that is to blame. Thus the “gouty” subject with atonic dyspepsia finds a glass of sound wine helps digestion. On the other hand, if he suffers from hyperacidity or chronic gastritis, the reverse will probably be the case.
Again, it is not the name, but the quality, of the wine that counts. It makes all the difference whether the wine taken is fine, mature, and of good quality, or some factitious, mixed, or adulterated product, passing muster, say, as claret. Fine mature clarets or red Bordeaux wines are most suitable for the gouty. But, as Burney Yeo rightly says, “a more injurious beverage than bad claret or imperfectly matured claret—and, speaking generally, all but the more expensive or most carefully selected clarets are bad—was never drunk.”
It seems opportune here to lodge a protest against fashions in wines for the “gouty.” At one time it was claret, then light white wines, Moselle, etc., and anon whisky, and even cider had its vogue. Fashions in wines, as in other spheres, postulate uniformity and lack of discrimination. Any one of the foregoing beverages may suit some particular “gouty” individual, but not all “gouty” subjects.
We have said that in some instances the wine, in others the stomach, is at fault. But intrinsically it may lie in neither, but simply in the quantity of the wine drunk. It may not, as judged by ordinary standards, be an excessive amount, but it may be excessive for that particular man. It is here that a medical man may often intervene with advantage. For a man may, quite unbeknown to himself, be really a heavy drinker, one of those unfortunates who are peculiarly tolerant of alcohol. A tactful reminder of the amount he is consuming per diem will frequently come as a shock, often a very beneficial one.
Apart from this, it is, I am sure, wise to fix the daily amount. The daily habit in the “gouty” is all-important. If accustomed to take one or two glasses, and they stick to it, all may be well; but it is on the occasions when the glass grows into a half-bottle that the trouble comes. Metabolically speaking, the “gouty” subject is most unstable, and disturbance of what one may call his daily alcoholic rhythm is always perilous. Unfortunately it works either way, too, both in the matter of “too little” as well as “too much.” Here experience and sound judgment will alone enable the physician to decide how far he may tamper with long-established habits.
At other times the amount, though, strictly speaking, not excessive, is so when judged in light of the victim’s habits. He may be an intellectual worker, but sedentary, and he must either lessen his drink or increase his exercise, or he may overeat as well as overdrink—a victim of the prevalent idea that the one evil counteracts the other. Between the Scylla of overeating and the Charybdis of overdrinking there is no safe course save by way of reduction of both.
We see therefore that in the matter of the choice of a wine for a “gouty” subject there are many points to be considered. Of these personal idiosyncrasy stands first. By this criterion, and none other, can the suitability of the wine be decided. Then the state of the digestive functions, if deranged, has to be considered. Is the gastric disorder such as will be benefited or, on the other hand, impaired by wine of any sort? Again, glycosuria, albuminuria, raised blood pressure, or cardiac degeneration may intervene to complicate the issue, and so our policy in regard to alcohol has constantly to be adapted and readapted to the varying requirements of the organism.
It will be seen that I have largely refrained from specifying the wines suitable or unsuitable for the “gouty.” To have done so would have been alien to the general tenor of my remarks, convinced as I am that our trend in the matter of alcohol for the “gouty” should be more in the direction of “individualisation” than of “standardisation.” Subject to the reservations that such an attitude portends, I would proffer the following suggestions:—
As a general rule, wines which are “dry” are much more suitable for the “gouty” than those which are “sweet.” Wines are termed “dry” when nearly all the sugar of the grape is transmuted into alcohol, as in “dry” sherries. They are termed saccharine or “sweet” when the process of fermentation is arrested before all the sugar has been exhausted, as in Malaga. Again, wines which are both “strong” and “sweet,” e.g., Malaga, sweet champagne, Tokay, etc., are more pernicious than those which are “strong” yet “dry,” e.g., port, sherry, Madeira.
Sir James Goodhart, discussing wines suitable for the “gouty,” confesses to a “personal leaning in favour of the wholesomeness of a glass of good old sherry in those cases where a little wine seems a judicious prescription.” With this I fully agree, and would suggest that of sherries the “gouty” should favour the “Manzanilla” rather than the “Amontillado” class. The former, save for the addition of a small quantity of spirit, are mostly shipped in the natural state; also they are light and “dry” as compared with the latter, which are generally “sweet” and full-bodied.
It is interesting to recall, too, that Sydenham regarded sherry as preferable either to Rhenish or French wines. He himself in his own person found “sack” or Canary the most helpful. “I have during the fits of the last years tried many things to lessen the symptoms. Nothing, however, effected my purpose so much as a small draught of Canary wine, taken now and then, when the faintness or sickness were most oppressive.” Here one may note that sherry was the first wine to be known as “sack” in this country, and that the wine shipped in Sydenham’s time was of the “dry” variety. Chemically the “sweet” sherry differs from the natural “dry” light wine through its relatively high content of alcohol and sugar.
Turning to port, Sir Alfred Garrod absolutely tabooed its usage by the gouty. But this appears too sweeping, and nowadays, at any rate, it is well recognised that, especially in asthenic types of gout, a glass or two of old port is well borne. Consequently in such cases we should not, in the absence of any adverse symptoms, forbid its continuance. The bad reputation achieved by port is, I am sure, a relic of the Regency. But “three-bottle” men are no longer with us, and, allowing for personal idiosyncrasy, I very much question if sound port taken in moderation wholly merits the aspersions cast upon it. I do not by that for one moment suggest its general adoption by “gouty” people, but that where an old or elderly gouty subject takes port and can be trusted not to extend his glass to half a bottle his inclination may be respected. The sugar content of port varies according to the vintage, ranging from 7 to 15 per cent., and the “gouty” man should favour the “drier” varieties.
As for champagne—a manufactured article rather than a natural wine—there is no question that, if taken at all, it should be a “dry” brand. Such contains from 9 to 12 per cent. of alcohol and from 1 to 4 per cent. of sugar, whereas the “sweet” brands may hold as much as 16 per cent. All depends on the quality of the champagne, and, as Ewart wisely remarks, “it is wiser for the ‘gouty’ patient not to incur considerable risks by trying brands with which he is not familiar, though he may sometimes with impunity, and occasionally with benefit, enjoy a glass of champagne which he can trust from personal experience.”
If, on the whole, the most unsuitable wines for the “gouty” are the strong sweet spirituous or liqueur wines, on the other hand the red or astringent and white wines are the most esteemed. As to the red wines, there is no doubt that the delicate Gironde (Bordeaux) wines are par excellence the most suitable. They have sufficient body and alcohol without being heavy or fiery, while their acidity and sugar content are very low. But of course the quality of the wines varies considerably with the vintage. Subject to this, sound, well-made clarets taken in moderation and somewhat diluted with water are the most wholesome wines we can prescribe for the “gouty.”
The more full, though still not coarse, wines of the Burgundy district are by some denounced. One authority, I note, states that in elderly gouty subjects he had often found that two or three glasses of claret or Burgundy were in the course of a few hours followed by eczema. While such idiosyncrasies may obtain, it is not true of the “gouty” as a class. I should consider a “gouty” subject in any case unwise to take two or three glasses of Burgundy. But I do not hesitate to order one or perhaps two glasses somewhat diluted with water. Being a stronger and more tonic wine than Bordeaux, it is useful in the more asthenic types of gout. The pity is, of course, that the cheaper Bordeaux and Burgundy wines are so largely adulterated, while the more mature clarets are available only for the rich. As good substitutes for French wines Burney Yeo commends the red Hungarian wines, such as Carlovitz, while we may add that some of the Dalmatian wines are of fair quality and somewhat resemble Burgundy.
Reverting to white wines, these, as compared with the red wines of the Gironde, contain less tannin and more free acid. According to Burney Yeo, they exert, too, a more diuretic effect, and to remove their excessive acidity he advises their dilution with some alkaline table water. Most of the white wines come from the Rhine or Moselle districts. The Rhenish are relatively full-bodied and of marked vinosity, while the Moselle wines are mostly light and of a somewhat delicate nature. Light hocks and still Moselles are quite permissible, also the white wines of France, such as vin de Grave, all varieties of the latter being fairly “dry” and light in character. On the other hand, the white wines of Sauterne, like some of the Hungarian wines—i.e., Ruster—are rich in saccharine constituents. In this respect they contrast with the Rhenish and Moselle wines. Of these last Johannisberg contains only 0·42 per cent. of sugar, Rudisheimer 0·39, Zeltinger 0·13, and Stein-Reisling 0·01, while Ruster contains no less than 21·74 per cent. of sugar.
In conclusion, I would re-emphasise the fact that, if wine be taken, the patient’s own experience is the best test as to which particular wine is the most suitable in his case. This elicited, the subject should be counselled to adhere to it, taking it only at meal-times, and establishing a rigid rule as to quantity. The least excess is harmful, and breaking of the ordinary routine in the matter of the amount drunk is a fertile source of “gouty” outbreaks. In any case the quality of the wine should be above suspicion, and if the expense is prohibitive, he had best eschew wine altogether in favour of mature spirits.
Spirits.—Brandy, whisky, and gin are the spirits most in vogue in Great Britain, and it has become an axiom with some that, if alcohol in any form be requisite for the “gouty,” the least harmful is one or other of these beverages when adequately diluted. Of the three whisky undoubtedly has found most favour, and the pernicious and far too prevalent idea is that whisky not only does not beget gout, but is actually beneficial for gout. The consequence is that many “gouty” people take far more whisky than is desirable, seemingly oblivious of the fact that, if whisky in moderation be suitable for the “gouty,” whisky in excess is as deleterious for them as for the non-gouty. In short, like any other form of alcohol, if taken immoderately, it will bring to fruition a latent gout, this, as suggested by Ford Robertson, not by the direct action of the alcohol, but by the “indigestion toxæmia” it sets up.
In advising therefore a “gouty” subject to take whisky we should insist that (1) it should be taken only at meal-times and (2) only in moderation. The habit of occasional “nips” at all times of the day should be unreservedly condemned. As to what constitutes a moderate quantity is often a difficult question to decide.
When feasible, I endeavour to limit the daily allowance to a wine-glassful, distributed over lunch and dinner. But it is quite impossible to lay down hard and fast rules in a matter in which personal idiosyncrasy plays such a strong rôle. Frequently, in addition to the above amount, one has to relent to the extent of a “nightcap,” or but too commonly one has to be content if one can compass reduction to an amount which for the particular individual under review seems apparently compatible with no appreciable damage to health.
Sometimes one of the frequent accompaniments of gout comes to our assistance. It may be raised blood pressure, glycosuria, albuminuria, obesity, etc. In such cases a word in season may reduce an otherwise recalcitrant subject to reason.
Needless to say, in regard to “ardent spirits,” as to wines or malt liquors, we must, when determining the quantity to be taken per diem, review the same in light of the person’s habits, whether active or sedentary, whether associated with overeating or not. For manifestly all these bear on the point at issue.
Lastly, as to whether the subject should take brandy or gin in preference to whisky is a matter for himself to decide. Whichever suits him best is the best for him. Albeit, I confess to a leaning in favour of “dry Plymouth” gin, this being more diuretic than other spirits by reason of the juniper contained therein. But, in whatever form “ardent spirits” be taken, it is most essential that it be sound. Brandy should be of the finest quality, the whisky mature, and inferior kinds of both wholly eschewed.
XXVIII. MEDICINAL AND OTHER MODES OF THERAPY—ACUTE GOUT
MEDICINAL THERAPY
The illustrious Sydenham, for more than thirty years a sufferer from gout, was clearly in doubt as to whether a cure of the malady was to be attempted or even desired. It was Nature’s prerogative, he contended, to dispose of the peccant matter after her own fashion by depositing it in the joints, whence it might be dissipated by insensible transpiration. Evacuant measures were, he thought, frankly prejudicial in that they occasioned reabsorption into the blood of morbid substances already cast forth from the system into the joints, with haply deflection of the same upon the viscera, with all its added perils.
In view of these conceptions, Sydenham naturally discountenanced any attempt to arrest or control the course of acute gout. “Nay, more,” said he, “I can confidently affirm that the greater part of those who are supposed to have died of the gout have died of the medicine rather than the disease.” Not only were purging, blood-letting, and alike the use of diaphoretics by him condemned, but, more, a policy of “inert expectancy” enjoined. The true rôle of the physician was that of the bystander viewing the workings of the vis medicatrix Naturæ, while for the tortured victim remained the pithy consolation that his gout was to be regarded as a minister of health, whose presence and stay ought by all means to be courted. Long years after Sydenham’s death his laisser faire attitude survived in Meade’s epigram, “the gout is the only cure of the gout,” and in Cullen’s depressing axiom that “in patience and flannel alone” lay salvation. Can we wonder that this policy of masterly inactivity made gout the happy hunting ground of the charlatan?
It may be admitted that an initial attack of gout often leaves the subject better than before, but the deep remedial forces of Nature, at first apparently all-sufficing, later prove unequal to their task. Secondary evils follow the attacks, and “the racking pains, unfitness of motion and other disorders which afflicted him during the greatest part of his life” are at once a proof of Nature’s limitations and the fallaciousness of Sydenham’s doctrines.
So much by way of prelude, but perhaps, as Heberden surmised, the chief reason why Sydenham and his disciples found it advisable to do nothing to curb the violence of gout was that they knew nothing wherewith to achieve such control. Thus, though colchicum had been used from time immemorial by the ancient physicians, it had in Sydenham’s time almost been abandoned as a remedy in gout, when, long after, according to Scudamore, a Mr. Want (“Essays in the Medical and Physical Journals,” No. 185, etc.) drew attention to its specific value in gout, and restored the drug to its pristine status.
ACUTE GOUT
In the main the general principles of treatment conform to those adopted for other inflammatory ailments, with, of course, the important reservation that our mode of procedure be adapted to the individual case; viz., due regard must be had to age, the intensity of the attack, and the presence of complications. For obviously the treatment suitable for a robust plethoric subject might prove the very reverse of salutary for a broken-down victim more or less worn out by previous attacks and haply the subject also of arterial and renal changes.
The medicinal treatment of acute gout necessarily divides itself into constitutional and local measures. In pursuance of the first, we seek to control the inflammation and febrile disturbance while assisting the organism to eliminate those toxic substances in the blood that have determined the incidence of the paroxysm.
The attack usually supervenes while the subject is in bed, and, generally speaking, keeps him there. Indeed, rest is imperative, and as far as possible sources of worry should be excluded. The nature of the diet suitable for the acute stages has already been adverted to, and, practically speaking, the first point that calls for investigation is the state of the bowels. Were they prior to the attack open regularly, loose, or confined? Constipation is the usual forerunner, and if so, a swiftly acting purge must be given. Indeed, even if previously the action of the bowels has been free, they usually, with the onset of the attack, become bound, the intensity of the local pain presumably exerting an inhibitory effect.
As to the advisability of initial purgation in acute gout, Sydenham was definitely opposed thereto. In contrast, others, who held with Scudamore that portal congestion was an etiological factor, highly eulogised free catharsis. The truth, as usual, lay between the opposing views. In other words, we must strike the happy mean between adequate evacuation and excessive purgation, for there is good reason to believe that the latter often so to speak, defeats its own end. It may determine more rapid recurrence of the disorder or its perpetuation in a chronic and asthenic form.
Incidentally one may recall that the objections unfairly launched against colchicum took origin in the misconception that its good offices were referable to its cathartic action. Hence by our forefathers the drug was pushed until the characteristic “colchicum stools” appeared, with their attendant nausea and prostration. This of course led to this valuable drug being looked at askance, whereas the error lay, not in the drug, but in the method of its administration, for, fortunately, its specific effect in gouty arthritis may be secured without the induction of depression, nausea, or purgation. Indeed, as Sir Alfred Garrod long since pointed out, it “frequently proves of most benefit when its operation is unattended with increased alvine evacuation.”
Albeit, from the tenor of our digression it must not be inferred that purgation is inadvisable in gout, but only that this salutary purpose must not be effected by colchicum. At the same time we must not think that mere purgation will of itself allay the articular inflammation, for it has been repeatedly shown that it exercises little or no control in this direction; but, on the other hand, it sweeps out irritating matter, promotes the return to a healthy state of the alimentary canal, and in this way reinforces the beneficial effect of colchicum.
My own opinion is that, if seen just before or just after the acute attack begins, it is wiser to secure a free action of the bowels before placing the subject on colchicum, this the more imperatively if it be a case of acute sthenic type supervening in a robust subject evidently labouring under constipation. If there be no palpable derangement of the liver, we may content ourselves with ordering at bedtime a full dose of Gregory’s powder, or Pil. rhei co. gr. 5-8, or Pil. colocynth co. gr. 5-8, followed in the morning by a saline aperient. French physicians, especially Robin, in such circumstances rely solely on sodium sulphate. The salt has the advantage of not lessening the secretion of urine, and the dose advocated is 1 ounce.
If the conjunctivæ show an icteric tinge or the character of the stools suggests that the liver is at fault, small doses of a mercurial preparation, such as calomel (gr. 4) or blue pill, may be given at night, either Pil. hydrarg. gr. 5 or Pil. hydrarg. gr. 1, in combination with Pil. coloc. cum hyoscy. gr. 4, and the same followed in the morning by 1-2 ounces of Mist. sennæ co. The nauseating flavour of the latter is best disguised by 1-2 drachms of Glyl. vanillæ, or for the “black draught” we may substitute 4-6 drachms of sodium sulphate, a Seidlitz powder, or a full dose of Carlsbad or Condal water.
When mercurials are contra-indicated or from experience known by the subject to disagree, podophyllin may be prescribed in some such form as the following: Podophyllin gr. ¼ c̄, Pil. coloc. hyoscy. gr. 4.
In other instances the cholagogue effect of the mercurial is procured by substitution for it of a small dose of the Ext. colchici in combination with the compound colocynth pill. Our forefathers, too, frequently prescribed colchicum and mercury conjoined with aloes or colocynth, and the following is an excellent and well-tried formula:—
℞ Ext. colchici acet. gr. ½ Ext. aloes barb. gr. 1 Ext. hyoscy. vir. gr. 1 Pil. hydrarg. gr. 1½ Fiat pil., 1.
In short, in the matter of the initial purgation the drug chosen must be suited to the individual and the degree of purgation also graded. The old rule was that if the belly is hard, the subject can stand purging, but not otherwise; and it is, I think, a fairly sound index. Mercurials in aged subjects are best avoided, and likewise in those with defective kidneys. Salivation in their instance is easily provoked, and Sir Alfred Garrod held that mercury “in advanced forms of gout should be altogether avoided.” French physicians think saline aperients preferable to the English method of giving calomel, and unquestionably they are eminently suitable for robust and plethoric subjects.
Colchicum in Acute Gout.
Whatever be its mode of action, colchicum still remains par excellence the remedy for acute gout. As before noted, Dixon and Maiden hold that colchicine has no action on the metabolism or excretion of purins, nor on the kidneys. On the other hand, it influences markedly the leucocytes, their number in the circulation undergoing a primary decrease and a secondary increase. Bain, it is true, found that under colchicum a slight increase in uric acid excretion occurred, but thinks it extremely doubtful if its influence in this direction is invariable.
That colchicine should exert such a marked effect in gout and yet apparently be destitute of any influence on uric acid excretion is of course very striking. It calls, moreover, for more reflection on the part of those who seem to contend that because a drug increases uric acid elimination it must necessarily be beneficial both for the gout as well as for the victim.
Method of Administration.—In initial attacks the drug must be exhibited with caution. Some persons are idiosyncratically sensitive thereto. Attacks of faintness may ensue, or even ordinary doses occasion purging or nausea and vomiting. Their incidence shows either that the subject is abnormally sensitive or the dose too large. Such untoward phenomena indicate its abandonment or drastic reduction. With these reservations, colchicum may be administered in every primary attack and most, if not all, of the succeeding paroxysms.
Albeit, the older the subject and the more ancient the gout, the more warily should we proceed, especially if there is marked irritability of the digestive system, renal disorder, or cardiac degeneration. Robin holds that if visceral gout is present, or the urine contains much albumen, no colchicum should be given.
It is notorious that old persons stand colchicum badly. In their instance we need be the less ready to resort to heroic doses when we recall that acute gout is a self-delimited disease, and while it would be improper to do nothing in elderly subjects exhibiting visceral lesions, etc., it is well that we proceed cautiously, so as to avoid the induction of circulatory depression or the excitation of nausea or a diarrhœa which may be, and often is, difficult of control. Moreover, if these untoward symptoms are allowed to ensue, there is a tendency for the gout to recur as soon as the effects of the colchicum have worn off.
Preparations of Colchicum and Dosage.—Those most commonly in use are the tincture and wine of colchicum, and of these the latter is most in favour. As to dosage, most authorities agree that a full dose—30-40 minims of the vinum colchici—should be given at the inception of treatment and followed by smaller amounts, from 10-20 minims two or three times a day.
By French physicians the tincture of colchicum is preferred, and by Robin that extracted from the flowers rather than the seeds. The dose of our own official Tinct. colchici seminum ranges from 5-15 minims, and by the French Codex the maximum single dose is placed at 25 minims, and the maximum intake during twenty-four hours at 100 minims approximately. It may be noted that preparations from the seeds are more purgative than those derived from the corn. Lastly, we have the official extract of colchicum and the acetic extract. The dose of the former ranges from ¼-1 grain, and it is frequently given in the form of a pill with ipecacuanha and mercury. The addition of a small dose of atropine is often advisable, to obviate the vomiting and diarrhœa often primarily induced by increase of peristalsis. By many the acetic extract is preferred, J. S. Matthews holding that the effective dose ranges from 2-6 grains.
Turning now to discuss the most opportune juncture at which to administer colchicum, certainly in the initial and the earlier paroxysms we may with advantage postpone the giving of colchicum pending free clearance of the bowels. No harm will follow its being withheld until the second day. Indeed, many physicians, both British and Continental, counsel delay in its exhibition until the fit is well established.
Again, in primary paroxysms—viz., while ignorant of the personal equation in respect of colchicum—it is well that our maximum dose should not exceed 20 minims, and when the bowels have not been previously purged, the drug should be combined with sulphate and carbonate of magnesia, as in the following prescription:—
℞ Magnesii sulphatis gr. 60 Magnesii carbonatis gr. 10 Potassii citratis gr. 30 Vini colchici ♏︎ 20 Aquæ menthæ viridis ad unciam. Misce. fiat mistura. Two tablespoonfuls with two of hot water every three hours until bowels have been freely opened.
This achieved, the sulphate of magnesia may be omitted, and the mixture taken every six instead of every three hours; but it is a good plan to keep the original mixture at hand, giving a dose every morning while the acute stage lasts. Then during the day the colchicum should be persisted with either in the form of the wine or the tincture.
Moreover, there are often special indications to be met. Thus the skin in acute gout is often hot and dry, and the urine unusually scanty and high-coloured. In this event the colchicum may with advantage be given with the citrate, bicarbonate or nitrate of potash, so as to produce a diaphoretic and diuretic effect. In other instances acidity is a prominent symptom, and here the combination of colchicum with the citrate of potash and magnesia will be found useful.
As the intensity of the inflammation wanes and the local pain and tension subside the dose of the colchicum should be gradually diminished; but even after convalescence is established it may advantageously be continued for a few days in small doses, say, 5 minims of the vinum colchici three times a day. The condition of the tongue will usually furnish a safe index, as rarely will it clean up prior to abatement of the gouty fit.
In subsequent paroxysms and alike in the acute exacerbations that chequer the course of chronic gout we may, in the absence of idiosyncrasy or other contra-indication, proceed more boldly. Thus, if the bowels have not previously been briskly purged, we may at once prescribe the following formula:—
℞ Vini colchici ♏︎ 15-20 Magnesii carbonatis gr. 15 Magnesii sulphatis gr. 60 Aquæ cinnamomi ad ℥j. Fiat mistura, ℥ij. statim sumenda et ℥j. quartis horis p.p.a.
The primary dose, as will be noted, will contain either 30 or 40 minims of the wine, and, though Sir Alfred Garrod prescribed up to a drachm, it will scarcely, if ever, be necessary to exceed 30-40 minims. The subsequent dose of from 15-20 minims may after a day or two be reduced, and instead the mixture given in ½-ounce doses three or four times a day. Or, if preferred, the mixture in its reduced dosage may be renounced in favour of a pill containing either the extract of colchicum or, what many consider even better, the acetic extract thereof. Thus the following pill may be taken every night for a few days, and then on alternate nights:—
℞ Ext. colchici gr. ¼ Aloin gr. ⅛ Ext. bellad. alcoh. gr. ⅛ Capsicin gr. ⅟₂₀ Ext. rhei gr. 1 Fiat pil., 1.
The acetic extract may be given in larger doses, and was in great favour as the chief constituent of many so-called “gout pills” in combination with ipecacuanha and mercury:—
℞ Ext. colchici acet. gr. 1½ Pulv. ipecac. co. gr. 1½ Ext. colocynth co. gr. 1½ Fiat pil., 1 nocte sumenda.
An excellent formula, in which the colchicum is combined with mercury, has already been furnished on a preceding page. Needless to say, it should, like the above pill, be followed in the morning, if necessary, by a mild saline purgative.
Colchicine.—This, the active principle of colchicum, has of recent years been widely and successfully employed in acute gout, as well as in exacerbations of the chronic type. By some subjects, especially the old, it is often better borne than colchicum preparations. The dose ranges from ⅟₁₀₀-⅟₃₂ grain in a pill. By the French Codex the maximum single dose is fixed at ⅟₃₂ grain, and the maximum administered during twenty-four hours should not exceed ⅟₁₆ grain approximately.
The following is a suitable combination in an elderly subject, and it may be noted that the drug has been found of use, too, in cerebral congestion and uræmia:—
℞ Colchicine gr. ⅟₁₀₀ Ext. belladon. alcoh. gr. ⅛ Ext. nucis vomicæ gr. ¼ Fiat capsule or cachet, 1 every three or four hours.
In robust subjects the colchicine may be given in larger doses. Luff states that few patients will tolerate ⅟₅₀ grain, because of the diarrhœa and griping pains produced. He found that colchicine (⅟₇₀ grain), in combination with henbane and nux vomica in the form of a pill, rapidly relieved gout when taken every three or four hours.
Or as a substitute we may use the salicylate of colchicine, the dose of which is ⅟₆₀ grain. Colchicine is readily soluble in methyl salicylate, and is conveniently administered in the form of capsules, each containing ⅟₂₅₀ gram (Martindale). In acute gout one capsule may be given every two hours, or two capsules three or four times a day. These doses are well within the limits of safety, and, if necessary, may be combined with nux vomica and belladonna; but with the alkaloids, as with the colchicum itself, it is essential that the bowels should be kept freely opened. Also with the waning of the pain and inflammation the colchicine or its salicylate should be given less frequently, so as to obviate any depression.
Atophan.—This is a yellowish cream-coloured amorphous powder of the composition 2-phenylchinolin 4-carbonic acid. Its use has been much extolled both in acute and subacute gout. The dose ranges from 30-45 grains daily for three to four days, according to some authorities, but others consider that it may be taken for prolonged periods with advantage. It is most conveniently exhibited in the form of tablets containing 4 or 8 grains. Agotan, a drug identical with that formerly sold under the German registered name “atophan,” is supplied in the form of crystalline powder and in 7½-grain tablets, and appears to be equally efficient.
Atophan is incompatible with sodium bicarbonate and other alkalies in vitro, but Martindale and Westcott “did not find it incompatible with potassium iodide.” It has been repeatedly noted that, following the intake of atophan, the uric acid content of the blood falls and the urinary uric-acid output increases. Weintraud in gouty patients on a purin-free diet noted that after atophan the quantity of uric acid excreted in the urine was more than doubled, but subsequently the excretion fell below normal.
Even in healthy individuals when taking atophan the urine becomes turbid from the presence of urates. This excess of uric acid in the urine may in gouty individuals be precipitated in the urinary tract, and so induce an attack of gravel. Consequently Weintraud advises that the drug be taken with alkalies, either sodium bicarbonate or alkaline waters. Drs. Jansen and Plum, of Copenhagen, during their recent visit to the Royal Mineral Water Hospital, Bath, informed me that they had met no instances of gravel, but in several of their cases atophan had induced urticaria.
As to the simultaneous intake of alkalies, while the precaution is probably desirable, I have known gouty patients take atophan without alkalies for several weeks in full doses without any apparent ill effects. Brugsch, indeed, states that in polyarthritis urica the subjects are able to take 15-30 grains of atophan per diem for a year without any affection of the kidneys. Moreover, uric acid excretion was increased throughout the whole period, and when the drug was discontinued, the pains recurred.
As to the usurpation of colchicum by atophan, I do not think it is at all likely, for it does not, I consider, exert the specific effect of the former on the gouty inflammatory process, taking the humbler rôle of obviating the formation or promoting the absorption and elimination of uratic deposits. In other words, colchicum influences the causa causans of gouty inflammation, atophan only the consequences or sequels thereof.
The most favourable juncture at which to prescribe atophan is at the close of a paroxysm. I have myself been much impressed with the manner in which it produces softening and palpable diminution in the size of tophaceous deposits, so much so, indeed, that I feel sure we have in this drug a valuable agent wherewith to prevent the formation of uratic deposits.
A two or three weeks’ course of atophan after an acute attack is, I have found, very advantageous, in doses of 30-45 grains per diem, after meals. It may, for the special reasons given, be well combined with an alkaline stomachic mixture taken half an hour or more before food.
℞ Potassii bicarbonatis gr. 15 Sodii bicarbonatis gr. 20 Spts. ammoniæ aromat. ♏︎ 20 Tinct. zingiberis fort. ♏︎ 5 Inf. aurantii co. ad unciam. Fiat haustus, thrice daily well diluted with water.
To sum up, our medicinal treatment of acute gout consists in initial purgation, followed by maintenance of an adequate daily evacuation; secondly, the exhibition of colchicum or its active principle and continuance of the same in diminishing doses until pain and inflammatory phenomena have departed. With the passing of the paroxysm atophan should be resorted to in combination with an alkaline stomachic mixture. Supervision of the subject should not cease until the digestive and assimilative functions have, as far as possible, attained functional efficiency, for it is certain that this is the most important point in the management of the gouty constitution. Conjoined therewith, the bowels should never be allowed to become constipated, the urine maintained free from acid lithates, and the skin active by regular exercise.
Alternative Remedies in Acute Gout.—Of the various drugs advocated as substitutes for colchicum the salicylate group alone seems to have evoked something like enthusiasm. Thus Germain Sée affirmed that sodium salicylate was the best remedy for gout, whether of acute or chronic type. In this country Haig strongly upheld its claim. On the other hand, Ebstein, when he used this salt in acute gout, found that the inflammation, though it quickly subsided in one joint, immediately reappeared in another, even though the administration of the drug was continued.
Lecorche, again, though he found it useful in acute gout, was equally certain that it was altogether inferior to colchicum. It did lessen the pain and the violence of the paroxysm, but in no way shortened its duration. But, on the other hand, he attached a prophylactic value to it in chronic gout marked by recurring subacute attacks. His method was to give it in the intervals of paroxysms in doses of from 60-80 grains a day, whereby he claimed to abort attacks, prevent ankyloses, and facilitate absorption of uratic deposits.
As to its mode of action, salicylate of soda, both in gouty and healthy subjects, determines an immediate increase in the uric acid excretion, 30-60 per cent. The increase, however, is but ephemeral, the excretion of uric acid sinking gradually to normal in about forty hours, and this whether the drug be persisted with or not. The increase in total nitrogen excretion does not reach 10 per cent.
Discussing this mode of response, MacLeod (who noted the same after citrates) is of opinion that salicylate of soda and citrate act, not by influencing the metabolic processes that originate uric acid, but by promoting the excretion thereof. Walker Hall and Magnus Levy, albeit, suggest that the increase is due to diminution in the normal destruction of purins in the organism, with resulting transmission of the same in larger quantities to the kidneys for excretion. It is possible therefore that in the presence of sodium salicylate there is diminished oxidation of uric acid.
Bain, however, studying the elimination of nitrogen in a gouty subject, found, contrary to expectation, that after sodium salicylate there ensued only a small increase in the uric acid, with a slight augmentation of the alloxur bases relative to the acid. We see therefore that all the above observers agree that an increased uric acid output in the urine follows the administration of salicylate of sodium, though they differ in opinion as to the manner of its production.
As to the employment of salicylate of soda in acute gout, it must, I think, be seldom called for, save in the presence of idiosyncratic sensitiveness to colchicum. Now, though of this latter much has been written, yet I venture to affirm it is exceptional, and the adverse symptoms are attributable rather to injudicious dosage of the individual than to inherent peculiarities on his side in respect to this valuable drug.
If we should encounter such an instance, there is no objection to our giving the salicylates of sodium or potassium a trial, especially in an acute febrile attack occurring in a healthy subject. In isolated cases the relief to pain may be swift and striking; but, generally speaking, the results are neither so decisive nor so prompt as those obtained in suitable cases by colchicum. The potassium and lithium salicylates are usually given the preference, and they may be combined with citrate or bicarbonate of potash. If the latter salt be used, the draught will prove more grateful if given in effervescent form, viz., by the addition of citric acid or lemon juice.
Frequently it happens that the patient, to begin with, has been placed on colchicum, and, symptoms of irritation having supervened, the drug has had to be withdrawn. The tardy resort then to salicylates is fortunately rather beneficial than otherwise, for, apart from its analgesic effect, it reinforces the increased uric acid output in the urine that follows the attack, and so tends to counteract the tendency to uric acid deposition.
There is yet another contingency in which resort to salicylates may be indicated, viz., in those long-standing cases of chronic gout with recurring exacerbations in which the colchicum, formerly beneficial, has now through acquired tolerance become impotent. Here, either during or immediately after the acute phases, the salicylates may be exhibited, if the stomach be tolerant and there be an absence of cardiac or renal degeneration. As to the employment of salicylates in massive doses in the inter-paroxysmal periods as a prophylactic measure, I think this is better attained by occasional courses of atophan.
Lastly, there are instances in which both colchicum and salicylates appear to be contra-indicated. In this event we may either rely simply on alkalies—and we have Duckworth’s authority that in many cases of acute gout they have proved satisfactory—or we may adopt Sir Alfred Garrod’s plan of giving quinine (2½-5½ grains) suspended by tragacanth in combination with the bicarbonate or citrate of potash. By this means the pyrexia is controlled, and, according to the above authority, any tendency on the part of the disorder to wander from joint to joint; and he holds it especially valuable in those subacute attacks that so commonly chequer the course of chronic gout.
Thyminic or nucleotin-phosphoric acid in doses of 5-10 grains has also been highly eulogised, being held to have an affinity for and a solvent action on uric acid. But Walker Hall, while he agrees that the results obtained in gout are encouraging, yet from his own experiments does not find that “the improvement is at all associated with any change in uric acid excretion—a result which also applies to citerin.”
As to quinic acid and its synthetic combinations, their popularity seems to have been evanescent. It is claimed that “urosin” or lithium quinate speedily controls the acute manifestations of gout, this apparently without any evidences of cinchonism, even though given in 7½-grain tablets ten times daily in acute paroxysms. Others give quinic acid in combination with piperazine, i.e. “sidonal” in doses of 1-1½ grains per diem. But of these, as well as of many other vaunted specifics, I feel inclined to say, with Bianca, “Old fashions please me best; I am not so nice to change true rules for new inventions.”
Anodynes in Acute Gout.—On this point it may be recalled that such was the prejudice at one time against colchicum that Ebstein thought it preferable to relieve the pain of acute gout by hypodermic injections of morphia, which, he thought, acted “quicker, more easily, and with less danger.” Fortunately, however, it is only very exceptionally that colchicum fails to mitigate the pain in acute gout.
In rebellious instances salicylate of soda in full doses for a few hours sometimes succeeds. Hypodermic injections of morphia must rarely, if ever, be called for, and I have never had occasion to invoke them. In fact, opium in any form is best avoided, and if unavoidable is best given in the form of Dover’s powder in combination with aspirin and phenacetin, viz., 2½ grains of each in a cachet at bedtime. Luff in some cases found a full dose of extract of hyoscyamus a very useful anodyne, and if sleeplessness through pain prevails, advises 7 grains of veronal or 10 grains of trional. Sir William Whitla’s “routine hypnotic in gout” is paraldehyde.
All these are preferable to opium in any form, for we deal with a disease in which defective elimination is a prominent feature, and that we should exhibit unnecessarily a drug which inhibits all excretory processes save that subserved by the skin seems wholly irrational. Of this we have an object lesson in the clay stools that in some gouty subjects, as Burney Yeo remarked, persist for some days after even a very small dose of morphia. My own rule is to rely on colchicum as far as possible, and for any extra anodyne effect on local applications, to the consideration of which I now proceed.
Local Measures in Acute Gout.
The affected limb must be kept at rest on a firm pillow and slightly raised above the body level. The inflamed part should be protected from pressure by a cradle. In the majority of instances, as the elder Garrod long since pointed out, the only local application needed is cotton wool covered with oiled silk, evenly and lightly bandaged. By this means the joint surface is kept both warm and moist, and moisture is important, as dry heat is not grateful and seems to aggravate the pain. The dressing soon becomes wet, requires changing two or three times in the twenty-four hours, when dry warm wool should again be applied, and in this way a local vapour bath of sorts is provided for the inflamed part.
If pain be marked, hot fomentations or stupes or even a foot-bath may be substituted. At one time warm spirituous lotions on lint covered with oiled silk were popular, whisky and water being much in vogue. Others (Pye-Smith) spoke well of a lotion containing 1 drachm of sulphuric ether to 6 ounces of water. Some pack the joint with warm alkaline lotions to which opium or belladonna, or both, are added; but, whether dealing with spirituous or alkaline lotions, all are agreed that cold applications should be carefully shunned.
As to anodyne preparations, we suffer from what may be truly described as un embarras de richesse; but the inexplicable variability of response is such that it is always well to have another shot in one’s therapeutic locker. Practically all the analgesic remedies in use have been recommended by some one or other as useful for the relief of pain in acute gout. The mere enumeration of these might be indefinitely extended, for in truth every one has a favourite remedy wherewith to meet certain indications, and the good results obtained are exactly proportional to the skill displayed in exhibiting their use. We should not, however, resort forthwith to the more potent analgesics. It is wiser to give the simpler remedies a prior trial, such as poppy-head fomentations. If these fail, the liniment or unguentum methyl salicylatis co. may be tried, applied on lint covered with oiled silk and a flannel bandage. Equal parts of chloroform and belladonna or of opium and menthol liniment are also very soothing when sprinkled on lint and covered with cotton wool.
In the more intense cases with great local sensitiveness the following preparations may be lightly applied to the affected area with a brush. Anodyne colloid is one of the most reliable, or we may use glycerine of belladonna or atropine, subsequently covering the part with warm, moist dressings or spongiopiline enveloped in oiled silk, cotton wool, and a flannel bandage. In using atropine preparations, however, care must be exercised, as absorption through the unbroken skin may readily cause toxic symptoms.
In less acute types or as local sensitiveness declines various ointments may be gently rubbed into the affected joint, and in this way the beneficial effects of massage superadded. The most suitable unguents are those containing methyl salicylate in hydrous wool fat with or without menthol, or the methyl salicylate may be mixed with equal parts of olive oil and applied with friction. Used in this way, it is rapidly absorbed, and is much to be preferred to the natural oil of winter-green, which not infrequently proves very irritating to the skin.
Under the influence of one or other of the foregoing methods, the pain in these forms of acute gout is usually quickly subdued. Occasionally, however, owing to incomplete absorption of inflammatory exudate, the case proves more obstinate, and a variable degree of pain and stiffness lingers on in the affected articulation.
If means permit, the ideal course to pursue is for the patient to be sent to some spa where, conjointly with the general treatment, he may enlist the advantage of hydrotherapy, massage, and so forth. In default of such facilities, we must of course fall back upon friction with liniments, being careful not to induce tenderness of the joint. Of these there are endless varieties, those containing ammonia, turpentine, camphor, or capsicum being most in vogue. Inasmuch as their efficacy is largely referable to the rubbing which accompanies their use, we should favour preparations containing oleic acid, either alone or diluted with a fatty oil. As an oily liniment perhaps one of the most useful is the linimentum succini co., containing equal parts of the oils of amber and clove combined with twice the quantity of olive oil, or one of the following excellent combinations may be selected:—
℞ Olei origani vel olei terebinthini Partes æquales. Linimenti ammoniæ. To be applied with friction to the affected part.
℞ Ætheris 1 drachm. Linimenti belladonnæ ½ ounce. Tinct. capsici To 2 ounces. To be well rubbed into painful parts night and morning.
When a joint is the seat of fixed pain with definite thickening, it may be necessary to resort to blisters; but frequently they are so utilised as to merit the aspersion of “adding additional distress to unrelieved pain.” They are of course unsuitable for cases with acute serous effusion of recent origin; but are often beneficial when applied over joints, bursæ, or tendon sheaths, when the seat of long-standing passive distension.
Garrod held them of most advantage in gout of asthenic character with lingering effusion; but he thought them inadvisable in the later stages of gout with defective kidneys and where the joints were the seat of massive uratic deposits, as in the last event sores difficult of healing may follow.
In the vast majority of instances such drastic counter-irritation is unnecessary, as the pain usually relents to less strenuous measures. For the dissipation of exudates and thickening nothing is superior to iodine and mercurial preparations. Painting with strong iodine may occasion soreness, but not if the glycerinum iodi be used. Better still is it if we use iodine preparations that admit of gentle inunction. The iodide of potassium and soap liniment is of course most reliable, or we may use one of the proprietary preparations, e.g., leukion. The oleate of mercury (10 per cent.) is often useful, and if pain linger on in the joint, may be combined with morphia (½ grain to 1 drachm). Ichthyol lanoline also deserves mention, and is best rubbed in after a fomentation followed by a dry pack. It is extremely probable that the stimulant and absorbent action of these agents is markedly reinforced by the friction which accompanies their usage.
In conclusion, it must be recalled that the swelling, stiffness, and pain are of dual origin, viz., in part due to inflammatory products and in part to uratic deposits, and it is the former that will be the most influenced by the foregoing measures. As to the means available for the reduction or dissipation of tophaceous matter, we shall best postpone their consideration until we come to discuss the treatment of tophi.
Ionisation in Acute Gout.—The introduction of medicinal substances into the interior of the joints by means of an electrical current is now in extensive vogue, both as a means of relieving pain and promoting absorption in periarticular and synovial affections. It is of course in the more accessible or superficial articulations that its beneficial effects are most easily attainable.
The sensitiveness of the parts in acute gout is such that I have never felt justified in invoking ionisation therein. Nevertheless Finzi tried it in two cases of acute gout. Instant relief of pain and diminution of swelling followed the first séance, while in sequence to a second all local tenderness disappeared. Finzi used a combination of lithium and iodine, the former at the positive and the latter at the negative pole. I would only add that in non-gouty forms of arthritis, if relief of pain be desired, salicylic ions, by general consent, would appear to be the most reliable. As far as I know, most authorities confine ionisation to chronic articular gout, and to this I shall refer later.
Massage.—The success that follows the application of stimulant or absorbent preparations in the after-treatment of acute gout largely depends on the skill and persistence with which the rubbing or kneading is performed. Hence it is that treatment by external medication has been largely superseded, and rightly so, by skilled massage, the outstanding advantages of which find increasing appreciation.
It need hardly be said that massage is contra-indicated in the acute, and its use should be confined to the subacute, stage. Moreover, I would suggest that its aid be sought more frequently during the decline of acute attacks, instead of its being reserved, as it very largely is, for the more chronic varieties of articular gout. In the latter instance organisation of the inflammatory products has already ensued, and their dispersal is correspondingly more difficult, whereas in the former the soft nature of the effused material renders dissipation more easy and, what is more important, minimises the chances of recurrence. Gentle massage also will promote the absorption and resolution of tophi, for the uratic deposits, even when pre-existing, are often found after an attack to be softened and more mobile, and now is the time to profit by these changes, so as to compass their elimination.
In these subacute stages, of course, vigorous excitation must be avoided, effleurage or light stroking being the only permissible measure at this stage; and of course it should be exercised centripetally. In presence of any marked sensitiveness, too, it is advisable that derivative massage of the limb above the joint should always precede any direct friction of the latter.
The measure of success will depend on the technique of the masseur. If he be unskilful or rough, aggravation of the inflammatory process will almost certainly ensue, with prolongation of stiffness and pain. He should proceed tentatively, the energy displayed being gradually increased as the parts grow more tolerant of manipulation.
Again, it is at the close of a massage séance that passive movements are most advantageously employed, and where irritation and pain follow their performance, gentle centrifugal stroking of the actual joint surface will exercise a grateful, soothing effect.
Surgical Methods.—The intensity of the inflammation and swelling in acute gout has, as before said, sometimes led to its confusion with purulent arthritis. It was just such a mishap that led Riedel to discuss seriously the operative treatment of gout when of monarticular type, e.g., in the great toe joint. He cites the case of a man, aged forty-five, suffering with acute gout of classic site which was operated on under the impression that the joint contained pus. None issued, but the synovial membrane was found covered with urates. The latter were removed, the wound healed in five weeks, and no recurrence of articular gout followed till fourteen years after. The second example occurred in a lady seventy years of age, who likewise suffered an acute attack of gout in the right great toe joint. An incision was made and the revealed urates removed, and the wound healed in a few weeks, and no subsequent attacks followed!
Despite the apparent good results obtained, one can scarcely believe that incision and removal of urates during acute gout will ever be seriously considered. Nevertheless the apparent impunity, if not actual benefit, that followed the above operative interference does, I think, indicate that in these aseptic days we need be less timorous; in other words, that, while the operative treatment of acute gout is unnecessary, yet in chronic cases surgery has its sphere. But to this I shall return later, when discussing the treatment of tophaceous deposits in chronic gout.
Chapter XXIX
MEDICINAL AND OTHER MODES OF THERAPY (continued)—INTER-PAROXYSMAL PERIOD
TREATMENT IN THE INTER-PAROXYSMAL PERIOD
Despite the fact that heredity plays so dominant a rôle in the genesis of gout, how relatively scanty the attention paid to prophylactic measures! It is the second, never the initial, attack of gout that we endeavour to avert. Surely to inhibit the development rather than to prevent the recurrence of the malady is the better part. The idea is not wholly utopian, for such shrewd observers as Scudamore, Austin Flint, and others, were convinced that by timely and judicious intervention a threatened outbreak might be averted or at least its severity mitigated.
It was to this end that in a preceding chapter I urged the desirability of more attention being paid to the prodromal symptoms of gout and the clarifying light that might be thrown on otherwise inexplicable derangements by the disclosure of a hereditary tendency thereto. The failure to elicit such familial predisposition is but too common, and so those who may be led to expect the gout by inheritance are bereft of all the benefit that might accrue from a prophylactic regimen.
The indications may, indeed, be more explicit, for, apart from hereditary proneness, some subjects, even though they may never have experienced an articular outbreak, yet exhibit tophi, and therewith frequently suffer from gastric or hepatic disturbance. Obviously, is not this the opportune time for prophylaxis—the institution of hygienic and dietetic rules conjoined with the occasional use of medicines? For the “potentially” gouty, as Scudamore said, cannot “too early be taught to pay the most careful regard to their constitution, nor too surely confirm the best habits by long practice.” We hear much nowadays of the “beginnings” of disease, and who can doubt that this is a fruitful sphere for their study?
Unfortunately it is, as a rule, only when the disease has made its invasion that we wake up to our responsibilities in this respect; but happily even then we may do much to prevent consolidation of its tyranny, for even in those who have experienced regular gout there are derangements to correct, warnings to note, if we do but take heed. Of these the more common are dyspepsia and costiveness, signs of portal congestion, etc., not to mention local symptoms, i.e., the onset of pricking and tenderness in already existing tophi, twinges in the toes, etc.
We see therefore that in regard to the prophylaxis of gout the victims fall into two main groups, i.e., firstly, the “potentially” gouty, who as yet have not experienced arthritic outbreaks, and, secondly, those who have, and wish to obviate their recurrence. Happily the premonitory gastric symptoms, though varied in character, are in both instances more or less similar; nor need I say that in either alike medicinal measures are but the smallest part of the prophylaxis, whose chief stay and strength must be the golden rule of temperance in eating and drinking conjoined with adequate exercise. For, whatever our views as to the proximate origin of gout, there is every reason to suppose that the principal exciting cause resides in the alimentary canal. As Sydenham long since said, “The more closely I have thought upon gout, the more have I referred it to indigestion or to the impaired concoction of matters both in the parts and the juices of the body.” Even so to-day do medical men suffering from gout tell me that they, like Sydenham, have found by experience that almost invariably dyspeptic symptoms are the forerunners of attacks, and that their avoidance or timely correction is the best means wherewith to avert paroxysms.
As to the nature of the “indigestion,” it is of subacute or chronic type, and only very exceptionally is it acute. As to symptomatology, there is nothing distinctive about the “dyspepsias” of the “gouty,” save perhaps their marked tendency to recurrence, the facility with which they are occasioned by trivial causes, their frequent obduracy to ordinary measures, and their response to such as take cognisance of the constitutional factor.
Nevertheless such is the frequency and persistence often of gastric derangements in the “gouty” that it may safely be affirmed that the treatment of these subjects in their inter-paroxysmal periods is essentially that of the “dyspeptic.” It is, in truth, the basal indication in their therapy, for correction of the “gouty” man’s digestive disabilities is the surest way to prevent articular outbreaks, or, failing this, to postpone their recurrence or mitigate their severity.
The primary object of medicinal treatment is the restoration to functional efficiency of the alimentary tract and its accessory glands and maintenance of the action of the kidneys and skin. While diet and general hygienic regulations are all essential, we often have to fight the vicious inclination of the victim who is desirous that some medicine may be found which will avert the threatened gout without his being obliged to forego his accustomed indulgence.
He must be promptly and firmly disabused of this fallacy. Indiscriminate drugging is the bane of these cases. They fly from one remedy to another rather than give up this or that excess, and so frequently superimpose a “drug dyspepsia” upon the original disorder.
The most common form of indigestion in the “gouty” is atonic dyspepsia. The primary indication is, of course, to correct the dietetic errors, i.e., to remove the cause, and, secondly, to stimulate the secretory and motor power of the stomach. To this end, the alkalies and alkaline carbonates should be administered shortly before meals in combination with nux vomica, bitters, and carminatives.
℞ Mag. carb. gr. 10 Sodæ bicarb. gr. 15 Tinct. nucis vomicæ ♏︎ 7 Spts. chloroformi ♏︎ 10 Infus. calumbæ ad unciam, ter in die sumenda ante cibos.
In the milder type of case the above may suffice, supplemented, if necessary, by some gentle aperient. Unfortunately in many instances the condition is apt to become complicated by fermentation with excessive formation of organic acids. It is to these that the “acid risings” are due, and not to excess of HCL. Indeed, the reverse is the case, viz., a deficiency of HCL. It is this that is responsible for the fermentation with the production of butyric, lactic, and acetic acids. Moreover, in middle-aged “gouty” subjects of sedentary habits there is often superadded motor defect, which may end in dilatation.
For treatment of this condition careful dieting alone may suffice. Indeed, attention to general health often succeeds where stomachic therapy alone conspicuously fails. The medicinal indications in these cases will vary according to the stage at which they are seen. In the milder forms we may stimulate the flow of gastric juice by alkalies and bitters before meals, or hydrochloric acid after food may be taken to replace the defect.
Now, theoretically speaking, this may sound very simple, but in practice it is often not so. Moreover, the less the attention paid to correction of diet and faulty habits, the more bewildering and disappointing the effect of drugs. Conversely, the more care expended on the selection of food and hygienic measures, the less need for drugs and the clearer the indications for such as may be helpful.
Thus simply under a revised diet the acid eructations may wholly disappear and the subject suffer only with languor, discomfort, or drowsiness after meals. Here dilute hydrochloric acid combined with strychnine and pepsine after food will be found useful.
On the other hand, many of these patients are impatient of dietetic control, yet nevertheless clamour for relief of their “acid” eructations. In such cases alkalies must be given an hour or so after meals to correct the excess of organic acids. The same may be combined with antiseptics—carbolic, B. naphthol, creosote, etc.—or some artificial digestive, such as papain, pancretin, or taka-diastase.
℞ Bismuth carb. gr. 15 Calcii carb. gr. 5 Acid. carbol. pur. ♏︎ ½ Oleum cajeput ♏︎ 2 Fiat cachet, 1 or 2 an hour or more after meals.
The calcium and bismuth carbonates are best, inasmuch as, though they act slowly, they give rise to no secondary hypersecretion. Of digestive adjuvants in these cases, Luff speaks highly of taka-diastase (gr. 2½) immediately before meals in addition to bismuth and alkalies. The taka-diastase assists the digestion of carbohydrate foodstuffs, and so lessens or inhibits the formation of organic acids. But as a digestive adjuvant in these cases of “dyspepsia” with acid eructations papain is most useful, acting in acid, alkaline, or neutral media. This indifference on its part enables us to combine it with alkalies, and so attain the dual effect of reinforcing the digestive capacity and neutralising hyperacidity.
℞ Mag. carb. pond. gr. 15 Sodii bicarb. gr. 10 Papain gr. 3 Oleum caryophylli ♏︎ ½ Fiat cachet, 1 or 2 after meals when acidity is at its height.
Our forefathers in such cases thought highly of rhubarb and magnesia, and certainly in hospital patients some such combination as the following is invaluable in so-called “gouty dyspepsia”:—
℞ Mag. carb. gr. 10 Sodii bicarb. gr. 15 Acid. carbol. pur. ♏︎ 1 Tinct. rhei co. ♏︎ 15 Spts. chloroformi ♏︎ 15 Inf. caryophylli ad unciam, ter in die post in cibos.
Almost always in these cases more or less constipation prevails, which must be corrected. To this end, of course, the magnesia contained in one of the above cachets may be all that is necessary; but often it is not so, especially if the subject be taking bismuth. Moreover, inasmuch as we have to take cognisance of the constitutional taint in these individuals, we may with advantage give an occasional aloetic pill containing colchicum or a nightly dose of guaiacum and sulphur. Again, if the urine be scanty, we may substitute a morning draught of phosphate of soda (¼-½ ounce), which not only stimulates the liver, but exercises also an antacid and diuretic effect.
℞ Ext. colchici gr. ¼ Aloin gr. ¼ Menthol gr. ½ Ext. rhei gr. 1 Fiat pil., 1 alternis noctibus sumenda.
As soon as the symptoms of fermentation and organic acidity relent to the above or similar measures we should, if possible, dispense with drugs and rely wholly on diet and general hygienic regulations; but unfortunately a case of atonic “dyspepsia,” if of prolonged duration, gradually merges into one of chronic gastritis. Especially in those given to alcoholic indulgence do we meet with a condition of mucous catarrh, with its associated deficiency of hydrochloric acid. Indeed, apart from alcoholic excess, such is the frequency in “gouty” subjects of this form of “dyspepsia,” i.e., fermentation with excess of organic acids, that I am inclined to think that the subacidity which permits of such developing is, if I may say so, the inherent digestive disability in “gouty” subjects. Unquestionably hyperacidity—i.e., excess of organic acids due to hypochlorhydria—is in their instance infinitely more common than hyperchlorhydria, or excess of HCL, that is, much more frequent than the latter as differentiated from organic acidity by the only possible means, viz., an examination of the stomach contents.
Again, accepting the view that infections are the chief excitants of gouty paroxysms, the desirability of reinforcing the antiseptic action of the gastric juice is obvious. In other words, the defensive powers of the stomach against intruding microbes must be raised by prescribing hydrochloric acid. For this purpose it is well to use strong or fuming hydrochloric acid in doses of from 5-10 minims, freshly mixed at the time of administration with 6-8 ounces of water, and the same taken at every meal. The hydrochloric acid may with convenience be placed in a drop bottle, and beginning with 5 minims, an extra minim may be added every few days until 10 or 15 minims are taken at each meal.
Some years ago Armstrong, of Buxton, spoke highly of its value in alimentary toxæmia, which is precisely the condition we are confronted with in gout. Falkenstein, again, highly eulogises it in the latter disorder. He gives from 40-60 drops of pure hydrochloric acid in a large quantity of effervescing water each day. It is taken during meals, and the dilution with water is arranged so that the patient is struck by the acid taste. The diet taken was an ordinary one, and yet Falkenstein noted that the dyspeptic symptoms disappeared and the attacks of gout grew more rare and much less severe. As an alternative to water, either still or effervescing, the hydrochloric acid in from 5-15 drops may be given in mucilage, or, if preferred, we may give the dilute hydrochloric acid in some such form as the following:—
℞ Acid. hydrochlor. dil. ♏︎ 10-15 Glycerin pepsinæ dr. 1 Liq. strych. hyd. ♏︎ 3 Tinct. capsici ♏︎ 1 Inf. aurantii co. ad unciam, ter die sumenda statim post cibos.
Sometimes it so happens that while taking the above acid mixture the subjects an hour or more after meals complain of acidity. If so, it is due to fermentation, and at the time of its occurrence must be met by an adequate dose of an alkali with or without some antiseptic preparation. It goes without saying that if such can be referred to dietetic errors—food-bolting, etc.—these also must be corrected.
In these cases, too, the liver is frequently inactive, though often their attacks of “biliousness” signify nothing but constipation; but when there are definite signs of hepatic torpor we may substitute for the hydrochloric acid in the above mixture the dilute nitro-muriatic acid. Simultaneously we may occasionally at night give a pill containing calomel, iridin, or podophyllin combined with aloes and belladonna, or we may instead invoke colchicum as a cholagogue, following it up in either case the morning after by a saline purge. As a substitute we may in suitable cases order every morning for some days a full dose of Rubinat, Hunyadi Janos, or other bitter water.
So much for the more common derangements of the inter-paroxysmal period and the measures wherewith to combat them. Collectively their aim is the restoration to functional efficiency of the alimentary canal and its accessory glands, this to the end that, as far as possible, a condition of intestinal asepsis may be attained, with its correlated diminution of the excitants most fertile of outbreaks.
Nevertheless, from time to time, either from failure of the patient’s co-operation or other mischances, our best efforts at prophylaxis fail, and it becomes clear that an attack is imminent. What then, save brisk purgation, can be done to avert the threatened outbreak? Our forefathers, in cases in which the fits recurred periodically and might be forecast with tolerable accuracy, were accustomed some time before the threatened attack to place the subject on a rigorous diet, this in combination with a course of alkalies, those of soda being given the preference in dyspeptic or hepatic disturbance and those of potash when the urine was scanty.
That this was sound treatment and abundantly justified by the results is well acknowledged, and all I would suggest is that this is yet another juncture at which atophan is indicated, viz., immediately before a paroxysm. At this particular time the urinary output of uric acid is often diminished, a clear indication for enlistment of atophan, which increases uric acid elimination. I note that both Retzlaff and Brugsch consider it an especially advantageous time for its exhibition. As a prophylactic measure the former gives 30-45 grains daily for three days at intervals of a fortnight, and if cardialgia or heartburn ensues, adds ¼-½ teaspoonful of bicarbonate of soda to each gramme of the drug.
Lastly, we have to recollect, too, that colchicum is credited with some prophylactic powers. Some, it is true, discountenance its employment in the inter-paroxysmal period, on the plea that it tends to favour recurrence and chronicity of attacks. While I think it is better to reserve it for acute or subacute attacks, still I have not found that colchicum, given in what Sir Thomas Watson called alterative doses, is anything but beneficial, provided that it be taken intermittently, not continuously, for long periods. As to special indications for its employment, I think it is more effectual in aborting a threatened attack when, in addition to dyspeptic phenomena, the imminence of a fit is betokened by what may be termed specific harbingers thereof, i.e., pricking and tenderness in existing tophi, twinges in the toes, etc.
In conclusion, are we not in this matter of the prophylaxis of gout somewhat too prone to resort, both in and out of season, to what we are pleased to term special medication? Almost every week some new and of course infallible “uric acid solvent” is lauded ad nauseam in the press. Are not we ourselves, too, somewhat overanxious to go with the tide in prescribing these vaunted “gout specifics”?
The true aim of prophylaxis is rather to prevent the incidence of those functional derangements that in some subtle way determine the disturbances in nuclein metabolism, with secondary accumulation of uric acid in the organism. That drugs, such as atophan, which diminish the uric acid content of the blood and increase its urinary output, fulfil an invaluable rôle in ridding the system of excessive amounts of this chemical outcast, I fully admit.
Albeit, this achievement does but deal with the consequences or sequels, not the exciting causes, of gout. In truth, there is no short cut to the cure of gout. Only under suitable treatment, applied to meet all the necessities of individual cases, will any long immunity from its onslaughts be secured or their intensity attenuated.