Part 17

Garrod, in a paper read at the International Medical Congress in 1881 {122} on "Eczema and Albuminuria in Relation to Gout," affirms that each year strengthens his conviction that gout and eczema are most closely allied. Since his attention was first called to this relation in 1860, he has found a gradually increasing percentage of eczema in the cases of gout that have come under his observation. Dividing all the cases from 1860 to 1881 into ten groups, he found the percentage rose from 10 in the first group to 47 in the tenth. He accounts for this rapid increase in the percentage in the fact that in the first few years the eczema was only observed when it was very patent; during the past two or three years he has had made more careful inquiries as to the presence of eczema or other skin eruption in every case of gout, and by these means has frequently discovered its presence when it might otherwise have been overlooked. Garrod believes that eczema is the special skin-lesion of gouty subjects, and does not regard psoriasis as having anything more than an accidental connection with gout. He admits that the latter is often associated with rheumatoid arthritis. It must be remembered, however, that Garrod does not admit that gout ever exists without lithatic deposits.

In regard to the location of gouty eczema, it appears to affect by preference the more tender and vascular regions of the skin. The eyelids, ears, the scalp, and back of the neck, the fingers and toes, particularly the dorsal and lateral surfaces, and in old people the legs, are especially liable to be attacked. The subjective symptoms of gouty eczema are often the source of great suffering; the burning and itching are sometimes intolerable. This is especially true of persons of highly neurotic constitution.

It is not possible to affirm that there are lesions of the mucous membranes which are strictly analogous in their transient character to the erythematous affections of the skin, but it is not unreasonable to suppose that many of the temporary disturbances of indigestion to which gouty patients are subject are caused by an evanescent hyperæmia corresponding to the vaso-motor derangements which are observed in the external integument. In regard, however, to the more persistent catarrhal lesions, there can be no question as to their analogy with those which affect the skin. The continuity of these lesions at the orifices of the mucous tracts, and the frequent association of external eczemas with catarrhs of mucous membranes, are facts of common experience. Greenhow of London first called attention to the frequency with which chronic bronchitis is associated with the gouty dyscrasia. In an analysis of 96 cases of chronic bronchitis he elicited the fact that in 34 out of the 96 a distinct gouty history attached either to the patients themselves or to some of their immediate relatives. In 14 of the cases the patients were subject to attacks of acute regular gout as well as to bronchitis. He also noted the association in a number of cases of bronchitis and psoriasis with gravel and gout. My own experience confirms these observations, and also the alternations of catarrhal and parenchymatous tonsillitis, of pharyngeal and laryngeal catarrh, and of asthma and chronic bronchitis, with the more common manifestations of regular and irregular gout.

The occurrence of subacute gastro-duodenal and intestinal catarrhs {123} with hemorrhoidal complications is even more common that the catarrhal affections of the respiratory tract. The lesion, in fact, which gives rise to the manifold dyspeptic symptoms in gouty subjects is doubtless a catarrhal one.

The genito-urinary tract exhibits also the tendency to catarrhal affections in sufferers from the gouty dyscrasia. It is certain that gouty persons are especially liable to vesical catarrh, and it is generally admitted that rheumatic and gouty persons are particularly susceptible to gonorrhoea. My own experience leads me to suspect that chronic urethral discharge resulting from acute urethritis is more common in rheumatic persons than in those not having this taint. The etiological relations of gonorrhoeal rheumatism and kerato-iritis are still involved in obscurity, though I am inclined to believe that a careful examination of the personal and family history in cases of these diseases would establish the opinion that has been maintained as to their gouty origin.

The presence of albumen in the urine of persons suffering from acute gout is occasionally observed. Under these circumstances it is transient, and has probably no more significance than is usually attached to this symptom in the course of any acute febrile disease. In chronic gout it is by no means infrequently observed as a more or less persistent symptom. It is associated under these circumstances with a copious discharge of urine of pale color and low density, and with the general signs of what Rayer first described as the néphrite goutteuse.

The importance of this symptom is very great when we consider the insidious development of this form of disease and the difficulty of its early diagnosis. Recent investigations point to the value of the changes in the urine in the progress of the gouty dyscrasia as bearing upon this question. It has already been noted that in the early history of gouty persons the urine is often scanty, high-colored, excessively acid, of high specific gravity, occasionally albuminous and saccharine, and frequently depositing sediments of urates and calcium oxalate. McBride of New York has recently called attention to this condition of the urine and its association with high arterial tension as the functional stage of the granular kidney--as the stage, that is to say, during which the necessity of eliminating large amounts of imperfectly oxidized nitrogenous material maintains a constant state of renal hyperæmia, which finally induces the changes in the tubular and intertubular structures which constitute the anatomical features of this form of disease.

The occasional presence of sugar in the urine of gouty persons has already been noted. I have repeatedly observed this symptom in the urine of gouty dyspepsia. It occurs more commonly in obese subjects, and is usually intermittent and easily controlled by dietetic restrictions. In these cases it is not necessarily associated with a very large amount of urine. In chronic gout and in connection with the granular kidney a more serious form of glycosuria is occasionally observed. Under these circumstances it increases largely the polyuria which is characteristic of gouty nephritis, and is sometimes overlooked because it occurs in a urine of a low density, often not more than 1.010. It is not controlled by diet {124} to the same extent that it is in the cases previously described, and is in my experience a prognostic sign of bad import.

Some of the most distressing symptoms to which gouty persons are especially liable are those connected with the passage of gravel from the kidney to the bladder. Where gravel alone passes, it may cause little uneasiness, and the fact is only recognized through the discovery of blood in the urine in connection with uric acid or calcium oxalate crystals. When, however, the sand forms concretions in the pelvis of the kidney, their dislodgment and passage through the ureter are accompanied by the well-known agonies of renal colic.

Dysuria is a symptom from which gouty persons often experience much inconvenience and suffering. It is usually associated with extremely acid urine of high density containing crystalline sediments. It may manifest itself only in frequent and painful micturition, or it may be associated with such a degree of vesical tenesmus as to cause retention and necessitate the use of the catheter.

DIAGNOSIS.--If the term gout be restricted to that form of arthritis in which an excess of urates is found in the blood with tophous deposits in the affected joints, the cartilages of the ear and nose, and in the subcutaneous connective tissue, then the diagnosis of this disease is a simple one. It is a disease with a pathognomonic sign. But if the pathology of gout consists rather in a more complex morbid condition of the blood, of which an excess of urates in the serum is only one of a number of phenomena, and not necessarily the sole and essential cause of the local lesions, then the question of diagnosis involves a consideration of all the correlated morbid conditions which are so frequently associated in gouty persons and gouty families as to justify the inference that they have a common origin in a perverted nutrition, the essential nature of which is imperfectly understood.

The very existence of the terms gouty rheumatism and rheumatic gout which are in common use shows that what is regarded by many excellent authorities as the confounding of distinct entities must have some foundation in clinical experience. If we consider gout, in its strictest pathological sense, acute inflammatory rheumatism, rheumatoid arthritis, or gouty rheumatism, and senile arthritis or the arthritis deformans and gonorrhoeal rheumatism as separate and distinct diseases, we shall find ourselves compelled to ignore certain common clinical facts which indicate a bond of union between them. Heredity, for example, is common to them all, and more than this, there appears to be a tendency to a differentiation of the taint in families. It is well known, for instance, that the children of gouty parents are especially liable to acute rheumatism, and acute rheumatism in youth is often followed by gout in later years. It is also a fact of common experience that while the men in gouty families are the victims of true gout, the women are apt to be the subjects of rheumatoid arthritis. The arthritis deformans which develops with the degenerations of advancing years is not infrequently associated with a family history of genuine gout. Gonorrhoeal rheumatism also, according to the experience of many trustworthy observers, often recognizes an inheritance to gouty lesions. But it is not alone in heredity and the differentiation of the type of the disease in families that the unity of these affections displays itself. The same disturbances of digestion which {125} characterize the history of true gout are observed in those who are liable to acute rheumatism, to rheumatoid arthritis, and to arthritis deformans. It is true that excesses in food and fermented liquors do not determine, as in gout, attacks of acute rheumatism nor of the chronic forms of arthritis, for these latter diseases are commonly due to causes operating upon the nervous system, as exposure to cold and dampness or to physical or emotional shock of some kind; still, there is in the subjects of these diseases a more or less marked tendency to the same dyspeptic disorders, and especially to the diminished capacity in digesting the carbohydrates, which the subjects of true gout exhibit. In the diagnosis of gout, therefore, it would seem that the question of differentiating this disease from those which simulate it is not one in which we are called upon to distinguish one morbid entity from another, as typhus from typhoid fever or syphilis from cancer, but rather to determine, first, the presence of a recognized constitutional vice; and, secondly, to differentiate the variety of the lesions by which this vice manifests itself.

In the diagnosis of the gouty dyscrasia the first point to determine is that of heredity. This requires a careful inquiry into collateral as well as direct descent, and does not necessarily involve the discovery of arthritic diseases in the ancestors, though these are doubtless the most striking and trustworthy proofs; but the tradition in the family of persistent dyspepsia, or what is commonly called biliousness, of chronic catarrhal affections of the skin and mucous membranes, and of the chronic forms of renal disease, are significant indications of this dyscrasia. In the personal history the evidences of the lithæmic tendency, as indicated by the characteristic dyspeptic symptoms which have been described, and especially by the feeble capacity for the digestion of carbohydrates, are of great diagnostic value.

The diagnosis of gouty joint-lesions, whether acute or chronic, depends partly upon the determination of the gouty dyscrasia, and partly upon the differential distinctions which separate gouty inflammations from acute rheumatism, rheumatoid arthritis, and from the arthropathies which result from traumatism and from lesions of nerves and nerve-centres.

Gouty arthritis may be distinguished from acute rheumatism by the fact that it is more often hereditary--that it occurs in older subjects, attacking generally the smaller joints, and, as a rule, in the acute form, localizing itself in one or two joints. It is also noteworthy that the constitutional symptoms are not as severe as in rheumatism. Gout deforms the joints, while acute rheumatism leaves no traces of the inflammatory process. In addition to these distinctions there is, according to Garrod, the crucial test of an excess of urates in the blood-serum.

From rheumatoid arthritis or rheumatic gout, gout in its acute and regular form is distinguished by the more acute local and constitutional symptoms. Gout is periodical in its attacks, while rheumatoid arthritis is progressive. It attacks the smaller joints or those most exposed to strain, while rheumatoid arthritis occurs in the large as well as the small joints, and appears to be more independent of traumatism as an exciting cause. Gout is more common in men, rheumatoid arthritis in women. According to Garrod and other excellent authorities, deposits of urates are never found in the joints in rheumatoid arthritis, and there is no excess {126} of urates in the blood. This statement is denied by Hutchinson. Ulcerations of cartilages, contractions of tendons, atrophies of muscles with subluxations of joints, are more common in rheumatoid arthritis than in gout.

While these local distinctions are undeniable, it is proper to observe that in rheumatoid arthritis the constitutional symptoms of the gouty dyscrasia, especially the dyspeptic derangements and the nervous disturbances, are often well marked; and it should also be noted that the principal distinction, the absence of urates in the blood and in the diseased joints, is one that is based on the exclusive theory that uric acid is the materies morbi of true gout. If, as is still maintained by some excellent authorities, uric acid is not essential to gout, then it must be confessed that the other distinctions are purely lesional, and that the common constitutional symptoms suggest that these diseases are divergent branches of a single trunk.

Gouty arthritis is not always easily distinguishable from traumatic inflammation of the joints, inasmuch as traumatism plays so important a part as an exciting cause of gouty attacks. The history of previous seizures and the presence of predisposing causes of gout are the points upon which the determination of the gouty nature of the inflammation would depend. A termination in suppuration would exclude the idea of the gouty nature of an arthritis.

With the arthropathies of purely nervous origin, such as occur in paralyzed limbs, in Pott's disease, and in tabes dorsalis, gout can hardly be confounded, although the arthritic complications in these diseases have been used to illustrate the neurotic theory of both gout and rheumatism.

The diagnosis of irregular gout--i.e. of gouty affections of the skin and mucous membranes, of the structures of the eye, and of the parenchymatous organs--must be based more upon the hereditary history and upon the correlated phenomena recognized in the personal history than upon any specific character in the lesions themselves. In the gouty form of nephritis there are, it is true, in the urinary symptoms, in the anæmia, in the arterial fibrosis, and in the cardiac hypertrophy, diagnostic signs of great value.

PROGNOSIS.--Acute, regular, articular gout is probably never a fatal disease where it occurs in a robust person without visceral complications. In rare instances the first attack may never be repeated, or only two or three attacks may occur in the course of a long life. In the majority of instances, however, frequent repetitions are the rule, the intervals between the attacks growing progressively shorter; occasionally repeated seizures go on through a long life, the attacks becoming milder with advancing years, and, save the crippling effects of the disease, the patient may enjoy in the intervals a fair degree of health. This, however, is the exception. With the increased frequency of the arthritic attacks the signs of the constitutional vice become more marked. The dyspeptic disorders become more persistent and rebellious to treatment, various transformations of the disease manifest themselves, and tissue-changes make insidious and inevitable progress. When this stage of the gouty disease is reached, the prognosis becomes more grave because of the complications and accidents to which the sufferer is liable. These complications and accidents are the result of the nervous, vascular, and visceral lesions which have been {127} described. Vaso-motor instability gives rise to a great variety of painful functional derangements resulting from serious cerebral, pulmonary, gastric, and renal congestions. Glycosuria is not an uncommon complication in chronic gout, and seriously affects the question of prognosis. Arterial degenerations may cause thrombotic accidents, and the formation of miliary aneurisms in the brain may determine a fatal issue by softening or hemorrhage. Anginal attacks due to cardiac muscular degeneration may also imperil life.

The principal visceral lesion which leads directly or indirectly to a fatal issue in gout is that of the kidney. This involves danger either through the induction of a hopeless anæmia and its consequences in dropsical effusions, or by determining inflammatory accidents of the gravest nature.

That gout shortens life in the majority of cases is unquestionable--a fact which is sufficiently attested by the care with which life-insurance companies exclude risks in which a well-pronounced inherited tendency or existing manifestation of the disease can be substantiated.

The prognosis varies of course with the rapidity with which the constitutional dyscrasia is developed, and this rapidity will depend on the intensity of the inheritance and the mode of life. Some gouty subjects escape the vascular and visceral complications of the disease for a long period, although crippled and deformed by its articular ravages, and attain advanced age; others may succumb in comparative youth to its most profound lesions. It is a happy circumstance that under wise hygienic management and judicious medication acquired gout may be checked in its progress, and even a strong inherited tendency may be largely controlled.

TREATMENT.--A logical consideration of the treatment of gout embraces, first, the treatment of the constitutional vice, based, as far as possible, on the nature and causes of the disease; and, secondly, the treatment of the lesions which the disease determines. If we regard the accumulation in the blood-serum of the salts of uric acid as the essential cause of the gouty lesions, then the origin of the constitutional vice is in the conditions which bring about this accumulation. As we have urged, none of the theories of the production of the lithæmic state harmonize all its phenomena. It is impossible to represent the complex processes of nutrition by chemical formulæ, and equally impossible to divorce chemical reactions from a share in their production. We can trace the metabolism of the azotized and carbonaceous foods through many changes to their ultimate disintegration into urea, carbonic acid, and water, but we do not know all the steps by which this conversion is effected, nor the organs or tissues in which it is accomplished. We may reasonably assume that the agent through which the potential energy of the food is evolved is oxygen, and that the process of nutrition is hence partly, at least, a process of oxidation. This chemical view of the digestion and assimilation of food may be said to be the rational basis of the treatment of the lithæmic state. To control the accumulation of azotized matters in the blood, and to secure their thorough combustion and conversion into urea, carbonic acid, and water are the recognized aims of the treatment of the vice upon which gout depends.

DIET.--The prevention of the accumulation of azotized matters in the {128} blood involves, first, a consideration of the question of the diet appropriate to the gouty dyscrasia. The almost uniform counsel upon this point of all the authorities from Sydenham to the present time is, that albuminous foods should be sparingly allowed in the diet of the gouty patient, and that vegetable foods, especially the farinaceous, should constitute the principal aliment. This counsel is based upon the theory that uric acid is the offending substance, and, this being the outcome of a nitrogenous diet, the nitrogenous element in diet must be reduced. My own observation has led me to believe that while this may be a legitimate deduction from the uric-acid theory of gout, it is not supported by the results of clinical experience. If there is one signal peculiarity in the digestive derangements of gouty persons, it is their limited power to digest the carbohydrates, the sugars and starches. In whatever form these foods are used, they are more commonly the source of the dyspeptic troubles of sufferers from gout than the albuminous foods. They provoke the acid and flatulent dyspepsia which so generally precedes the explosion of the gouty paroxysm; and it must have attracted the attention of every observer who has studied the dyspeptic disorders of sufferers from inherited gout, who have sought to control their unhappy heritage by abstemious habits, that these disorders are especially provoked by over-indulgence in saccharine and amylaceous foods.

It is not possible to explain satisfactorily why the lithæmic condition should be induced by the carbonaceous aliments, but we believe there can be no question as to the fact. If, as modern physiological investigations tend to show, the liver is the organ in which urea as well as glycogen is formed, it may be that the overtaxing of its functions manifests itself more readily in the conversion of the albuminous than in that of the carbonaceous foods; or it is possible that the carbonaceous foods are destined chiefly for the evolution of mechanical energy, and that when this destiny is not fulfilled through indolence and imperfect oxygen-supply, they escape complete combustion, and so vitiate the blood. But whatever may be the cause of this anomaly, the clinical fact remains that in gouty persons the conversion of the azotized foods is more complete with a minimum of carbohydrates than it is with an excess of them--in other words, that one of the best means of avoiding an accumulation of lithates in the blood is to diminish the carbohydrates rather than the azotized foods.

The diet which a considerable experience has led me to adopt in the treatment of the gouty dyscrasia is very similar to that which glycosuria requires. The exclusion of the carbohydrates is of course not so strict. Abstinence from all the fermented preparations of alcohol is perhaps the most important restriction, on account of the unfermented dextrin and sugar which they contain. This restriction accords with the common experience respecting the part which wine and beer play as predisposing causes of the gouty disease and as occasional exciting causes of gouty lesions.