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A System of Practical Medicine. by American Authors. Vol. 2 · William Pepper — chapter 15 of 249 · ~4,186 words · public domain

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The course, termination, duration, and prognosis need not be insisted upon after what has gone before. The duration is very variable. Many recover in four to eight weeks, many not for three to six months and longer; relapses are of frequent occurrence; complete and tolerably prompt recovery is not uncommon in first attacks and in young and healthy subjects; rebellious persistency, and even deformity, with impairment of the articular movements, and not infrequently even fibrous ankylosis of one or many joints, sometimes including the vertebral, may be observed. Indeed, the most formidable examples of spondylitis are associated with gonorrhoeal rheumatism as its exciting cause. These unfavorable issues are most apt to follow repeated attacks in unhealthy and especially scrofulous persons. Both rheumatoid arthritis and strumous articular disease have appeared as sequels of gonorrhoeal rheumatism. Life is not endangered, except in very rare instances in which cardiac or cerebral {107} complications obtain; and to stiffened enlarged joints the functions may often be restored by efficient treatment.

DIAGNOSIS.--In some instances no doubt what appears to be ordinary gonorrhoeal rheumatism, owing to the coexistence of urethral discharge and articular inflammation, is really pyæmic arthritis. The intermediate link in the causation may be suppuration in the prostate or its veins or in the testicle or the penis or in its dorsal vein, or the urethral pus may undergo changes and become septic and be absorbed. In other instances it is highly probable that true primary acute articular rheumatism sometimes occurs coincidentally with gonorrhoea. If in addition to the presence or recent existence of gonorrhoea the case present several of the following features, gonorrhoeal rheumatism may be said to exist: moderate or mild pyrexia and articular pain; the number of joints attacked being few, with a tendency to concentration in one, either from the first or secondarily; no migration from one joint to another; no delitescence, but marked chronicity and indolence, with a tendency to hydrarthrosis and to implication of the synovial sheaths and bursæ; an absence of cardiac complications; the frequent and often early coincidence of special ophthalmic affections.

TREATMENT.--The patient should be confined to bed, so as to secure rest to the inflamed articulations, and when severe arthritis (third form) exists an efficient splint is peremptorily required, and its application is often followed by prompt relief to the pain. It should be retained until not only all pain, but all tenderness on pressing the articulation, has disappeared. In short, the principles and details of local treatment suited to gonorrhoeal rheumatism are the same as those recommended for rheumatoid arthritis, which it so closely resembles; and the reader is referred to that article for information. Although there is a greater proclivity to copious effusion into the joints in gonorrhoeal rheumatism than in rheumatoid arthritis, there is less to those deeper lesions which affect the bones, and complete recovery is usually more certain and more prompt in the former than in the latter. Measures to prevent stiffness and even ankylosis of the articulations are often an urgent indication. In the general treatment, also, almost the same remedies are indicated as have been recommended for rheumatoid arthritis. The salicylate of sodium, given freely, is sometimes signally useful, more especially when several joints are acutely inflamed. In the more chronic stages, when much articular effusion exists, a prolonged course of potassium iodide is occasionally beneficial. The local measures, however, simultaneously employed, doubtless co-operate efficiently. Iron and quinia will frequently be demanded by general debility, anæmia, and impaired nutrition; and the same may be said of cod-liver oil, extract of malt, etc. The circumstances under which the various baths are likely to be useful have been mentioned in connection with the treatment of rheumatoid arthritis.

The gonorrhoea should be treated in the same way that it ought to be if no arthritis existed. The rest, the moderate diet, and even the salicylate of sodium, favor its removal, but the frequent employment of mild astringent injections should not be omitted.

{108}

GOUT.

BY W. H. DRAPER, M.D.

DEFINITION.--Gout, as a disease, in the traditional acceptation of the term, is a specific arthritis, characterized by the deposit of the salts of uric acid in the affected joints. Gout, as a diathesis, is a blood crasis in which there is an accumulation in the blood serum of the uric acid salts, the consequence either of the increased formation or of the defective excretion of these products of proteid metamorphosis. The manifold irritations of the different tissues, and the accompanying subjective and objective symptoms provoked by this dyscrasia, are termed gouty.

SYNONYMS.--(a) Eng., Gout; Lat., Gutta; Fr., Goutte; Sp., Gota; Ger., Gicht--derived from the nomenclature of humoral pathology and descriptive of the distillation (goutte à goutte) of the poisonous humor into the joints--arthritis uratica. (b) Gouty diathesis; constitutional gout; irregular gout.

CLASSIFICATION.--(a) Gout as a specific form of articular inflammation is classified according to its location--cheiragra, onagra, podagra, gonagra, etc. (b) Gout as a constitutional disease is classified, 1st, according to the structures affected--e.g. articular gout; tegumentary gout, embracing mucous as well as cutaneous affections of gouty origin; nervous gout; parenchymatous or visceral gout; 2d, according to the degree of the inflammatory process--acute, subacute, and chronic; 3d, according to certain irregularities manifested in the development and progress of gouty lesions as metastatic, retrocedent, and suppressed gout. This classification of constitutional gout is based upon the well-recognized clinical observation in the history of gouty persons and gouty families, that the characteristic lesions of the joint-structures are often correlated with lesions of the skin, mucous and serous membranes, vessels, nerves, and parenchymatous organs, which are marked by the same blood dyscrasia that exists in articular gout, and which are most successfully treated by the same measures which experience has suggested in the management of the arthritic disease.

Musgrave in his work treats of a great number of varieties of gout, as follows: De arthritide anomala; de colica arthritica; de diarrhoea arthritica; de dysenteria arthritica; de abscesse intestinorum arthritica; de melancholia arthritica; de syncope arthritica; de calculo renum arthritico; de asthmate arthritico; de catarrho, tussi, et peripneumonia arthritica; de phthise arthritica; de angina arthritica; de capito dolore et {109} vertigine arthritica; de apoplexia arthritica; de paralysi arthritica; de doloribus in corpore vagis, fixis; de ophthalmia, de erysipelate et achoribus arthriticis; etc.

HISTORY.--The records of medicine furnish simple evidence of the prevalence of gout in all ancient as well as in modern civilized communities. Its origin in the perversion of physiological functions was as clearly recognized by the prophets of the old testament of the medical art as it is by the founders of the gospel of modern science. The refined processes of animal chemistry have simply revealed the materies morbi which was foreshadowed in the "peccant matters" of the humoralists, which were supposed to be distilled into the joints and other structures, provoking inflammation and tophous deposits. This is the most notable and interesting fact in the history of gout, that it has from the earliest times been regarded as a specific form of arthritis and dependent upon the circulation in the blood of peccant matter. It was not, however, until the latter part of the eighteenth century, when Murray Forbes, and a few years later Wollaston, called attention to the fact that uric acid was the chief ingredient in urinary calculi and in tophous deposits, that our knowledge of the pathology of gout may be said to have had its beginning. The demonstration by Garrod, in 1848, of the presence of lithate of soda in the blood of gouty persons, also marks an era in the history of the pathology of gout.

While the humoralistic theory of gout has prevailed almost to the exclusion of all others, it is historically interesting to note that the views of the solidists, as represented by Cullen, who maintained that "gout was an affection of the nervous system in which the primary moving powers of the whole system are lodged," have been recently revived and are attracting considerable attention.

ETIOLOGY: PREDISPOSING CAUSES.--Heredity may be regarded as the most prominent of the predisposing causes of gout. Statistics of arthritic gout show this tendency in a varying but always large proportion of cases. Scudamore observed it in nearly 60 per cent. of his cases; Garrod, in 50 per cent. of his hospital cases and, in a much larger proportion, in his private practice; Gairdner found it in 140 out of 156 cases. If all the manifestations of the gouty vice were taken into consideration in determining the influence of heredity, it would doubtless be shown in a still larger percentage of cases.

It is generally supposed that there is a greater frequency of inheritance from the male ancestors and in the male descendants. This may be explained by the fact that men are more exposed to the other predisposing and to the exciting causes of gout. My own experience leads me to suspect that if we took into consideration the irregular manifestations of this morbid inheritance, we should find it as frequently in the female, both in the ascending and descending line; of the greater frequency of acute articular gout, however, in the male, there can be no question. While it is true that acute attacks are comparatively rare in women, both before and after the menopause, it is undeniable that the subacute and chronic forms of gouty arthritis are by no means rare in them, both before and after the cessation of menstruation. The Hippocratic proposition that women enjoy immunity from gout by reason of the menstrual flux can hardly be entitled to much consideration in view {110} of the fact that they are commonly less exposed to the exciting causes of the disease, and that when they subject themselves to the same vicious habits which entail the disease in men they suffer like men.

Statistics as to the age at which articular gout is most often developed show that the larger proportion of cases occurs in the decade from thirty or forty. It is rare before twenty, and the frequency diminishes rapidly after sixty. Some well-authenticated cases have been observed before puberty in children in whom the hereditary taint was strongly developed. Gairdner claims to have seen several cases in infants at the breast. Trousseau saw a case in a boy aged six, and Garrod in a youth of sixteen. At the other extreme Garrod reports a first attack at the age of eighty, and another in the ninetieth year. The cases at the extremes of age are certainly rare, and other causes of arthritic inflammation might easily be invoked to explain them. It is a significant fact that the largest proportion of attacks of acute articular gout occurs after the period of complete development is ended and before the period of degenerative changes has begun, when the necessities of growth have ceased and food is required only for the nutrition of the tissues, the maintenance of vital energies, and the demands of work.

Much stress was laid by the earlier writers on the effect of temperament as a predisposing cause of gout. The vague ideas involved in the classification of mankind according to temperament may be said to have lost their influence in the scientific conceptions of modern pathology. Gout is observed in persons exhibiting the most diverse peculiarities in physical conformation and physical disposition. The true interpretation of the facts in regard to the relations of temperament to gout, so far as those relations exist, would seem to be that the conditions which give rise to gout are responsible also for the physical and moral idiosyncrasies of gouty subjects.

A vicious hygiene may be regarded as one of the chief predisposing causes of gout. The disease is essentially one of advanced civilization, and is alike the product of the luxury and the misery which a high civilization entails. It is a common error to suppose that gout is the consequence only of luxurious living. If the essential cause of the disease is the circulation of imperfectly oxidized plasma, then there are two ways in which this defective oxidation may be brought about: either there is an excess of food ingested beyond the capacity of the individual, under the most favorable conditions, to consume, or the conditions of oxidation may be so impaired that the complete combustion of even a moderate supply of food is impossible. Perfect oxidation requires an even balance between the amount of food ingested and the oxygen inhaled. A consideration of this axiom explains several circumstances in the history of gout. As has been remarked, the disease is rare during the period of growth and development, when the processes of nutrition are active and the consumption of food in excessive quantities is rendered possible by the large demands for the needs of the growing body and for the development of active energy. It is common in adult life when the processes of nutrition are less active, when growth is complete, and when the supply of food must be regulated according to the amount of energy to be developed. It must also be observed that while the disease is most frequently caused by excesses in the consumption of {111} food, it is also often the consequence of an insufficient supply of pure air; hence we find it often among those who cannot be accused of gluttony, but whose occupations or poverty compel them to live and work in a vitiated atmosphere.

The influence of alcoholic liquors in the production of gouty dyscrasia is generally acknowledged. There seems to be a striking difference, however, in the effects of the distilled and fermented preparations of alcohol in this respect. Gout is certainly more prevalent in countries where large amounts of fermented liquors are used than in those where distilled spirits are chiefly consumed. The disease is more prevalent, for example, in England than in Scotland or Ireland, especially among the lower classes; it is said also that it is rare in Russia and Poland, where spirits are more exclusively used. There is a difference also in the predisposing influence of the different varieties of fermented liquors in the production of gouty dyscrasia. The heavier wines, sherry, madeira, and port, are known to be more mischievous in this respect than the lighter wines of France and Germany, though there is abundant clinical evidence of the fact that even these wines, and especially the richer clarets. Burgundies, and Rhine wines, frequently give rise to acute gout and the gouty habit. There can be no question as to the pernicious effects of the malt liquors as gout-producers. The great frequency of gouty diseases particularly among the lower classes who consume these beverages in large quantities is undeniable. This is true especially of the stronger English and Scotch ales, and to a less degree of the lighter English, American, and German beers. The effect of cider and perry as gout-producers is also well recognized. It has been observed in certain districts of England where cider is largely consumed, and, though acute articular gout is said not to be a common disease in New England, where cider has always been much used, there can be no question that it often leads to the development of the irregular forms of gout. As one of the forms of fermented alcoholic beverages containing, in its fresh state especially, a large amount of sugar, it favors the production of the acid dyspepsia which is a common antecedent in the formation of a gouty dyscrasia.

In 1854, Garrod called attention to the fact that a considerable proportion of the gouty patients in hospital practice--at least 30 per cent.--was represented by painters and other workers in lead. This statement has since been confirmed by other observers, and the association of the characteristic symptoms of this form of metallic poisoning, such as the blue line on the gums, colic, and the different forms of paralysis, with both articular and visceral gout, especially the contracted kidney, is certainly frequent. The relation, however, of saturnine poisoning to gout in this association is not easy to determine, Garrod himself pointing out that while the women in the lead-works frequently had the colic, they but rarely had gout. The difference in susceptibility of different individuals to all forms of metallic poisoning is well recognized. It is more strikingly observed perhaps in mercurial and arsenical poisoning than in that of lead. It is well known that the internal use of lead as an astringent in cases of hemorrhage and intestinal catarrh is occasionally, though very rarely, followed by the evidences of lead-poisoning. This difference in susceptibility is perhaps explicable on the theory that persons inclined to gout have less power in eliminating the {112} metal than those who are not gouty, so that it is possible that plumbism is the effect rather than the cause of gout, as has been commonly supposed.

Tanquerel des Planches found none of those changes in the kidneys as the result of plumbism such as are frequently met with in gout, and Rosenstein, who was able to produce saturnine epilepsy in dogs, found no renal changes to have occurred. Charcot and Gombault in recent experiments of feeding guinea-pigs with lead found changes in the kidneys similar to those produced by tying the ureters.

EXCITING CAUSES.--Paroxysms of acute or subacute gouty inflammation of the joints, skin, or mucous membranes, as well as the neuroses of gouty origin, are excited by a variety of causes: errors in diet, both as to quantity and as to specific articles; excesses in the use of fermented liquors--even moderate indulgence, in persons with strong gouty tendencies--are perhaps the most common exciting causes. Sudden changes in temperature, and especially sudden changes in barometrical pressure, sometimes excite and often aggravate the sufferings of gouty persons. Blows, contusions, and mechanical strain frequently determine arthritic attacks; the large proportion of paroxysms affecting the metatarso-phalangeal joint of the great toe is explained by the fact that this joint is more exposed than any other to strain and injury. Finally, nervous exhaustion, from any cause, from overwork or sexual excesses, from grief, anger, or shock, may provoke any of the inflammatory or neurotic consequences of this disease.

PATHOLOGY.--It would be impossible in the limits of this article to review the many theories that have prevailed in regard to the pathology of gout, or even to discuss fully those that may be said to divide professional opinion at the present day. Since the discovery, by Garrod, of the salts of uric acid in the blood-serum of gouty patients, the humoral pathology of gout has certainly had the largest number of adherents.

The lithæmic pathology may be said to be based primarily upon the chemical theory of digestion or food-transformation. This theory proceeds upon the idea that every atom of albuminous or carbonaceous food that enters the body, whether it goes to the construction of tissue or is destined for the direct conversion of potential into active energy, is finally eliminated, for the most part, as urea, carbonic acid, and water. This transformation, of course, is supposed to be effected by a process of oxidation, but neither the exact mode of transformation nor the share which the different organs and tissues take in its accomplishment can be said to be certainly known. Recent investigations seem to indicate that the liver is chiefly concerned, not only in the metamorphosis of the carbohydrates, but also in the formation of urea, so that the arrest in the conversion of starches and sugars which results in glycosuria, and the check in the metabolism of the proteids which give rise to lithæmia, may both have their origin in hepatic derangement. The not infrequent association of glycosuria and lithæmia in the same patient, and the frequent alternation of gout and saccharine diabetes in gouty families, are significant facts in support of the common origin of these diseases.

The purely chemical theory of gout and diabetes, that they are diseases of suboxidation--a theory most ably advocated by Bence Jones--has {113} much to commend it from the valuable suggestions which it affords in the clinical management of these maladies; but it must be acknowledged that while a defective oxidation seems to be an essential factor in the production of gout and diabetes, it is impossible to reduce the process to the simplicity of a chemical equation. It cannot be claimed that the complex chain of transformations which organic chemistry has demonstrated in the destructive metamorphosis of albumen and starch in the laboratory is represented in the vital chemistry of the body. All that can be said in the present state of knowledge is, that the metabolism of food is in its nature a chemical analysis, modified and regulated by vital force, and resulting in the building up of tissues and in the conversion of potential into active energy. Imperfect blood-elaboration must depend upon much besides a disturbance of the balance between the amount of food ingested and the oxygen inhaled, though this must unquestionably be an important factor in its production. Heredity and the mysterious influence of the nervous system complicate the problem of the malnutrition which leads to gout, in such a way that while the general proposition may be maintained that gout is a disease in which suboxidation occurs, it is not possible to affirm whether suboxidation is the essence of the disease or only one of its phenomena.

It is probable, however, that the pathogenesis of the gouty dyscrasia involves a much more complex process than the simple accumulation of uric acid salts in the blood. Uric acid, like urea, is one of the normal results of the metamorphosis of the albuminous foods and tissues. In birds and reptiles it takes the place of urea as the final issue of this metabolism. It has been supposed, as one atom of uric acid can be split by oxidation into two atoms of urea and one of mesoxalic acid, that uric acid was the penultimate of urea, the result of a lower degree of oxidation. It is by no means certain, however, that it is a necessary antecedent of urea. In birds, who consume by their rapid breathing an enormous proportion of oxygen, as well as in the slow-breathing reptilia, the nitrogenous excrements are in the form of urates; and under such divergent conditions it is impossible to explain the variations in the proteid metabolism by varying degrees of oxidation. The only reason that can be assigned for the elimination of the nitrogenous waste in some animals in the form of urea and in others in that of urates is the teleological one that the urea is destined for a fluid and the urates for a solid excretion.

But apart from these physiological objections to the theory that uric acid is necessarily the offending substance in gout, it is well known that uric acid salts accumulate in the blood in febrile diseases, in disorders of digestion, and in anæmia--notably in splenic anæmia--and do not produce either the symptoms or lesions of gout. Todd maintained that gout might occur without an excess of uric acid in the blood; and it is certain that in the atonic and irregular forms of the disease uric acid may not be found in excess in the blood or appear in excess in the urine. Another significant circumstance in the history of gouty persons tending to show that uric acid may be, after all, only an epiphenomenon in the disease, and not its exciting cause, is that the power of digesting farinaceous and saccharine foods in this disease is markedly diminished. To such a degree is this true that sufferers from the gouty dyscrasia are most {114} promptly relieved of their symptoms of primary indigestion by restricting their diet very largely to albuminous foods; and not only does such a diet diminish the dyspeptic symptoms, but I am persuaded by a considerable experience that it is one of the surest prophylactics against the recurrence of gouty lesions. It is well known that the fermented preparations of alcohol are among the most frequent exciting causes of acute gout, and cases are by no means infrequent in which indulgence in sweet foods and in fruits will provoke many of the well-recognized local lesions of the disease.

The explanation of this anomaly in the uric acid pathology of gout may possibly be found in the suggestion of Garrod, that the deposition of the urates is caused by their insolubility, and, as this insolubility is increased by the diminished alkalinity of the serum, that the evolution of the acids in the digestion of the carbohydrates so diminishes the normal alkaline state of the blood that the uric acid salts are more readily precipitated. But even if we accept this explanation, the fact remains that as efficient factors in the production of the gouty diathesis the carbonaceous foods may play as large and perhaps a larger part than the albuminous foods. It would seem, therefore, in view of the conflicting evidence in regard to the theory of the uric acid origin of gout, that the chemical pathology of this dyscrasia is still involved in considerable obscurity.

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