Chronic Articular Gout
In delineating the features of the acute polyarticular variety, we have to a certain extent trenched on the clinical territory of the chronic form; this is scarcely avoidable, inasmuch as the line drawn between acute and chronic gout is purely arbitrary. Thus one authority remarks of acute gout: “If the disease continue beyond three or four weeks, it is to be considered as persistent or chronic” (Flint). Trousseau, again, discussing the acute variety, more particularly the acute polyarticular type, states that it “may last for some weeks, or even for three months,” adding: “Should it extend beyond that period, it is no longer acute gout; it is chronic gout.”
The truth is that articular gout in this respect is very prone to vagaries. Thus, in rare instances an attack of acute or sub-acute gout, more particularly the latter, may merge without break into the chronic form of the disease.[35] Far more commonly the tragedy is more slowly played out. The unfortunate victim, after passing through several more or less classical attacks, finds that the intervals become shorter and shorter until they merge, as it were, one into the other. Fortunately its course is not one of continuous uniform severity. Remissions, but not complete intermissions, occur, and every now and again intercurrent acute attacks take place.
But, the reader may observe, surely this is very reminiscent of acute gouty polyarthritis, with its serial content of acute paroxysms?[36] Quite so; but there is this difference, that, although such may last six weeks or three months, still there is a period put to the sufferings. A respite of months or years of immunity, and relative health may then supervene.
Not so, unfortunately, when such paroxysmal waves sweep over the subject of long-standing or chronic gout. Not only do the recurrent acute outbreaks occur with increasing frequency, but also with increasing length of duration. It is here no longer a question of the intercurrent acute attack lasting days, but weeks. Also during such exacerbations either four, five, or six joints are simultaneously attacked, or in such rapid sequence that before one joint is free another is involved.
But a word here as to the variations in distribution of the articular lesions in chronic gout. The well-marked penchant of acute gout for the great toe continues throughout the life history of the disorder, the predilection for this site being equally a characteristic of the chronic type. As to the subsequent articular involvement, Garrod held the sequence to be as follows: heels; ankles; knees; the smaller articulations of the hands; lastly, the shoulders and hips. It has never been my lot to see either the shoulders or hips involved; but I have seen osteo-arthritis of the hip in men displaying auricular tophi, and I am inclined to think that, in the presence of the latter, it has sometimes been assumed that the hip mischief was of gouty nature—the “hip gout” of the older authors.
Moreover, the order of sequence is by no means invariable, for oftentimes a local circumstance, i.e., injury or sprain, determines the location. Again, chronic gout is very erratic in respect of the number of joints implicated. In some almost all the joints may be affected, while in others, no matter how ancient the disorder and how oft its recurrence, it remains localised to but a few joints; or it may progress after a leisurely fashion, with each attack invading different joints in succession.
Naturally, if the disorder confine itself to a few joints, and these, and these alone, are the seat of the oft-recurring attacks, permanent changes sooner or later make their appearance. Nor are the morbid effects limited to the joints, but they invade the continuity of the limb, for the oft-repeated inflammatory reactions lead to engorgements of persistent nature. The contour of the affected members is distorted by the œdematous tumefaction, which, more pronounced at the level of the joints, extends in lesser degree beyond their confines. The skin, too, especially over the fingers, undergoes a change in texture, often becomes smooth and glossy, and through its dusky pink subjacent uratic deposits may be discerned.
Old gouty subjects are often of sallow or parchment-like complexion. The blood in these cases of polyarticular gout conforms in attenuated degree, in the matter of leucocytosis and secondary anæmia, to that observed in the more acute types, as witness the following blood pictures.
All were males, the subjects of chronic articular gout of many years’ standing. They all exhibited tophi, which were verified microscopically. The examinations were conducted during the inter-paroxysmal periods.
(1) Blood Count.
| Red corpuscles, per c. mm. | 4,832,000 | = | 96·6 | per cent. |
| Hæmoglobin | = | 64 | ” | |
| Colour index | = | ·66 | ” | |
| Leucocytes, per c. mm. | 11,000 |
Differential Count.
| Lymphocytes | 42 | = | 4,620 |
| Large mononuclears | 4 | = | 440 |
| Polymorphonuclears | 52·5 | = | 5,775 |
| Eosinophils | 0 | = | 0 |
| Mast cells | 1·5 | = | 165 |
(2) Blood Count.
| Red corpuscles, per c. mm. | 5,040,000 | = | 100·8 | per cent. |
| Hæmoglobin | = | 72 | ” | |
| Colour index | = | 0·72 | ” | |
| Leucocytes, per c. mm. | 13,400 |
Differential Count.
| Lymphocytes | 15 | = | 2,010 |
| Large mononuclears | 2·5 | = | 335 |
| Polymorphonuclears | 78 | = | 10,452 |
| Eosinophils | 1 | = | 134 |
| Mast cells | 3·5 | = | 469 |
(3) Blood Count.
| Red corpuscles, per c. mm. | 4,280,000 | = | 85·6 | per cent. |
| Hæmoglobin | = | 66 | ” | |
| Colour index | = | 0·77 | ” | |
| Leucocytes, per c. mm. | 12,000 |
Differential Count.
| Lymphocytes | 23 | = | 2,760 |
| Large mononuclears | 3 | = | 360 |
| Polymorphonuclears | 74 | = | 8,880 |
| Eosinophils | 0 | = | 0 |
| Mast cells | 0 | = | 0 |
In these chronic forms, save during exacerbations, there may be little or no febrile movement, and local pain, heat, and redness may be slight or wholly lacking. But the articular swellings never wholly disappear, and the mobility of the joints is never entirely regained. The articulations, few or many, become stiff, ankylosed, and deformed, by the growth of tophaceous deposits. But to detailed description of these latter we shall return later.
In inveterate cases of this nature the victim grows more and more crippled and infirm, the inroads of the disease upon the constitution more and more palpable. Pelion is heaped upon Ossa, as one ailment sets in after another, now of the digestive organs, now of the heart, or of the kidneys. These subjects of chronic gout are more often than not dyspeptic, show signs of arterio-sclerosis. Their blood pressure is raised, their vessels tortuous and thickened, and the left ventricle enlarged.
As to the variations in uric acid excretion, these, as before remarked, show no appreciable deviation from normal. Occasionally, however, there is a tendency to uric acid gravel. Of more sinister significance, albeit, is the fact that in many of these cases the urine is copious, of low density, paler than normal, and shows a trace of albumen with hyaline casts.
As the disease marches to its fell end the appetite becomes impaired, gastric catarrh and diarrhœa may sap the waning strength, or palpitations, fits of dyspnœa, or angina-like attacks, sometimes fleeting, but often of organic source, may portend a fatal issue. Ripe for the sickle, a kindly “stroke” perchance puts an end to his protracted misery. Or symptoms, long since manifest, of progressive renal failure may usher in the closing scene, and happy the victim if he pass muttering, half conscious, into that dream-like stupor drifting by insensible graduations to death.
“The life of all his blood
Is touched corruptibly, and his pure brain
(Which some suppose the soul’s frail dwelling-house)
Doth by the idle comments that it makes
Foretell the ending of mortality.”
Shakespeare.
So much in attempted portraiture of the long-drawn-out tragedy of inveterate chronic gout. But, fortunately, it is not always thus, and nowadays, at any rate, the evils wrought on the constitution by the malady are seldom so malignant. For not only, as before stated, has gout become less frequent, but its virulence also much attenuated. States of so-called “gouty cachexia” were, however, more familiar to our forefathers. It more commonly ensues in subjects of strongly hereditary tendency, and particularly in those in whom the initial attacks ensue before thirty years of age. I recall the instance of a colonel who sustained his first attack of gout when a subaltern of but eighteen, brought on, as he thought, through exposure while shooting snipe in Peshawur. It is in such cases that this so-called “gouty cachexia” may overtake a man while yet in his prime, and vest him untimely “with all the characters of age.”
As to the milder types of regular chronic gout, such usually arise, not in youth, but in men past the meridian of life. In their instance the recurrence of gouty paroxysms is often erratic. Periodicity becomes less pronounced or wholly lost. The life history of the disease may be summed up in a few sporadic outbreaks, occurring irregularly throughout a long life. Even when at first the attacks occurred regularly in the spring and fall the rhythm of incidence becomes broken. An attack comes before its time, is belated, fails of appearance wholly, or an intermediate paroxysm comes as a surprise. Moreover, in many such the gouty manifestations with the passing years tend to become more and more attenuated, maybe even to extinction. Thus, a man who in the middle decades was a martyr to gout in old age gains freedom from its visitations, the disease having apparently exhausted its vicious potentialities.
Reviewing articular gout as a whole, one cannot but realise that it does in respect of the recurrence of gouty paroxysms exhibit inexplicable vagaries, inexplicable in that, as Sir William Roberts long since said, “in many instances they are dependent neither upon medical treatment nor upon altered dietetic habits, but are due to spontaneous changes in the constitution. They form part of the natural history of gout; and it is important to bear their existence in mind when we seek to estimate the value of therapeutic means in order to prevent ourselves from becoming the dupes of misinterpreted sequences.”
Albeit, we would not end on too sombre a note. For, in respect of the graver consequences of gout, it is unquestionable that right living, aided by efficient therapy, may arrest the course or mitigate the severity of the disorder. Moreover, as long as the attacks do not follow quick upon each other, but are separated by long intervals, there is little fear of a cachectic condition supervening. Life may not be appreciably shortened, and such textural degenerations as may ensue, though frequently attributed to gout, may often with at least equal plausibility be assigned to advancing years, but this with reservation, for, as Duckworth says, “the wilful libertine is likely soon to become cachectic, while the prudent man may altogether avoid this state or avert its evils for many years or decades of years.”