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.”
The Joint Deformities of Chronic Gout
The palpable changes in the affected joints differ widely in different cases, and why is not apparent. Thus, the first attack, if of prolonged duration, may bequeath a legacy of crippledom comparable to that met with after repeated paroxysms. On the other hand, some, although they have suffered from the disorder off and on throughout their lives, yet escape those consecutive deformities which in others deform and cripple the hands and feet, though the disease may be of relatively brief duration.
But in the less fortunate cases the continued ravages of gout lead to a pitiful disablement of the affected limbs, reaching its acme in the hands and individual fingers, flail-like and semi-paralytic as they so frequently become.
Not only are the digits variously distorted, their joints more or less ankylosed, but the overlying skin, distended by the ever increasing subjacent uratic deposits, becomes thinned and purplish red in hue, and occasionally ulcerates. Similarly at ankle, knee, wrist and elbow thickening and deformity ensue as the concretions accumulate in and around the affected joints, these further accentuated by the correlated inflammatory and degenerative processes. Coincident deposits in the tendon sheaths and related bursæ contribute their quota, and at knee and elbow the bursal masses may reach extraordinary dimensions. Not only do the joints become deformed, but distorted also, through reflex muscular spasm and instinctive adoption of unnatural attitudes for the avoidance of pain.