The pain is aggravated in that frequent “startings” of the limb prevent the victim keeping the foot at rest. The slamming of a door, or the incautious shaking of the bed, so quickens its throbbing intensity as provokes a literal frenzy of rage. But fortunately it is not always so. For though the pain of gout is unquestionably severe, at times excruciating, yet it presents infinite grades of severity. Also one must recollect that but too many of its victims are already in a high state of irritability before the outbreak. Moreover, their powers of self-control are too often sapped by unbridled self-indulgence, and they have but slight reserves of patience and fortitude to draw upon.[32]
Apart from the personal factor, in subacute cases the pain is notably less severe than in the acute sthenic form. The pain of gout, as a rule, is more intense than that of acute rheumatism, and, I fancy, than that of all other varieties of acute arthritis.[33] Sir Thomas Watson in his fascinating lectures tells of a witty Frenchman who, comparing acute gout and acute rheumatism in respect of pain intensity, remarked: “Screw up the vice as tightly as possible, you have rheumatism; give it another turn, and that is gout.”
Lastly, in respect of the duration of the pain, it is not always true that it wholly intermits at the approach of dawn. It does so frequently, it is true, but in some instances pain, more or less severe, continues during the day as well as the night. Occasionally, on a crescendo scale, it continues increasing almost up to the crisis. Generally speaking, too, the shorter the duration of the paroxysm the more intense the pain, and the more prolonged the less the degree of suffering.
Following the crisis, the pain gradually becomes less and less, giving place to a feeling of numbness of the toe, which in older subjects may endure for some days.
General Phenomena.—Symptoms, other than those referable to the affected part, vary widely in different cases. In this respect the acute sthenic forms contrast with the acute asthenic types. In the former the pulse quickens; the temperature rises, but rarely exceeds 101°-102°, though Garrod saw it reach 104°. The tongue is furred, the breath foul, with anorexia and thirst. Though the appetite is frequently impaired or lost, yet in some instances it is retained. Dyspeptic symptoms, hiccough, eructations, etc., are sometimes prominent, but often wholly lacking. The bowels are constipated, as a rule, the stools pale, or dark and extremely offensive. The urine is generally scanty, high-coloured, with a lateritious sediment on cooling. It may contain a trace of albumen. Severe cramps affecting muscles of the leg, thigh, and upper parts of the body, are more or less prominent symptoms in a considerable number of instances.
The pyrexia appears to be symptomatic, more or less in proportion to the acuteness of the local phenomena. Comparably the highest temperatures are usually met with in sthenic forms in relatively young or robust middle-aged subjects. Duckworth noted the interesting point that “a preliminary rise is commonly noted for one, two, three or four days before a joint is actively involved.” With the articular outbreak the febrile movement becomes more active. The temperature runs up to 100° or over, but with the morning abatement sinks to normal or nearly so. The following evening it rises again frequently to a higher level, 102° with a morning remission, and so it continues for a variable number of days, it may be only two or eight to ten. It then subsides, and frequently for a few days remains sub-normal. Lastly, the acute asthenic forms, that occur often in women (Garrod), may be wholly afebrile.
Changes in the Blood.—Apart from its increased content of uric acid, further morbid changes take place in the blood in gout.
Neusser in 1894 described what he termed “perinuclear basophilic granules” over and about the nuclei of the leucocytes in the blood of gouty patients. He held that the dark granules constituted the mother substance from which uric acid was derived, and that their presence in the blood was distinctive of the “gouty diathesis.” Subsequent researches, however, by Futcher and others appear to have shown the absence of any interrelationship between the amount of these granules and uric acid elimination, though Neusser claimed that cases showing them excreted uric acid in excess.
More significant, however, is it that the blood in acute gout may show a high grade leucocytosis with secondary anæmia.
In a case under my care of acute gout at classic site, though by no means of unusual severity, the following was the content of the blood picture:—