Detailed Consideration of Phenomena
Onset.—From Sydenham’s classical account it might be inferred that the onfall of gout is always fulminant. But this is far from being the case. For I find myself in agreement with Hilton Fagge that in many, if not the majority of instances, even the initial outbreak of the disorder is installed in a far less dramatic manner. Certainly in not a few cases its manner of approach is insidious, not to say stealthy. At onset then the nature of the case is therefore frequently misinterpreted both by victim and physician. The free liver, fearing that Nemesis has overtaken him, is fertile in suggestion. He has overwalked, his boot pinched him, or it is a sprain. Local appearances may be non-committal. There may be no swelling nor redness, and no access of pain at night. Still there is discomfort when he walks. The so-called sprain lingers, and one morning the great toe, instep, or ankle, is swollen, tender, flushed, and the victim’s fears and the physician’s suspicions are converted into certainty: it is gout!
Still in this matter of the onset I must not overlook the findings of my colleague James Lindsay. In 569 cases, the onset was sudden in 458, and in the remaining 111 examples gradual. It was noted that only 14·5 per cent. of the male cases were of gradual onset. But no less than 47·1 per cent. of the female cases developed after this fashion.
Again to resume, it is by no means invariably the case that the onset is nocturnal. For, as Duckworth has pointed out, many attacks begin during the day, and this is perhaps more often the case after the disorder is fully established.
Locality.—Gout in its classical form is monarticular in distribution. In 375 out of 512 initial seizures, Sir Charles Scudamore found that the metatarso-phalangeal joint of the great toe of one or other foot was the joint affected. Garrod, too, noted that, excluding the great toe, in not more than 5 per cent. were other joints implicated. As to the frequency of incidence in joints other than the big toe, opinions differ. For Scudamore it is the ankle, for Garrod the instep, and afterwards the outer side of the foot and the knee. In contrast, Hilton Fagge holds that next to the great toe gout vents its initial fury with greatest frequency upon the metacarpo-phalangeal joint of the index finger, adding, “certainly not the thumb.” Most authorities however agree that gout in its early stages rarely attacks the joints of the upper limb, and even in its most inveterate form the shoulder and hip joints are immune. Personally, I have never seen a case of gout in the shoulder or hip; such cases are usually examples of osteo-arthritis.
Exceptionally, even in first seizures, more than one joint may be affected. Thus it may migrate from one big toe to its fellow, or travelling further afield, may invade ankle, knee, wrist, or elbow, or small joints of hand. W. Gairdner held that in gout the joints of the left were more commonly attacked than those of the right limb. But James Lindsay’s figures would appear to indicate precisely the reverse, viz. a predilection for the right side of the body.
Pain.—If we may accept the lurid imagery of its victims, even the tortures of the Inquisition failed to transcend in agony the—
“... pangs arthritic
that infest the toe of libertine excess.”
Cowper.
Sydenham said that at its onset the pain was as that of a dislocation (ossium dislocatio). At its zenith it was as if the flesh was being gnawed, squeezed in a bootscrew, or scalded by molten lead or boiling water. Sensory perversions are superadded, and, as Ambrose Paré said, “some patients say they burn, while others complain of icy coldness.”
Its peculiarly exasperating nature is well illustrated by Hosack, an old time Professor of Medicine of New York, who thus delivered himself: “Some compare it with the gnawing of a dog, the pressure of a vice, or the pain of the actual cautery; this probably is not far from the truth, judging from the anecdote I have heard of a man subject to gout. This man falling asleep barefooted before a large fire, the fire fell, and a large coal found its way to his foot; half awake and half asleep, he cried out: ‘There’s that d——d gout again!’ He at length awoke, when he found a large coal frying his great toe. The sensation of the two evils was probably the same.”
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:—
Blood Count.
| Red corpuscles, per c. mm. | 3,692,000 | = | 73·8 | per cent. |
| Hæmoglobin | 80 | ” | ||
| Colour index | 1·08 | ” | ||
| Leucocytes, per c. mm. | 25,920 |
Differential Count.
| Lymphocytes | 8·0 | per cent. | = | 2,074 | per c. mm. |
| Large mononuclears | 3·5 | ” | = | 907 | ” |
| Polymorphonuclears | 87·0 | ” | = | 22,550 | ” |
| Eosinophiles | 0·5 | ” | = | 130 | ” |
| Mast cells | 1·0 | ” | = | 260 | ” |
| 100·0 |
The salient feature of the blood picture is the high grade leucocytosis of leucoid type with moderate anæmia—appearances quite compatible with, and suggestive of, an infective arthritis. To these interesting blood changes we shall again refer when dealing with the acute polyarticular variety, the above case being of monarticular type, i.e., the big toe.
Uric Acid Excretion.—If when on a purin-free diet a gouty subject develops a paroxysm, the curve of uric acid excretion in the urine is so characteristic as to be almost pathognomonic of the disorder. As His pointed out, immediately before the onset of the paroxysm the endogenous uric acid sinks to a lower level (termed by Umber the anacritical stage of depression). With the onset of the attack the uric acid content of the urine quickly increases, to reach its zenith on the second or third day. F. Pfeiffer, who first noted this point, termed it an uric acid wave. Subsequently, with the gradual subsidence of the paroxysm, it again drops into what Umber termed the post-critical stage of depression. While this curve of endogenous purin excretion may be modified by oft recurring exacerbations, still Umber holds that nevertheless it is of decided value in differential diagnosis.
Local Phenomena.—The site and character of the pain having been dealt with, we now pass on to consider the objective changes in the affected part. The local engorgement of veins that precedes the articular outbreak becomes more pronounced, extending from the vicinity of the painful joint as far as the leg. The overlying skin of the joint quickly becomes red and tumid. It is not a bright, but a dark red, the superjacent skin taking on a shining smoothness that has been compared to the peel of an onion. Indeed, in its more violent form it resembles but too closely the ordinary appearance of an abscess, over which the skin is becoming thin. The redness is not strictly confined to the surface of the joint, but spreads a little beyond, and where it ceases œdema is perceptible.
The redness in its intensity attains its zenith in from twenty-four to forty-eight hours, and then in hue becomes more violaceous. On the other hand, the œdema may go on increasing for some days. At first, owing to tension, the presence of œdema may not readily be elicited. But with the subsidence of inflammation the swollen parts readily pit on pressure. It is scarcely possible to detect intra-articular effusion unless it be the ankle joint that is involved.
According to Duckworth, in the more sthenic forms there may be local ecchymoses. With the crisis the redness, œdema, and venous turgescence die down. The previously distended skin becomes wrinkled, and with complete subsidence of inflammation desquamation ensues. This process is generally attended with troublesome itching. It is most noticeable about the feet and hands, but more rare at other sites. Scudamore said that in seventy-eight out of 234 cases no peeling occurred, but, as Garrod observed, it may readily be overlooked unless especially sought for.
The exquisite sensitiveness of the parts, as before noted, gives way to numbness. The diminished sensibility, coupled with stiffness of the joint, renders walking difficult for some days, and, indeed, a month or more may elapse before the joint, even in favourable cases, recovers its customary mobility.
In acute asthenic forms great contrasts appear. Pain and tenderness in the toe may be moderate, but there may be little local heat or redness and no pyrexia. But œdema is generally in evidence, and the usual desquamation of skin follows.
Tophus Formation.—To the local changes that mark their eruption at ab-articular sites we have already alluded. Here we would only reiterate that their formation follows the local joint inflammation. Consequently if a few days after the attack local pain or tenderness, with or without swelling in the vicinity of the joint, should be complained of, it should not be dismissed as of no account, but the affected parts should be scrutinised carefully and, where possible, at short intervals. This in the interests of diagnosis of a joint affection which may at the time have been of doubtful nature, more especially if the primary attack occur elsewhere than at the classical site. Some observations of Trousseau are well worth quotation: “Physicians who have watched the progress of the evolution of tophus believe that it is formed during the paroxysm of gout. They are mistaken: the deposit appears during the interval between attacks, or at least when the attacks have not been of long duration, and when they do not recur in such rapid succession as to run into one another, in which cases their secretion has commenced during the preceding and continued during the succeeding attack.”