Acute Generalised Gout
While gout may throughout its life history confine its ravages to the foot, if not solely to the toe joints, it may, even in the initial attack, involve many articulations. Such cases usually, if not always, occur in persons of marked gouty heredity. In its simplest forms the orthodox monarticular seizure is simply exchanged for a sequential implication of each big toe joint. If so, as Trousseau pointed out, the joint that is the last to be involved is least affected, and the soonest to get well again, while the accompanying œdema is of shorter duration. But in more severe cases not only the big toe, but the tarsal joints, the knee and the hand, may be invaded in the first attack. Occasionally, too, the disorder displays concomitantly its tendency to involve other structures, tendons and aponeuroses, e.g., the tendo Achillis, plantar fascia. Such widespread initial involvement is usually preceded by prodromal phenomena of unusual severity and prolonged duration. These initial attacks of polyarticular distribution are extremely rare.
Far more commonly acute gouty polyarthritis supervenes after several attacks of classic location have been suffered. The gouty inflammation in these cases invades the joints after a serial fashion. But each joint as it becomes involved goes through the same painful cycle. Thus, for five or six days the pain goes on increasing, then abates, and finally the wished-for crisis comes. So it happens that the gout may be raging simultaneously in several articulations, though in each at different stages of evolution. Consequently the symptoms do not pursue an even tenor, but are made up rather of a series of little attacks—series et catena paroxysmulorum, to invoke Sydenham’s expression.
Frequently periods of apparent recovery take place. The temperature remains normal for some days, and welcome convalescence seems established, when, to the victim’s despair, the temperature again rises, and the same weary cycle, though perhaps shorter, is yet to be endured. Running this chequered career, the disorder may last for six weeks or two or three months.
In such attacks not only the feet, knees, hands, and elbows, may be promiscuously involved, but often also the ligaments, bursæ, tendon sheaths, and aponeuroses. The suddenness with which the disorder shifts its seat from one joint to another, or from joints to bursæ or muscles, often leads to its confusion with acute rheumatism. In other words, that fixity distinctive of gout in its monarticular forms is here exchanged for mobility, that specific quality of acute rheumatism.
Naturally, the implication of so many varied structures casts its impress on the clinical picture, inasmuch as the physical characters vary with the different textures involved, their capacity for inflammatory distension, etc. On the dorsum of the hand and foot redness and œdema will be prominent, and Scudamore noted that the flush might be widely diffused, simulating erysipelas, with here and there small ecchymoses.
When structures more deeply placed, i.e., tendon sheaths at ankle, knee, and wrist, are singled out for attack, swelling is less marked and redness of the skin more patchy in distribution. The bursæ at the elbow or back of the knee may swell with extraordinary rapidity. The parts become exquisitely tender and painful, while the overlying skin takes on an angry blush. They may subside, but more often continue permanently enlarged, defiant of reduction.
Involvement of the olecranon bursa is very typical of gout. Pratt, of Boston (1916), tells of a case in which the subject had during twenty-seven years suffered from recurring attacks of acute gouty polyarthritis. The eight or ten physicians who had treated him had all regarded the disease as rheumatic fever. Pratt himself observes: “I did not feel sure of the diagnosis until I saw the swelling on his elbow, which presented the typical picture of a chronic gouty olecranon bursitis.”[34] Occasionally the bursæ when filled with uratic deposit undergo suppuration following injuries. The bursa in connection with the great toe frequently becomes acutely inflamed, and Scudamore in a gouty hand saw an old ganglion take on the same inflammatory reaction.
The tendon sheaths when involved lead to great disablement, as even the most tentative attempts at movement give rise to sudden and agonising cramp. The tendo Achillis is a favourite site, or the tendons of the wrist, or the ligament of the patella. The same is true of the aponeuroses, the predilection being for the lumbar or gluteal fascia, in which instance it may extend to the sheath of the sciatic nerve. These extensions of gout to tendon and nerve sheaths frequently outlast the articular lesions, and may become the dominant element in the clinical picture.
Naturally, when not only joints, but bursæ and other structures, are involved and implicate both upper and lower limbs, the victim presents a pitiful spectacle, one of almost complete helplessness. Œdema and general venous turgescence may be very pronounced in one or more members, giving a subjective sensation of almost overwhelming weight in the limb.
Reverting to the constitutional symptoms, the outstanding feature is that, notwithstanding the widespread involvement of joints with manifest local inflammatory reaction, the pyrexia is of moderate grade, and so frequently, indeed, is it afebrile that this peculiarity is of diagnostic significance.
Changes in the Blood.—The findings are extremely interesting in view of the high grades of leucocytosis to be met with both in pyrexial and apyrexial examples.
In a case of acute gouty polyarthritis under my care the blood picture was a very striking one. The patient had suffered from gout for some eleven years, with recurrent acute exacerbations. There was widespread involvement of the joints both in upper and lower limbs. On the dorsum of the mid-phalangeal joints small semi-solid swellings were present, the exact nature of which was somewhat puzzling. But inasmuch as the pinna in both ears was studded with tophi, this seemed to provide a clue. The auricular tophi were verified microscopically. The extra-articular phalangeal swellings were then aspirated with a hypodermic syringe. A turbid straw-coloured fluid issued, which microscopically was found to contain biurate crystals. His temperature rose nightly from 101° up to 102° F., with morning remissions. The left knee and wrist were the seat of effusion, and some of the small finger joints were inflamed.
Blood Count.
| Red corpuscles, per c. mm. | 4,432,000 | = | 88·6 | per cent. |
| Hæmoglobin | 60 | ” | ||
| Colour index | ·68 | ” | ||
| Leucocytes, per c. mm. | 27,200 |
Differential Count.
| Lymphocytes | 9 | = | 2,450 |
| Large mononuclears | 13 | = | 3,540 |
| Polymorphonuclears | 78 | = | 21,220 |
| Eosinophiles | 0 | = | 0 |
| Mast cells | 0 | = | 0 |
| 100·0 |
The left knee joint was aspirated by Dr. Munro. A clear fluid of straw yellow tint was withdrawn, which yielded some fibrin on standing. The cytological examination gave the following results:—
Total Count.
| 44,800 per c. mm. (nearly all leucocytes). |
Differential Count.
| Polymorphonuclears | 92 |
| Lymphocytes | 7 |
| Large mononuclears | 1 |
| Eosinophiles | 0 |
| Basophiles | 0 |
| 100 |
Attempts at culture on broth and agar proved sterile. In addition three separate blood cultures, taken at intervals of a few days, on agar slopes and broth, all gave negative results.
In another instance of polyarticular distribution the subject was seen during the inter-paroxysmal period. He displayed auricular tophi, the crystalline content of which was verified microscopically.
Blood Count.
| Red corpuscles, per c. mm. | 5,732,000 | = | 194·6 | per cent. |
| Hæmoglobin | 65 | ” | ||
| Colour index | ·57 | ” | ||
| Leucocytes, per c. mm. | 13,200 |
Differential Count.
| Lymphocytes | 34 | = | 4,490 |
| Large mononuclears | 3 | = | 400 |
| Polymorphonuclears | 61·5 | = | 8,120 |
| Eosinophiles | ·1 | = | 130 |
| Mast cells | ·5 | = | 66 |
Chalmers Watson some years previously investigated the blood in cases of acute gouty polyarthritis both during an exacerbation and in the inter-paroxysmal period. His findings were as follows:—
During the attack the films showed very marked leucocytosis. Also there was present a large number of peculiar myelocyte-like cells, these more than half as numerous as the ordinary finely granular oxyphil leucocytes.
“Each of these cells contained a large oval or horse-shaped nucleus, poor in chromatin. The nucleus occupied about half of the total area of the cell. It did not stain uniformly, and it was usually situated to one side, coming right up to the cell outline, and occupying from a third to a half of the total circumference. In many of these cells the nucleus was almost round, with but one slight indentation; in others the indentation was pronounced. The whole cell stained a pale blue, presented a degenerated appearance, and contrasted markedly with the ordinary leucocyte seen in the same film, with its brilliant blue nucleus and bright red eosinophil granules. The special cells under description were also remarkable for their size, measuring about 15 m. in diameter, a few being smaller, about 10 m. Some of them contained vacuoles in the cytoplasm. The general appearance of these cells suggested exhaustion in so far as the cytoplasm did not contain the typical fine oxyphil granules characteristic of the myelocyte. From the character of the nucleus and cytoplasm, they were undoubtedly distinct from lymphocytes. The large lymphocytes were scarce; small lymphocytes were numerous. True eosinophil cells were also scarce. The main bulk of the leucocytes consisted of the ordinary finely granular oxyphil leucocytes and the peculiar myelocyte cells described.
“Blood plates.—Some of the blood-plates were large (4 m. in diameter), and often formed very irregular torn-looking masses. The red cells were apparently normal.”
Shortly after Chalmers Watson, Bain published his results of blood examination in acute gouty polyarthritis. He also noted the presence of a distinct leucocytosis. A differential count disclosed a marked increase of the eosinophil cells, and he adds: “There was present a moderate number of the peculiar myelocyte-like cells originally described by Chalmers Watson.”
Dr. Munro, though he carefully examined the gouty blood films to this end, was unable to identify the myelocyte-like cells noted by these observers.
Recently, through the kindness of my colleague Dr. Waterhouse, Dr. Munro and I had again an opportunity of examining the blood in a case of this kind during the inter-paroxysmal period. The subject, a male, had had repeated attacks at the classic site, with subsequent extension to other joints. Multiple tophi were present in both ears, and the crystals of uric acid were demonstrated microscopically.
Blood Count.
| Red corpuscles | 7,364,000 | = | 147 | per cent. |
| Hæmoglobin | 74 | ” | ||
| Coloured index | 0·5 | ” | ||
| Leucocytes | 21,400 |
Differential Count.
| Lymphocytes | 28·5 | per cent. | = | 6,099 | per c. mm. |
| Large mononuclears | 2·5 | ” | = | 535 | ” |
| Polymorphonuclears | 64 | ” | = | 13,696 | ” |
| Eosinophiles | 3·5 | ” | = | 749 | ” |
| Basophiles | 1·5 | ” | = | 321 | ” |
The blood picture, it will be seen, is one of erythræmia—a marked leucocytosis, a normal differential percentage count, pronounced secondary anæmia.
Da Costa also notes, in a case of gout, erythræmia (7,125,000) with a leucocyte count of 14,000. Ewing, too, records an instance of chronic gout with huge tophi, seen in an acute exacerbation, in which the blood gave a leucocyte count of 21,000 with 70 per cent. hæmoglobin. In another severe instance of subacute type the same observer again met with leucocytosis (15,000).
In regard to these interesting blood findings, it is to be cordially hoped that as the somewhat rare opportunities occur they will be taken full advantage of.
As to the other general clinical features the nervous system, as might be expected, is often greatly perturbed, and the mental distress and anxiety in some instances appear to cause even more irritation than the bodily pain. Febrile movement when present accords with that observed in monarticular sites, save only in the tendency to relapses. Sweating is not a common feature, as in acute rheumatism. Neither does acute endocarditis occur in gout. On the other hand, as this acute polyarticular form may recur throughout years, it may in its later stages be complicated by nephritis.
Furthermore, in its differentiation from acute rheumatism the more advanced age of the sufferer, always over thirty-five and more often nearer fifty or over, will be of help. The presence of an hereditary taint, the nature of the occupation and personal habits, and more pertinently the history of a classical attack in the great toe, may give a clue.
But in this, as in all other varieties of gouty arthritis, the one and only unequivocal objective proof of the nature of the disorder is the presence of tophi. Lamentable indeed is the frequency with which this fact is forgotten, to our confounding and the patient’s detriment. As Hilton Fagge, discussing the diagnosis of gout, long since observed: “All those parts which are apt to be the seat of tophi should be examined. If a single deposit of urate of soda can be found it settles the question.”
In conclusion, before passing to consideration of chronic articular gout, it will be convenient here to discuss certain concomitant phenomena of the acute types. We refer to the muscular and nerve forms of fibrositis, which, we hasten to add, are of common occurrence also in the chronic types of articular gout.