Gout, with a section on ocular disease in the gouty

by Llewellyn J. Llewellyn

The only morbid structural changes, therefore, that can legitimately be defined as specific of gout relate to its regular or articular lesions. As to the anatomical alterations in the articulations, their specificity depends essentially on the uratic deposits, rather than upon the associated inflammatory and degenerative processes.

Given death during an acute paroxysm, examination reveals the usual tokens of inflammation, hyperæmia, effusion, and swelling of the ligamentous tissues. The synovial lining is injected and spongy, while the exuded fluid is thick, scanty and turbid, containing polymorphonuclear leucocytes as well as crystalline deposits. Charged therewith, not only is the synovia thick, but of a milky appearance. Examined microscopically, it is found to contain the acicular crystals of sodium biurate. The synovia has occasionally been found covered with blood, but no pus formation has ever been known to occur in uncomplicated acute gouty arthritis. The reaction of the synovial fluid is generally neutral or alkaline, but exceptionally Garrod found it acid.

Uratic deposit has a predilection for cartilage, and in some instances is strictly confined thereto; but in the more chronic forms it permeates all the component elements of the articulation. In the synovial membrane and fringes deposition takes place in the subepithelial and subserous layers. It invades also the ligaments, the tendons, and even the periarticular fibrous tissues become impregnated with biurate. Moreover, like the synovial sheaths of the tendons, the neighbouring bursæ are specially prone to deposits, which again encroaching upon the subcutaneous connective tissues, infiltrate the skin itself, forming chalk stones or tophi.

Inspected after death, the articular cartilages are seemingly overlaid with a white mortar or chalk-like material, i.e., sodium biurate. Their surfaces, however, though defaced by stains, streaks, or dull patches, nevertheless, at any rate at first, retain their pristine smoothness. This because closer scrutiny reveals that the deposit is not in reality upon the surface of the cartilage, but is located interstitially in its substance.

Microscopic examination of a vertical section, taken at the site of the deposit, shows clearly that it is composed of felted masses of acicular crystals. Lying in the matrix of the cartilage, they are more densely packed just below its free surface. The crystals do not penetrate further than one-third or one-half of the depth of the cartilage. Becoming more and more sparse towards the deeper layers, those near the bone are entirely free from deposit. This clearly indicates that the uratic matter originated from the synovial fluid bathing the articular ends and was precipitated therefrom.

As to the primary site of the deposition, it usually takes place at the centre of the articular cartilage. Opinions differ as to whether the cartilage cells are foci of deposition. Garrod thought so, but Duckworth found no relationship between it and any histological elements, while others locate it in the matrix.

While, as before stated, the cartilage at first retains its smoothness, later it becomes pitted in patches. Ultimately the cartilage, through atrophic changes and erosions, may disappear, the joint cavity becomes filled with a plaster-like material, and the joint structures undergo more or less disorganisation. Pari passu with the central atrophy of the cartilage, hypertrophic outgrowths form at its free margin. In late stages the bones, too, undergo changes; their outer layers become more dense through proliferative osteitis, while their spongy tissue becomes rarefied, and the cells of the marrow fatty. Duckworth held that uratic deposits might occur primarily in the bone without any similar implication of the related cartilage. On the other hand, Garrod dissented, claiming that when the bone was involved, it was only secondarily to uratic deposition in the cartilage, of which indeed it was but an extension.

In reviewing the foregoing findings, it must be admitted that morbid anatomy fails to shed light on the essential cause of gout. This, at any rate, is true of the older studies with which, up to the present, we have been engaged. Still, as Berkart’s more recent researches show, our knowledge of even the morbid anatomy of gout is as yet but in its infancy.

Histological examination of the articular ends adjacent to gouty joints reveals the presence of certain cystic changes in the diaphyses. Thereupon Berkart propounded an hypothesis, explanatory of the acute phenomena of a paroxysm of gout. His view was that these cysts in the bone, at first minute, gradually enlarge. Ultimately, through concomitant thinning of the surface bone, there comes a day when the cyst bursts into the joint, its content voided into the cavity thereof.

An interesting point noted by Berkart was that in many cases of “acute” gout the articular cartilage was found apparently normal and devoid of uratic deposits, and this although the attack had been sufficiently severe. This would appear to contravene Garrod’s dictum that “gouty inflammation is invariably attended with deposition of urate of soda.” The same inference was drawn from a case of Sir Dyce Duckworth’s. The subject had had two attacks of gout in the right great toe joint. Yet at the autopsy neither toe joint contained a speck of uratic deposit. Nevertheless, this does not prove that uratic deposition had not ensued during the gouty attacks. All it can be held to prove is, that such deposits are not always permanent, and that, under certain conditions, they may undergo resolution. That this is so is almost certain, seeing that tophi in the ear have been seen to come and go, and equally certainly, after an acute attack, tophi in the neighbourhood of a joint may lessen even though fresh ones form coincidently at another site.