In early stages the skin over the joint is waxy white or semi-asphyxial in tint, outline of joint smooth, rounded, and spindle in shape, with, as a rule, no irregular bony projection at the level of the articulation. If seen at a later stage, the swollen joint will be found shrunken from atrophy of all the articular structures as well as the skin. Ultimately it becomes reduced even below its normal size, the small “end-joint” of atrophic or rheumatoid arthritis. The deformities due to muscular spasm are usually in the direction of luxation and hyperextension, and differ from those of gout and osteoarthritis, in which there is more generally lateral displacement.
Nerve Arthropathies
The joint disorders incidental to tabes and syringomyelia do occasionally find their way to spas for treatment under the mistaken conception that they are instances of “gout,” “rheumatism,” or “rheumatic gout.” In the case of tabes the mistake is often referable to the confounding of its lightning pains with “gout” or “rheumatism,” with subsequent relegation of the swollen joints, whether single or multiple, to one or other of these categories. In the syringomyelic it is, I think, the close resemblance that obtains between the joint lesions and those of osteoarthritis or so-called “rheumatic gout” that accounts for their uncalled-for and utterly useless transference to spas. I have known a case of syringomyelia with multiple arthropathies in the hands sent to Bath under the mistaken idea that they were of “gouty” origin.
These remarkable joint affections will be distinguished by their fulminant onset with marked effusion and absence of pain, tenderness, and heat. In addition, associated phenomena will be present, viz., ataxic pupillary changes and lost knee-jerks in tabes, while syringomyelia is characterised by dissociated anæsthesia, trophic disturbances of bones, progressive muscular atrophy with paralysis.
Hæmophilic Arthritis
It will be recalled that Rieken held the view that so-called “bleeders” were prone to attacks of gout, and that sometimes these alternated with intra-articular hæmorrhages. Nor was he devoid of supporters, for Sir Dyce Duckworth maintained that a definite hereditary relationship obtained between gout and hæmophilia, while that astute observer Jonathan Hutchinson also contended that the vascular weakness was the outcome of gout and aggravated by serial hereditary transmission. Wickham Legg, however, in his masterly contribution questioned the correctness of Rieken’s proposition.
Personally, I cannot out of my own experience confirm or rebut the view that “bleeders” come of gouty stock, nor have I ever met an avowed gouty subject who was likewise the victim of hæmophilia. Quâ its joint complications, hæmophilia to our mind would appear to display closer affinities with peliosis rheumatica than with gout; but, in view of Duckworth and Hutchinson’s claims, it were wiser on our part to withhold judgment, while paying them the deference of being alive to the possibility of there being some obscure connection, though not proven, between the two disorders. Again, as emphasising the necessity for discrimination, we would draw attention to the fact that Konig recognised three stages in hæmophilic arthritis: (1) hæmarthrosis; (2) an inflammatory process, with pyrexia and spindle-shaped swellings apt to be confused with tuberculosis; (3) extensive arthritic changes reminiscent of arthritis deformans. Confusion with gouty arthritis clearly is only likely in the second or third stages, and in the matter of diagnosis the personal and family tendency to hæmorrhages is the most important clue.