In renal disease gout is widely recognised as a possible precursor. So we are again in the same quandary that we experience in considering the relationship of gout to iritis. Are the retinal hæmorrhages due to gout or to the resulting renal disease? The claim of gout to be the deus ex machina once more seems to be superfluous, for retinal hæmorrhages are an end result which may be reached by a variety of pathological routes. Gout may be one, but if so it acts viâ interstitial nephritis. In other words, hæmorrhagic retinitis is the apanage of nephritis and the appendix of gout.
It is impossible to affirm that a retinitis is gouty, for there are no distinctive features, but it occurs in gout when vascular disease has supervened, not gouty retinitis, therefore, but retinitis in the gouty. This is all that can be affirmed when we find albumen in the urine and tophi in the ears, eyelids, etc. Moreover, it is wiser in the interest of the patient to take this broad view. There may be a link between the kidney and the diathesis, but it is invisible.
Neither are we absolved from searching for some other cause of renal disease. The case may be fundamentally one of arterio-sclerosis with a secondarily induced sclerotic kidney, or, on the other hand, the hæmorrhages may be symptomatic of pernicious anæmia and due to toxins. With regard to prognosis it is helpful to remember that retinal hæmorrhages, especially when they are isolated, suggest the possibility of death ensuing suddenly from cerebral hæmorrhage; but albuminuric retinitis is itself frequently a terminal stage of chronic renal disease. We have not sufficient proof to call retinitis gouty, and we should adhere to the more catholic appellation “nephritic retinitis.”
James Taylor, writing on neuro-retinitis in the gouty,[59] states that—
“Commonly, of course, it occurs in association with albuminuria, yet it is met with apart from this even in cases where no very obvious cardio-vascular changes can be demonstrated in other regions. And thromboses in retinal veins, apart from cardiac hypertrophy and demonstrable changes in the arteries or in the blood pressure, are of frequent occurrence. In such cases gout is possibly—in many cases demonstrably—a very important factor in the etiology.”
The opinion that cases of neuro-retinitis may be gouty is based upon (a) the fact of the apparent absence of cardio-vascular disease elsewhere, (b) the lack of any other ostensible cause. Doubtless many cases of retinal hæmorrhage are seen for which we are unable to assign a cause; in some of these there is no suggestion of gout and nothing to support a postulation of a latent form of that diathesis. Taylor’s statement that gout in many cases is demonstrably a very important factor in the etiology cannot be lightly set aside, but as the appearances of neuro-retinitis are similar whether gout is present or absent, it is legitimate to question if the diathesis is really necessary.
Glaucoma.—Brudenell Carter, Hutchinson and Nettleship have claimed that gouty people are more apt than others to suffer from glaucoma, but no convincing argument has been brought forward in proof of any definite nexus.
The conclusion I would arrive at is that it is unwarrantable to speak of “gouty” ocular disease, for there is nothing in the character of the inflammation specific of gout. We renounce the prefix in order—
(1) That we may not be lulled into false etiological security, and
(2) That we may approach the elucidation of the case and the treatment thereof free from preconceptions. The mouth and its accessory cavities are the primary sphere of our investigation. This is no mean task, including as it does the radiography of the teeth, even though these are apparently healthy. In the tortuous route of elimination we look for concealed dental roots, rarefying osteitis, buried tonsils, post-nasal infections, antral disorders.