A. St. Clair Buxton
1888 The Lancet  
He complained of rapid loss of sight during eleven weeks, culminating at the time of nig visit to the hospital in the .condition described on his eut-patient letter, which gives the following details :-" Diagnosis: (?) Albuminuric retinitis. Vision with each eye=. Cannot read any near types. Cannot see to write. Colour blindness for red. Says be could see perfectly eleven weeks ago. Appearance of fundus normal in both eyes, except a few minute white specks near macula in right eye. ,Ordered
more » ... t eye. ,Ordered mist. ferri. aper." This treatment was after a while changed to syrup ferri iodidi, two drachms three times a day, and subsequently five grains of iodide of potassium were added to each dose of the syrup. A note now appears on the letter to the effect that °° he owns to having been a heavy drinker and smoker." No order, however, was given him to discontinue smoking, though alcohol was strictly forbidden. Apparently the diagnosis remained unchanged. He attended regularly once a week until April 1st, when, to use his own words, he "became sick ot it," for his vision was steadily becoming worse. On Jan. 18th, 1888, rather more than a year after the onset of the amblyopia, he called on me in the faint hope that something might yet be done to mitigate his desperate condition. It was at this time that I had the opportunity of inspecting the hospital letter above mentioned. The ophthalmoscopic appearances described therein were in accordance with those I observed myself, except that I noticed a marked diminution in the calibre of the retinal arteries and a distension of the veins. The discs were normal, neither pale nor cupped, and the tension of the globes was also perfectly normal. But the vision had now declined to scarcely more than mere perception of light. By keratoscopy a amall amount of hypermetropia was detected. There was nothing save the group of white specks to suggest retinitis, to my mind, as the cause of blindness. Nor did the closest questioning elicit any fact on which could possibly be based any suspicion that syphilis had played a part in the ocular tragedy. A careful examination revealed no trace of albumen in the urine, the specific gravity of which was M22. I was forced to the conclusion that his case had been incorrectly diagnosed, and that he was in reality suffering from tobacco amblyopia. I mentioned the fact that stimulants had been entirely abandoned for a year, but smoking was still indulged in. So that, admitting my diagnosis to be correct, it was evident that tobacco alone was keeping up the trouble, whether originally produced by the combined action of that drug with alcohol or not. In by far the greater number of cases of this kind that have come under my observation I have noticed a more or less well-marked diminution in the calibre of the arteries, and a corresponding increase in that of the veins. Indeed, I believe this to be a prominent feature, at some stage, in most cases of tobacco amblyopia. I am not aware that the primary seat of the lesion in the disease has yet been accurately determined, but I am inclined to think that the central (axial) portion of the optic nerves is the region 'first affected. 1. The peripheral portions of the field of vision are the last affected. 2. Lateral hemiopia is not met with, as far as I know. 3. Papillitis is noticed in some cases as an advanced symptom, hypersemia of the disc being frequently seen in the early stages. 4. Atrophy of the disc ia known to occur in cases of long standing. How are these facts to be accounted for? If we admit axial neuritis (resulting from a specific action of tobacco on this portion of the optic nerve), we seem to have an answer to the question. Inflammatory action would cause swelling, and perhaps exudation. The flow of blood in the arteries and the return current in the veins would be interfered with; hence the appearance of the vessels as seen with the ophthalmoscope. The stasis would in time react on the surrounding nerve fibres, first setting up irritation, and ultimately causing atrophy by pressure, nutrition being denied by reason of mechanical obstruction. For this reason I am of opinion that absorbents offer a better chance of rapidly successful treatment than any other class of drugs, tobacco, the origo mali, being of course strictly forbidden. In the case of E. L ----the medicinal treatment was as follows: Liq. hydrarg. perchlor., 2 dr.; pot. iodidi, 12 gr.; aq. dest. ad 1 oz.; three times a day. Ext. nucis vom., 2 gr.; ext. hyoscyam.,1 1 gr.: ft. pil.; one pill with each dose of mixture. This was taken regularly since Jan. 18th, 1888, and when I saw him, four weeks later, on Feb. 15th, his vision had improved very remarkably, as the following shows: With + 1 D, to correct hypermetropia, reads ; with + 4 D, for presbyopia and hypermetropia, reads No. 10 Jaeger at 16 in. He can also read handwriting, and is able to resume his duties, which he had been forced to abandon for over a year. Whether the simple abstinence from tobacco brought about the restoration of useful vision, or whether the mercury and iodide played any part in his recovery, I cannot of course determine with certainty; but I may say that the vessels have already resumed their natural proportions, and the colour-blindness is no longer marked. This is one case out of many of which I could give a very similar account.
doi:10.1016/s0140-6736(02)26731-8 fatcat:ubgit77hxjb3zdwks67i3ejtoy