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causing swelling around rim of cornea), lid edema, blepharospasm, photophobia, blurred vision, and tearing. The 10 percent of patients with corneal involvement exhibited corneal edema, keratitis, ocular pain, temporary blindness, tissue necrosis, iridocyclitis (inflammation of iris and ciliary body), glaucoma, vascularization, and, rarely, ulceration or perforation of the eye.

Anatomical investigations by Ashoff and colleagues, cited in Oswald (1920), have shown that sulfur mustard poisoning probably causes blood clots in the precapillary arterioles of the eye. This might explain a report of progressive narrowing of the retinal blood vessels in a 34-year-old man who had sustained a relatively mild exposure to sulfur mustard in 1917 that nevertheless resulted in bilateral blindness (Oswald, 1920).

Chronic Course

Many patients continue to have recurrent corneal erosions and inflammatory keratitis for an indefinite number of years after the serious corneal injury. Approximately 243 cases of late recurrent ulceration of the cornea have been reported following severe sulfur mustard burns in WWI (Scholz and Woods, 1945).

In the acute stage the limbal region frequently presents a marbled appearance in which porcelain-like areas of ischemia (decreased or blocked blood flow) are surrounded by blood vessels of irregular diameter. Later, the vascularized scars of the cornea often contain deposits of cholesterin, calcium, and fat. There were reports of a sudden increase in these symptoms and findings some 8 to 25 years after the initial injury. This information first appeared in the U.S. literature in a 1947 article by Scholz and Woods, but many such cases had already been reported in the British, French, and German literature (Genet, 1925; Heckford, 1937; Moore and Heckford, 1929; Proceedings of the Royal Society of Medicine, 1940; Rohrschneider, 1937; Sourdille, 1936; Weill, 1939).

Phillips, who collected 70 cases, called attention to the delayed keratitis due to sulfur mustard exposure (Proceedings of the Royal Society of Medicine, 1940). He noted that, after the initial early and intermediate hospitalization from 4 to 6 months, these patients were often symptom free for 10 to 13 years, whereupon delayed keratitis developed, characterized by photophobia, lacrimation, and failing vision. Superficial ulcerations also occurred in these patients, and the sensitivity of the cornea to touch and other stimuli was reduced. Marbling of the cornea appeared in the acute stage of these cases along with additional linear marks referred to as "skate marks on fresh ice." Also found were pale triangular patches on either side of the cornea,

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