THE PROGRESSIVE nature of severe alkali burns of the eyes and the frequency of secondary complications are well known. The purpose of this communication is to outline the distinctive clinical and pathologic features, which may yield clues to the mechanism of action, and to emphasize the secondary reactions, against which are directed many of the therapeutic measures.
Except for minor differences in the rate of penetration and the intensity of opacification, the clinical courses of burns produced by a variety of alkalis, e. g., lye, lime (calcium oxide) and ammonia, are remarkably similar.1 The alkalinity of the solution is probably the most important factor governing the severity of the lesion, and the rabbit cornea is damaged by solutions more alkaline than those with pH of 11.5.2 The material for the present study included sodium hydroxide burns of the rabbit eye and clinical observations on several types
HUGHES WF. ALKALI BURNS OF THE EYE: II. Clinical and Pathologic Course. Arch Ophthalmol. 1946;36(2):189–214. doi:10.1001/archopht.1946.00890210194005
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