A new classification system predicting keratomalacia after trauma in vitamin A deficiency: sodium citrate does not prevent disease progression.

ABSTRACT

PURPOSE: The purpose of this study was to develop a classification system to predict keratomalacia after trauma in vitamin A-deficient eyes and to determine whether citrate impedes polymorphonuclear leukocyte infiltration into the cornea, thus preventing keratomalacia. METHODS: Preliminary classification studies showed that a 7.0-mm corneal epithelial scrape, before clinical findings of corneal xerosis, did not induce keratomalacia. Primary studies were conducted concurrently on the same animals to develop the classification system and test the effect of citrate in vitamin A deficiency. A 7.0-mm corneal epithelial scrape was performed on vitamin A-deficient eyes in various stages of corneal xerosis and treated as follows. Experiment 1 group 1, 10% citrate drops; group 2, phosphate buffer solution (PBS) drops; experiment II group 3, drops and subconjunctival injection of 10% citrate; group 4, drops and subconjunctival injection of PBS. RESULTS: Corneal abrasion in eyes with 2+ corneal xerosis yielded keratomalacia in 50% of cases; the remainder healed with xerotic epithelium. Eighty-three percent of eyes with > 2+ xerosis developed keratomalacia after corneal abrasion, whereas only 7.1% of eyes with < 2+ xerosis advanced to this stage. In experiment I, 27% of citrate-treated eyes and 38% of PBS-treated eyes developed keratomalacia (not significant). In experiment II, two of six citrate-treated eyes perforated and one eye developed keratomalacia. One of six control PBS eyes perforated and four developed keratomalacia. CONCLUSION: We correlated the degree of corneal xerosis with the occurrence of keratomalacia after corneal trauma. This led to the development of a classification scale that is of research and clinical significance. Additionally, citrate did not significantly reduce keratomalacia or perforation in the vitamin. A-deficient eye.