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A Vidan, A Amir, J Turetz, H Buch, T Kadar; Corneal Neovascularization in Two Models of Chemical Burn: Alkali and Sulfur Mustard . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1742.
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Purpose: The pathogenesis of corneal neovascularization in alkali and sulfur mustard (HD) burns is still unclear. Both injuries cause a permanent damage that might lead to blindness. The present study was designed to evaluate the clinical and histological characteristics of chemical burns in New Zealand White rabbit caused by an alkali agent in comparison to those caused by a chemical warfare agent, sulfur mustard (HD). Method: Alkali burns were induced in eyes by applying a 9 mm filter paper soaked in 1N NaOH for 30 seconds (n=8). In HD experiments, eyes were exposed to HD vapor for a period of four minutes (n=8). A 3-month follow-up was carried out, based on slit lamp examination, fluorescein staining and pachymetry. Animals were then sacrificed and eyes enucleated and processed for histological evaluation. Results: Alkali caused immediate sloughing of surface epithelium, whitening of the cornea and within 96 hours the majority of eyes showed neovascularization. Corneas remained opaque and thick (≷ 1000µ) and recurrent epithelial defects were noticed throughout the follow-up period. Eyelid and conjunctival signs were minimal. 2 - 6 hrs after exposure to HD, eye closure, eyelid swelling, conjunctival hyperemia and corneal erosions occurred in all eyes. Clinical signs reached a peak 24-72 hrs post-exposure and healed within 1-2 weeks. A second phase of pathological processes started as early as two weeks post-exposure in about 60% of eyes and was characterized by corneal edema, recurrent erosions and neovascularization. Corneal thickness in HD-exposed eyes increased during the acute phase (900-1000µ) and then decreased (600µ) but never returned to the normal value (400µ). Conclusions: Neovascularization appears in both models. While in alkali injury it appears instantly, HD causes a primarily mild corneal injury followed by a latent period in which the cornea seems to heal, and then new blood vessels appear. These findings are consistent with those observed in patients. The clinical course of injury suggests that different mechanisms are involved. These mechanisms merit further study. The latent period, characteristic of HD injury, may open a window of opportunity for potential treatment.
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