Ocular hydrofluoric acid burns: animal model, mechanism of injury and therapy

A series of ocular HF burns was produced in rabbits in order to clarify the nature of the injury and to provide a description of the animal model. Burned eyes were evaluated clinically and allowed to progress for up to 65 days before histologic examination. The mechanism of HF toxicity was investigated through the study of burns produced by chemicals chosen to mimic its pH effects, osmotic effects, and effects of the free fluoride ion alone. The severe progressive caustic effect of HF on the eyes was found to depend on the combination of pH and the toxic effects of the free fluoride ion, together causing extensive dose-related damage to superficial and deep structures of the eye. Mild burns caused reversible ocular injury; whereas more severe burns lead to corneal stromal scarring, vascularization, edema, formation of calcific band keratopathy plus iris and ciliary body fibrosis. An investigation was made of potential treatments for experimental ocular HF burns in rabbits. Topical ointments containing MgO or MgSO4 and irrigations with or subconjunctival injections of H2O or solutions containing NaCl, MgCl2, CaCl2, LaCl3, hyamine, zephiran, calcium gluconate or a mixture of divalent metal ions were tested for toxicity and for therapeutic value in ocular HF burns. Immediate single irrigation with H2O, NaCl or MgCl2 solution was most effective. Other therapeutic agents commonly used in HF skin burn therapy were either too toxic in normal eyes or caused additive damage to burned eyes.