[Eye burns].

Eye burns are frequent among eye traumas. They induce different effects on the ocular structures, depending on the type of burn: chemical, with an important difference between acids and bases, thermal, or ionizing rays. The physiopathology of eye burns reflects the different stages of progression, with a first stage of destruction, a second stage of cleaning and inflammation, and a last stage of reconstruction and scarring. The final prognosis depends on the initial lesions, not only involving the eye ball, but also the conjunctiva and eyelids. Chemical burns by basic fluids have the worst prognosis because they are able to penetrate the tissues quickly. Burns by acids have a better prognosis and thermal burns are located only at the injured area. Treatment is most effective at the initial stage of destruction and can dramatically change the prognosis. The secondary phase of cleaning includes the entire biochemical cascade of inflammation and the production of proteases. At this stage, treatment can be effective but must be closely monitored because it can inhibit progression to the last stage of scarring. At the scarring stage, neovascularization begins, induced by initial ischemia, the reconstruction of epithelium with a probable role of stem cells, the reconstruction of nerve fibers depending on the nerve growth factor (NGF), and the reconstruction of extracellular matrix in which matrix metalloproteinases (MMPs) are essential. At this stage, therapy can only be surgery of functional after effects and esthetic anomalies.

Eye Burns↗

PubMed2004

[Medical treatment of ocular burns].

Chemical burns, especially alkali burns, can induce severe damage to the eye, not only of its surface, but also of its deep structures. Ocular chemical burns require urgent medical care and sometimes surgery. Medical management of chemical burns of the ocular surface includes controlling the inflammation of the underlying corneal stroma, preserving limbal vasculature, and restoring the limbal stem cell population if necessary, as early as the 3rd week following the injury, which sometimes also requires surgery consisting for the most part of amniotic membrane and/or limbal stem cell transplantation.

Eye Burns↗

PubMed2003

A new model for laser-induced thermal damage in the retina.

We describe a new model for laser-induced retinal damage. Our treatment is prompted by the failure of the traditional approach to accurately describe the image size dependence of laser-induced retinal injuries and by a recently reported study which demonstrated that laser injuries to the retina might not appear for up to 48 h post exposure. We propose that at threshold a short-duration, laser-induced, temperature rise melts the membrane of the melanosomes found in the pigmented retinal epithelial cells. This results in the generation of free radicals which initiate a slow chain reaction. If more than a critical number of radicals are generated then cell death may occur at a time much later than the return of the retina to body temperature. We show that the equations consequent upon this mechanism result in a good fit to the recent image size data although more detailed experimental data for rate constants of elementary reactions is still required. This paper contributes to the current understanding of damage mechanisms in the retina and may facilitate the development of new treatments to mitigate laser injuries to the eye. The work will also help minimize the need for further animal experimentation to set laser eye safety standards.

Eye Burns↗