Navegando por Palavras-chave "ceratoprotese"

Agora exibindo 1 - 1 de 1
  • Nenhuma Miniatura disponível
    Item
    Somente Metadadados
    Avaliação do dano ocular após queimadura química grave na córnea e suas possíveis implicações no implante da ceratoprótese de boston
    (Universidade Federal de São Paulo (UNIFESP), 2015-12-31) Jorge, Fabiano Cade [UNIFESP]; Siqueira, Wallace Chamon Alves de Siqueira [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    A severe chemical burn to the eye usually results in an opaque cornea. Its prognosis depends on the immediate treatment and prevention of further complications. Regardless of medical efforts, surgical rehabilitation with standard penetrating keratoplasty, often repeated, is usually fruitless in the long run, due to limbal stem cell deficiency. Boston Keratoprosthesis (KPro) is reported to give better outcome. However, in chemical burn eyes, optic nerve and retina seem to become more sensitive, developing intraocular complications, such as glaucoma, even with normal intraocular pressure, and retinal detachment. A retrospective review of patients with KPro and severe chemical burns was performed; the number of eyes with a preoperative history or signs of glaucoma was 21 (75%) out of 28 eyes, nine of which had glaucoma progression after KPro implantation. Thus, anti glaucoma medication must be prescribed, and therefore pressure evaluation must have priority in the early burn follow-up. Protection against optic nerve injury should have importance post burn. In addition, inflammation control plays an important role in this scenario. It has been showed that post burn inflammation results in a cloudy cornea and neovascularization. Retina may also be damaged. Two possible mechanisms of retinal damage after ocular surface burn can be hypothesized: first, direct pH-related alkali diffusion from the anterior chamber to the back of the eye, leading to cell cytotoxicity and retinal injury. And second, diffusion of inflammatory cytokines, especially tumor necrosis alpha (TNF-?) from the site of the injury to the posterior segment, causing cell death and retinal damage. The use of infliximab was tested to block TNF-? in mice. In pilot in-vivo and ex-vivo experiments, using larger eyes form pigs and rabbits, respectively, direct pH measurements revealed that the alkalinity in the anterior chamber was significantly elevated. In contrast, pH measurements in the vitreous remained unchanged, suggesting that prompt alkali diffusion posteriorly through the vitreous is very unlikely. In our model, early retinal damage after ocular surface alkali burns, and the protective effects of TNF-? blockade were evaluated. There was significant damage to the retina by 24 hours after corneal burn. TUNEL positive labeling was present in the retinal ganglion cells. Increase in the retinal inflammatory cytokines levels was showed in burned eyes. A single dose of anti-TNF-? antibody provided substantial retinal and corneal protection. This finding could lead to novel and more efficient therapies for chemical injury patients treatment.