Ocular toxicity long-term effects

These findings should have two consequences. First, the development of potential long-term ocular endotamponades should consider harmonising viscosity and density to avoid mechanically induced side effects. And secondly, the evaluation of the biocompatibility should include effects not directly related to classic toxic phenomena. 

Abuse of topically administered drugs by practitioners or patients can cause significant ocular toxicity. Infiltrative keratitis has occurred from long-term use of anesthetic eyedrops for relief of pain associated with corneal abrasions. Bilateral posterior subcapsular cataracts have developed after the topical administration of prednisolone acetate 0.12% twice daily over long durations. Practitioners should closely monitor patients treated with drugs known to have potentially significant ocular or systemic side effects. 

Adverse effects, in up to 60% of patients, are closely related to indometacin s strong anti-inflammatory potency. Gastric irritation, including ulcers, bleeding, and perforation, predominates. Nervous system comphca-tions are related to cerebral edema. Headache is common. Hematological effects are infrequently reported. Nephrotoxicity is exacerbated by pre-existing renal impairment. Ocular toxicity can follow long-term use. 

The exact mechanisms of MIC toxicity are not known, however, carbamylation of globin and other blood proteins have been speculated to contribute to MIC-induced toxicity. Acute exposure via inhalation of MIC vapors is known to cause irritation to the respiratory tract causing severe pulmonary edema and injury that can lead to death. It is also corrosive to the eyes causing severe corneal damage. Survivors of acute exposures may exhibit long-term respiratory and ocular effects. Direct skin contact of MIC in the liquid or gaseous form causes irritation of the skin. 

Recognizing the fact that ROS play a role in the pathogenesis of mustard-induced ocular injuries, compounds that inhibit the formation of ROS or prevent their toxic effects would be beneficial in the treatment of mustard-induced ocular injuries. The topical application of low concentrations of Zn/DFO or Ga/DFO after comeal exposure to nitrogen mustards markedly reduced conjunctival, comeal, iris, and anterior chamber injury. In the cornea, the healing of epithehal erosions was faster, the long-term opacification was reduced, and the levels of neovascularization were lowered. In the anterior chamber, decreased inflammation and better maintenance of intraocular pressure were achieved. Cataractous changes were also notably milder (Banin et al., 2003). 

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