Retinal Injuries/damage

Improving giycaemic control may not only reduce the rate of non-enzymatic glycosyiation and monosaccharide autooxidation, but lower polyol pathway activity. In addition, it should have a beneficial effect on other haemodynamic and hormonal factors involved in the development of diabetic vascular disease. However, in studies of diabetic retinopathy, rapid control of glucose levels by intensive insulin therapy has been shown to worsen vascular disease initially and it could be postulated that a sudden improvement in retinal blood flow promotes further free-radical damage as part of a reperfusion-ischaemic injury. 

Historically retinal autoimmunity has been considered pathogenic. So, active suppression of retinal immunity was thought to be necessary for the health of the eye. However, later studies have demonstrated the presence of retinal autoan-tibocUes in normal controls (Yamamoto et al., 1993). Animal optic nerve injury studies suggested possible beneficial roles of retinal autoimmunity in controlling collateral damage to the retinal ganglion cells (Kipnis et al., 2002). Thus, rednal autoimmunity can be viewed as both protective and destructive phenomenon. 

Specific cell injury or cell functional disorder occur with individual drugs or drug classes, e.g. tardive dyskinesia (dopamine receptor blockers), retinal damage (chloroquine, phenothiazines), retroperitoneal fibrosis (methysergide), NSAIDs (nephropathy). Cancer may occur, e.g. with oestrogens (endometrium) and with immunosuppressive (anticancer) drugs. 

Retinal damage appears to be an undesirable companion of transscleral iontophoresis. Retinal edema occurs within seconds of current application (56). Disruption of the normal retinal architecture, hemorrhagic necrosis, fibrosis, and RPE hyperplasia are evident beneath the iontophoretic site (68,69), and multiple applications exacerbate these injuries (70). Loss of tissue integrity, although spatially confined, may permit drug entry into the vitreous cavity or even the anterior segment tissues. Drug stability to possible electrochemical reactions is another possible limitation of this approach. 

If there is a nuclear detonation, bodily injury or death may occur as a result of the blast itself or as a result of debris thrown from the blast. People may experience moderate to severe skin burns, depending on their distance from the blast site. Those who look directly at the blast could experience eye damage ranging from temporary blindness to severe retinal burns. 

---