Objective: To investigate a possible correlation between final visual acuity and the presence at baseline of various systemic and local (orbital/ocular) signs in patients affected by indirect traumatic optic neuropathy. Methods: 35 cases of traumatic optic neuropathy were examined retrospectively and 13 variables were tested. Univariate analysis with "no recovery of visual acuity" as the primary outcome was performed. Relative risk (RR) and 95% confidence intervals (CI) were calculated. Fisher's exact test was used for two variables to test differences between proportions. Results: Four variables showed a significantly increased risk for no recovery of visual acuity: presence of blood within the posterior ethmoidal cells (RR = 2.25, 95% CI 1.25 to 4.04); age over 40 years (RR = 1.79, 1.07 to 2.99); loss of consciousness associated with traumatic optic neuropathy (RR = 2.21, 1.17 to 4.16); and absence of recovery after 48 hours of steroid treatment (p < 0.01, Fisher's exact test). Recovery documented at the first follow up visit after treatment was significantly associated with recovery at the last follow up visit (p < 0.01, Fisher's exact test). Conclusions: These four negative prognostic signs in patients affected by traumatic optic neuropathy may be useful in predicting the visual outcome in patients developing visual loss after head trauma and in deciding on the need for surgical treatment.

Open globe injury in Northern Sardinia varied with age, gender, and residence, was associated with lack of eye protection, and often resulted in severe visual loss. People engaged in domestic or leisure activities, especially the retired, are at highest risk, suggesting the need for targeted messages. This could reduce the incidence of open globe injury and its associated costs on the community.

Diagnosis of Münchausen syndrome is difficult to make in the ophthalmic department. Münchausen patients have little or no ability to control their self-destructive behavior. A sympathetic and supportive approach is therefore required and these patients should be urgently referred to a psychiatrist with experience in factitious disorders. Even with psychotherapy, which is often refused, the prognosis remains poor.

The aim of this study was to determine the levels of human tissue kallikrein in the vitreous fluid of patients with severe proliferative diabetic retinopathy (PDR). Tissue kallikrein levels were measured using a specific ELISA (range: 0.4–25 ng/ml) in 7 vitreous fluids from eyes with severe PDR. Seven vitreous samples from eyes which underwent vitrectomy because of rhegmatogenous retinal detachment served as non-PDR controls. Enzymatic activity was also tested by an amidolytic assay using a chromogenic substrate. In the PDR patients, vitreous tissue kallikrein was <0.4 ng/ml (5 eyes) or very low (0.52 and 0.58 ng/ml). Vitreous tissue kallikrein was <0.4 ng/ml in all non-PDR controls. These results were confirmed by the amidolytic test. Results suggest that vitreous tissue kallikrein probably plays either a secondary or no role in the pathogenesis of PDR.

The results suggest that grafts for keratoconus in patients with Turner's syndrome might have an increased risk of immunologic rejection. Corneal grafts in Turner's syndrome need to be monitored closely. Early detection of graft rejection and aggressive treatment with topical and systemic steroids and systemic cyclosporine A can save the graft and restore useful vision.