Corneal epithelial ingrowth after perforating corneal injury: a case report.

BACKGROUND: Epithelial ingrowth is a rare complication after ocular perforation and can become manifest many years after the primary trauma. CASE PRESENTATION: A 49-year-old patient presented with a positive Seidel test of unclear origin at her left eye, as well as a sharply defined anterior-stromal corneal scar at both eyes. Prior operations included a bilateral laser-assisted blepharoplasty 3 months earlier. The patient indicated to have been on holiday to France 5 months earlier, during an ongoing oak processionary moth caterpillars infestation. The examination using confocal microscopy confirmed a corneal perforation at the left eye and revealed corneal epithelial ingrowth capped with scarred stroma in both eyes. We performed a penetrating keratoplasty at the left eye. The scarred and perforated host cornea was divided into 4 pieces for further investigation: microbiology (negative), virology (negative), histology and transmission electron microscopy (TEM). Histology revealed differently structured epithelium, centrally inverted into the stroma through defects in Bowman's layer. TEM revealed full thickness corneal perforation with an epithelial plug extending to the lower third of the cornea, but without evidence of epithelial cell migration into the anterior chamber. Our differential diagnosis of the unclear positive Seidel test with epithelial ingrowth was as follows: (1) corneal perforation by hairs of the oak processionary moth caterpillar, although no hairs could be found histologically; (2) corneal perforation during laser-assisted blepharoplasty, which may be supported by the presence of pigmented cells on the posterior surface of Descemet´s membrane, pointing to a possible iris injury. CONCLUSION: Consequently, we highlighted that contact lenses can be useful, safe and inexpensive protective devices in upper eyelid procedures to protect the cornea against mechanical iatrogenic trauma.

Chromatic Full-Field Stimulus Thresholds in Patients with Treatment-Naive Age-Related Macular Degeneration.

PURPOSE: To evaluate retinal sensitivity using chromatic full-field stimulus thresholds (FST) in patients with treatment naive exudative age-related macular degeneration (e-ARMD) before and during the first intravitreal anti-vascular endothelial growth factor (anti-VEGF) treatment. PATIENTS AND METHODS: After general ophthalmological examinations to diagnose patients with e-ARMD the FST, the central foveal thickness (FCt) and the visual acuity were assessed in 20 eyes of 20 patients during this prospective study. Examinations were performed before and during the first treatment series with three intravitreal anti-VEGF injections. Normal values for FST were assessed in 19 eyes of 19 healthy subjects. Results were analyzed using Student's two-tailed t-test and Pearson's correlation coefficients between all functional parameters. RESULTS: At baseline and before the 1st intravitreal anti-VEGF treatment, a moderately significant negative correlation between VA and FCt was found in the e-ARMD group (p = 0.02, r = -0.45 and p = 0.03, r = -0.45), respectively. After the 2nd intravitreal anti-VEGF injection, no significant correlation between VA and FCt was found (p = 0.12). However, a significant correlation between FCt and blue FST was evident (p = 0.04, r = 0.4). After the 3rd intravitreal anti-VEGF treatment, there was no correlation evident between VA and FCt (p = 0.31) but a high significant correlation between FCt and FST using red (p = 0.01, r = 0.53), green (p = 0.002, r = 0.6) and blue light (p = 0.007, r = 0.66). CONCLUSION: During anti-VEGF treatment in patients with e-ARMD, the FST test showed higher significant correlations with the morphology measured by FCt, as it is the case for VA. These findings support that the FST test might serve as a valuable diagnostic tool for monitoring patients with e-ARMD and enhance functional assessment of retinal function under treatment with anti-VEGF.

Cyclosporine A Protects Retinal Explants against Hypoxia.

The retina is a complex neurological tissue and is extremely sensitive to an insufficient supply of oxygen. Hypoxia plays a major role in several retinal diseases, and often results in the loss of cells that are essential for vision. Cyclosporine A (CsA) is a widely used immunosuppressive drug. Furthermore, treatment with CsA has neuroprotective effects in several neurologic disorders. No data are currently available on the tolerated concentration of CsA when applied to the retina. To reveal the most effective dose, retinal explants from rat eyes were exposed to different CsA concentrations (1-9 µg/mL). Immunohistochemistry with brain-specific homeobox/POU domain protein 3a (Brn3a) and TUNEL staining was performed to determine the percentage of total and apoptotic retinal ganglion cells (RGCs), as well as the responses of micro- and macroglial cells. Furthermore, optical coherence tomography (OCT) scans were performed to measure the changes in retinal thickness, and recordings with multielectrode array (MEA) were performed to evaluate spontaneous RGC spiking. To examine the neuroprotective effects, retinas were subjected to a hypoxic insult by placing them in a nitrogen-streamed hypoxic chamber prior to CsA treatment. In the biocompatibility tests, the different CsA concentrations had no negative effect on RGCs and microglia. Neuroprotective effects after a hypoxic insult on RGCs was demonstrated at a concentration of 9 µg/mL CsA. CsA counteracted the hypoxia-induced loss of RGCs, reduced the percentage of TUNEL+ RGCs, and prevented a decrease in retinal thickness. Taken together, the results of this study suggest that CsA can effectively protect RGCs from hypoxia, and the administered concentrations were well tolerated. Further in vivo studies are needed to determine whether local CsA treatment may be a suitable option for hypoxic retinal diseases.

Hypothermia protects retinal ganglion cells against hypoxia-induced cell death in a retina organ culture model.

BACKGROUND: Hypoxia contributes to retinal damage in several retinal diseases, including central retinal artery occlusion, with detrimental consequences like painless, monocular loss of vision. Currently, the treatment options are severely limited due to the short therapy window, as the neuronal cells, especially the retinal ganglion cells (RGCs), are irreversibly damaged within the first few hours. Hypothermia might be a possible treatment option or at least might increase the therapy window. METHODS: To investigate the neuroprotective effect of hypothermia after retinal hypoxia, an easy-to-use ex vivo retinal hypoxia organ culture model developed in our laboratory was used that reliably induced retinal damage on a structural, molecular and functional level. The neuroprotective effect of hypothermia after retinal hypoxia was analysed using optical coherence tomography scans, histological stainings, quantitative real-time polymerase chain reaction, western blotting and microelectrode array recordings. RESULTS: Two different hypothermic temperatures (30°C and 20°C) were evaluated, both exhibited strong neuroprotective effects. Most importantly, hypothermia increased RGC survival after retinal hypoxia. Furthermore, hypothermia counteracted the hypoxia-induced RGC death, reduced macroglia activation, attenuated retinal thinning and protected from loss of spontaneous RGC activity. CONCLUSIONS: These results indicate that already a mild reduction in temperature protects the RGCs against damage and could function as a promising therapeutic option for hypoxic diseases.