Consideration of angle kappa is important for correct centration of refractive treatments. Decentered refractive treatment can cause photic phenomena including glare, halo, and deterioration of vision. This review highlights the concept of angle kappa, its measurement and distribution in normal populations, and the methods to compensate for large angle kappa in refractive surgery using laser or intraocular lenses (IOLs). Determination of the treatment center is very important in refractive surgery. Moving the ablation center from the center of the entrance pupil to points near visual axis, such as the corneal light reflex (line of sight) or corneal vertex normal, results in less induction of higher order aberrations (including coma aberration) and either the same or better visual outcomes both in hyperopic and myopic eyes when compared to laser ablation centered on the entrance pupil. Decentration of multifocal IOLs can result in deterioration of postoperative visual function with induction of higher order aberrations. The occurrence of photic phenomena positively correlated with preoperative values of angle kappa. There is a growing body of evidence that emphasizes the consideration of angle kappa in refractive surgery. Ignoring angle kappa may sometimes result in decentered treatment and aggravation of visual symptoms. Compensation for angle kappa is important for optimal correction of refractive error by either laser ablation or IOLs, especially for hyperopes and any eyes with large angle kappa.
Toxic anterior segment syndrome (TASS) can be a rare complication of anterior segment surgery. Here we reviewed the most recent advances in the understanding of TASS. English articles related to TASS were retrieved from “PubMed” using the following keywords; “toxic anterior segment syndrome” or “TASS”. The authors of this paper reviewed all the retrieved literature and critical findings were summarized. The onset of TASS can vary from hours to months. The clinical manifestations are also variable. The causes of TASS are broad and continue to expand and could not be elucidated in over half of the reported cases. Prompt and thorough investigation to explore the causes of TASS is critical. Surgeons should be fully aware and updated regarding possible etiologies and make ceaseless efforts to prevent TASS. This effort begins with establishing TASS prevention protocols and regularly training surgical staff. Proper cleaning of surgical instruments is critical and should follow the guidelines set by The American Society of Cataract and Refractive Surgery TASS Task Force. When TASS occurs, sharing information with other ophthalmologists and reporting new causes is crucial for the prevention of outbreaks. Anterior segment surgeons should be reminded that TASS is mostly preventable by the establishment of TASS prevention protocols, regular surgical staff training and thorough adherence to recommendations for cleaning and sterilizing intraocular surgical instruments.
Ocular drug delivery is an interesting field in current research. Silica nanoparticles (SiNPs) are promising drug carriers for ophthalmic drug delivery. However, little is known about the toxicity of SiNPs on ocular surface cells such as human corneal epithelial cells (HCECs). In this study, we evaluated the cytotoxicity induced by 50, 100 and 150 nm sizes of SiNPs on cultured HCECs for up to 48 hours. SiNPs were up-taken by HCECs inside cytoplasmic vacuoles. Cellular reactive oxygen species generation was mildly elevated, dose dependently, with SiNPs, but no significant decrease of cellular viability was observed up to concentrations of 100 μg/ml for three different sized SiNPs. Western blot assays revealed that both cellular autophagy and mammalian target of rapamycin (mTOR) pathways were activated with the addition of SiNPs. Our findings suggested that 50, 100 and 150 nm sized SiNPs did not induce significant cytotoxicity in cultured HCECs.
Nonporous silica nanoparticles (SiNPs) have potential as promising carriers for ophthalmic drugs. However, the in vivo safety of ocular topical SiNPs remains unclear. This study investigated the in vivo safety of oral and ocular topical applications of 100 nm-sized SiNPs in Sprague-Dawley rats. The rats were divided into the following four groups: low-dose oral administration (total 100 mg/kg of SiNPs mixed with food for one week), high-dose oral administration (total 1000 mg/kg of SiNPs mixed with food for one week), ocular topical administration (10 mg/ml concentration, one drop, applied to the right eyes four times a day for one month), or a negative control (no SiNP treatment). The rats were observed for 12 weeks to investigate any signs of general or ocular toxicity. During the observation period, no differences were observed in the body weights, food and water intakes, behaviors and abnormal symptoms of the four groups. No animal deaths occurred. After 12 weeks, hematologic, blood biochemical parameters and ophthalmic examinations revealed no abnormal findings in any of the animals. The lack of toxicity of the SiNPs was further verified in autopsy findings of brain, liver, lung, spleen, heart, kidneys, intestine, eyeballs, and ovaries or testes.
Nonporous silica nanoparticles (SiNPs) are promising drug carrier platforms for intraocular drug delivery. In this study, we investigated the safety of three different sizes of SiNPs (50, 100, and 150 nm) in a human corneal endothelial cell (HCEC) line, B4G12. The HCECs were exposed to different concentrations (0, 25, 50, and 100 µg/ml) of three sizes of SiNPs for up to 48 h. Cellular viability, autophagy, lactate dehydrogenase (LDH) assay, and mammalian target of rapamycin (mTOR) pathway activation were evaluated. Intracellular distribution of the SiNPs was evaluated with transmission electron microscopy (TEM). TEM revealed that the SiNPs were up-taken by the HCECs inside cytoplasmic vacuoles. No mitochondrial structural damage was observed. Both cellular viability and LDH level remained unchanged with up to 100 µg/mL of SiNP treatment. Autophagy showed a significant dose-dependent activation with 50, 100, and 150 nm SiNPs. However, the mTOR activation remained unchanged. Human corneal tissue culture with 100 µg/ml concentrations of SiNPs for 72 h revealed no significant endothelial toxicity. In vivo corneal safety of the SiNPs (0.05 ml intracameral injection, 200 mg/ml concentration) was also verified in rabbit models. These findings suggested that 50, 100, and 150 nm SiNPs did not induce acute significant cytotoxicity in corneal endothelial cells at concentrations up to 100 µg/mL. However, long-term toxicity of SiNPs remains unknown.