Mechanical protective effect of lens anterior capsule disc on corneal endothelial cells during femtosecond laser-assisted cataract surgery in a rabbit model.

PURPOSE: To evaluate the effects of a novel technique using an isolated lens anterior capsule disc (LACD) to protect corneal endothelial cells in rabbit eyes during femtosecond laser-assisted cataract surgery. METHODS: Experimental study. 40 rabbits were divided into endothelium-protected (experimental) and control groups, with 20 rabbits in each group. In the experimental group, after femtosecond laser capsulotomy, the isolated capsule disc was lifted to the corneal endothelium by an ophthalmic viscosurgical device. The endothelium was damaged for 1 min with an ultrasonic probe. The control group underwent the same surgery, except that the disc was removed immediately after capsulorhexis. Corneal endothelioscopy was performed preoperatively and on postoperative days (PODs) 3 and 7 to observe endothelial cell counts (ECC) and endothelial cell loss rate. Central corneal thickness (CCT) was measured before and at PODs 1, 3 and 7. RESULTS: There were 3.59%±1.88% (p < 0.001) and 2.92%±2.14% (p < 0.001) loss of ECC in experimental group at POD3 and POD7, respectively, while those in the control group were 11.62%±7.43% and 10.34%±5.77%, respectively. On POD 1, the difference in central corneal thickness was significant(P = 0.019) between the two groups. At POD 3 and POD 7, CCT was not significantly different (P = 0.597;0.913) between the two groups. CONCLUSIONS: The isolated LACD technique significantly reduced damage to the endothelium caused by ultrasonic energy and protects corneal endothelial cells during phacoemulsification.

Continuous administration of voriconazole enhances therapeutic effect for recalcitrant fungal keratitis.

PURPOSE: To evaluate the therapeutic effect of incorporating continuous administration of voriconazole in the treatment of recalcitrant fungal keratitis. METHODS: In this prospective case study, 5 consecutive patients (5 eyes) with fungal keratitis were treated with a standard protocol after the failing maximal conventional medical treatment. The protocol involved continuous lavage of the ulcer with 1% voriconazole through an irrigator for 2 h, twice a day, combined with local and systemic antifungals. Visual acuity, slit lamp findings of the ulcer, and fungal hyphae density by confocal microscope were documented, respectively. RESULTS: In 4 patients, the clinical symptoms and slit lamp examination were significantly improved after only 3 days of treatment. The hyphae were shown to decrease in number and morphologically fragmented in corneal stroma by confocal microscopy. After the infection was controlled, 2 cases required further keratoplasty. In one case, the treatment was deemed ineffective and a conjunctival flap had to be created to help control the infection. In all 5 patients, the best spectacle-corrected visual acuity had improved after treatment. With more than 3 months of follow-up, no recurrence of infection was seen in any cases. CONCLUSION: Our treatment protocol demonstrated improvement in the treatment of clinically resistant fungal keratitis. Continuous lavage of voriconazole is easy to be implemented and well-tolerated by patients. Modification of the current protocol should be further explored to optimize the therapeutic effectiveness in future.

α-Melanocyte-stimulating hormone ameliorates ocular surface dysfunctions and lesions in a scopolamine-induced dry eye model via PKA-CREB and MEK-Erk pathways.

Dry eye is a highly prevalent, chronic, and multifactorial disease that compromises quality of life and generates socioeconomic burdens. The pathogenic factors of dry eye disease (DED) include tear secretion abnormalities, tear film instability, and ocular surface inflammation. An effective intervention targeting the pathogenic factors is needed to control this disease. Here we applied α-Melanocyte-stimulating hormone (α-MSH) twice a day to the ocular surface of a scopolamine-induced dry eye rat model. The results showed that α-MSH at different doses ameliorated tear secretion, tear film stability, and corneal integrity, and corrected overexpression of proinflammatory factors, TNF-α, IL-1ß, and IFN-γ, in ocular surface of the dry eye rats. Moreover, α-MSH, at 10(-4) µg/µl, maintained corneal morphology, inhibited apoptosis, and restored the number and size of conjunctival goblet cells in the dry eye rats. Mechanistically, α-MSH activated both PKA-CREB and MEK-Erk pathways in the dry eye corneas and conjunctivas; pharmacological blockade of either pathway abolished α-MSH's protective effects, suggesting that both pathways are necessary for α-MSH's protection under dry eye condition. The peliotropic protective functions and explicit signaling mechanism of α-MSH warrant translation of the α-MSH-containing eye drop into a novel and effective intervention to DED.