[CyPass microstent trimming with special cutting forceps : Video article]. / CyPass-Mikrostent-Kürzung mittels spezieller Schneidezange : Videobeitrag.

OBJECTIVE OF SURGERY: A CyPass®-microstent (Alcon, Fort Worth, TX, USA) extending too far into the anterior chamber should be trimmed as close as possible to the scleral spur to avoid progression of endothelial cell reduction. INDICATIONS: After CyPass implantation, if there is a significant loss of corneal endothelial cells due to the Cypass microstent extending too far into the anterior chamber, trimming or removal of the CyPass stent is necessary. CONTRAINDICATIONS: There are no contraindications. SURGICAL TECHNIQUE: As shown in our video, which is available online, a special cutter (19 Gauge Ahmed Micro Stent Cutter, MicroSurgical Technology Inc, Redmond, WA, USA) is inserted into the anterior chamber via a 1.5-mm wide corneal paracentesis made directly opposite to the CyPass stent. It is then possible to trim the anterior part of the stent. The severed fragment is removed using the head of the forceps. Finally, the previously inserted viscoelastic agent can be aspirated and the paracentesis can be hydrated. POSTOPERATIVE TREATMENT: After the surgery vision testing as well as control of intraocular pressure and location of the stent are carried out. Antibiotic eye drops and ointment are postoperatively applied. EVIDENCE: There is still no standardized protocol for the procedure to trim the CyPass stent. Performing the trimming in our clinic using the procedure described here has so far not led to any complications. Long-term data about the development of the endothelial cell measurement after CyPass trimming are not yet available.

The effect of Rho Kinase inhibition on corneal nerve regeneration in vitro and in vivo.

PURPOSE: Impairment of corneal nerves can lead to neurotrophic keratopathy accompanied with severe ocular surface damage, which due to limited treatment options, can result in severe visual deterioration. This study evaluates a possible new treatment by enhancing the corneal nerve regeneration using a Rho Kinase inhibitor (Y27632). ROCK is known to play an important role in regulating cell morphology, adhesion and motility but little is known about its role in corneal nerve regeneration. METHODS: Effects of ROCK inhibition on murine peripheral nerves was assessed in single cell- and wound healing assays as well as a 3D in vitro model. Furthermore, Sholl analysis evaluating neuronal branching and life-death assays evaluating toxicity of the inhibitor were performed. An in vivo mouse model was established, with monitoring weekly corneal nerve regrowth using confocal microscopy. Additionally, corneal nerve fiber length was evaluated by immunofluorescence staining. Underlying pathways were examined by qrtPCR. RESULTS: ROCK inhibition leads to a significant enhancement of fiber growth in vitro. Sholl analysis revealed a higher degree of branching of treated fibers. Cytotoxicity assay showed no influence of Y27632 on cellular survival. In vivo measurement revealed significant enhanced regeneration after injury in the treated group. QrtPCR of trigeminal ganglia confirmed ROCK knock-down as well as altered pathways. CONCLUSION: The inhibition of ROCK after corneal nerve injury resulted in an enhanced regrowth of fibers in vitro and in vivo. This might be a step towards a new therapeutic concept for the treatment of impaired corneal nerves in diseases such as neurotrophic keratopathy.