Scleral fixation of a single-piece foldable acrylic IOL through a 1.80 mm corneal incision

A new scleral fixation technique of a single-piece acrylic foldable intraocular lens (IOL) (enVista MX60, Bausch & Lomb, Inc.) through a 1.80 mm corneal incision, using the IOL eyelets as anchoring point, is described. It was a retrospective review of 26 cases. The preoperative mean corrected distance visual acuity was 0.51 \ub1 0.21 logarithm of the minimum angle of resolution (logMAR). It improved significantly to 0.25 \ub1 0.27 logMAR (P < .01), 0.18 \ub1 0.16 logMAR (P < .01), and 0.17 \ub1 0.16 logMAR (P < .01) (at 1 month, 3 months, and 6 months postoperatively, respectively, repeated measures analysis of variance, P < .0001). No astigmatism increase of more than 0.75 diopters was recorded at any time point. In all 26 patients, the IOL was well centered and stable for the entire monitoring period. No complications were observed during follow-up. Scleral fixation of the foldable IOL through a 1.80 mm corneal incision provided excellent IOL stability during the 6-month follow-up of this study and might be an effective and safe surgical technique

State-of-the art pharmacotherapy for non-neovascular age-related macular degeneration

Introduction: Age-related macular degeneration (AMD) is the most common cause of blindness among the elderly in the industrialized world. While effective treatment is available for neovascular AMD, no therapy is successful for the non-neovascular form. Herein, the authors report the current knowledge on non-neovascular AMD pathogenesis and the promising research on treatments. Areas covered: In the present review, the authors summarize the most recent advances in the treatment of non-neovascular AMD and provide an update on current treatment strategies. Evidence available from preclinical and clinical studies and from a selective literature search is reported. Expert opinion: When investigating AMD, numerous pathological cascades and alterations of physiological processes have been investigated. It is well-known that AMD is a multifactorial disease, with environmental causes and genetics playing a role. Perturbations in multiple pathogenic pathways have been identified and this led to the development of several molecules directed at specific therapeutic targets. However, despite the huge research effort, the only proven approach so far is oral antioxidant supplementation. We believe that, in addition to successful advancement of promising drugs, further research should be directed at tailoring therapy to specific patient groups, eventually employing a combinational therapy strategy

Spectral-domain OCT changes in retina and optic nerve in children with hypoxic\u2013ischaemic encephalopathy

Purpose: To evaluate the effect of neonatal hypoxic\u2013ischaemic injury on the retina and the optic nerve and to correlate ocular damage with systemic parameters, laboratory tests, neurological imaging and therapeutic hypothermia at birth. Methods: Forty-one children with hypoxic\u2013ischaemic encephalopathy (HIE) at birth (9.09 \ub1 3.78\ua0years) and a control group of 38 healthy subjects (9.57 \ub1 3.47\ua0years) were enrolled in a cohort study. The HIE population was divided into three subgroups, based on the degree of encephalopathy according to Sarnat score and the treatment with therapeutic hypothermia (TH): Sarnat score I not treated with hypothermia, Sarnat score II-III treated with TH and Sarnat score II-III not subjected to TH. Total macular thickness, individual retinal layers and peripapillary nerve fibre layer thickness were measured with spectral-domain optical coherence tomography. Clinical data of perinatal period of HIE children were collected: APGAR score, pH and base excess of funiculus blood at birth, apnoea duration, brain ultrasound, cerebral MRI ischaemic lesions and blood chemistry tests. Results: Children with Sarnat score I did not show a reduction of peripapillary nerve fibres and ganglion cell layer compared to the control group (p = 0.387, p = 0.316). Peripapillary nerve fibre layer was 109.06 \ub1 7.79\ua0\u3bcm in children with Sarnat score II-III treated with TH, 108.31 \ub1 7.83\ua0\u3bcm in subjects with Sarnat score II-III not subjected to TH and 114.27 \ub1 6.81\ua0\u3bcm in the control group (p = 0.028, p = 0.007). Ganglion cell layer was thinner in children with Sarnat score II-III treated with TH (50.31 \ub1 5.13\ua0\u3bcm) compared to the control group (54.04 \ub1 2.81\ua0\u3bcm) (p = 0.01). Inner retinal layers damage correlated with C-reactive protein and lactate dehydrogenase increase, while higher levels of total bilirubin were protective against retinal impairment (p < 0.05). Cerebral oedema was related to peripapillary nerve fibre layer damage (p = 0.046). Conclusions: Thickness reduction of inner retinal layer and peripapillary nerve fibre impairment was related to encephalopathy severity. Ocular damage was associated with inflammation and cerebral oedema following hypoxic\u2013ischaemic damage. [Figure not available: see fulltext.