On the dark side of light: Genesis and prevention of two spectral types of retinal light damage

This thesis is on light damage to the retina. Photochemical light damage to the retina can even occur under ambient light conditions as demonstrated by Noell et al. (1966) They found green light (500 nm) the most powerful in causing retinal damage. Under higher irradiance conditions the action spectrum changes: Short wavelengths are then the most harmful (Ham et al., 1979; Ham, Mueller and Sliney, 1982; Gorgels and van Norren, 1995). With ever increasing irradiance the domain of thermal damage is entered. The highest retinal irradiance used in the experiments in this thesis is approximately 300 mW/ cm . This is a rather high 2 level, but insufficient to increase the retinal temperature over 10 C; the generally accepted safety o limit (Ham et al., 1979). Another argument against thermal damage, is the duration of the exposure. Thermal damage occurs in less then a second, or not at all (Ham et al., 1979; van Norren, Keunen and Vos, 1998). In the experiments in this thesis longer exposures (from 8 to 100 minutes) were required to cause damage. Thus, we have always dealt with photochemical rather than thermal mechanisms in retinal light damage as investigated in this thesis. The aims of the studies in this thesis were: (1) To document the development of two spectrally determined types of photochemical light damage. (2) To obtain more information about the mechanisms of these two spectral light damage types, and to evaluate possible protectors against retinal light damage

Temporal sequence of changes in rat retina after UV-A and blue light exposure

AbstractTwo spectral types of retinal light damage were induced in pigmented rats by irradiating small retinal patches at either 380 or 470 nm. The temporal sequence of changes in the retina was followed for up to 2 months by funduscopy and histology. For both damage types, fundus changes were best visible after 3 days. Histology showed that 380 nm specifically damaged photoreceptor cells, particularly the rods. All cell compartments of the rods, including the nucleus were affected already after 3 h. In the next days, damaged rods degenerated. At high doses (2.5×the funduscopic threshold dose) all rods in the irradiated area were lost, resulting in a local photoreceptor lesion, which was still present at 2 months after the irradiation. At 470 nm, damage occurred both in the photoreceptor layer and in the pigment epithelium. Acute changes, at 1 h after irradiation, consisted mainly of damaged mitochondria in these layers. Next, the pigment epithelium showed swelling, an altered melanin distribution and, at high doses (2.5×threshold), interruptions of the monolayer. Degeneration of photoreceptor cells was initially limited to a few scattered cells, but 3 days after high doses focal areas of massive degeneration were seen. At late stages, the cells of the pigment epithelium recovered and the photoreceptor layer showed a loss of cells. The results show that the spectral damage types are distinct in the early phases, indicating that different mechanisms are involved. Yet, the end effect of both damage types after exposure at doses up to 2.5×the funduscopic threshold is remarkably similar and consists of local photoreceptor lesions

Mydriatic Visual Acuity in Diabetic Patients: A Randomized Controlled Trial

Purpose. The aim of this randomized controlled equivalence trial was to demonstrate that, in diabetic patients, dilating the pupils before as compared with after refraction and visual acuity assessment would not lead to different advice given to patients. Methods. Three hundred sixteen adult patients with diabetes mellitus were randomized. The experimental group was administered tropicamide 0.5% before refraction and visual acuity assessment and the control group after refraction and visual acuity assessment. Study outcomes were the advised time till next visit, the advice on adjustment of refractive correction, further diagnostics, treatment, duration of the eye examination, and patient satisfaction. Results. No difference was seen in advised time till next visit between the experimental group (12.39 +/- 5.01 months) and the control group (12.84 +/- 4.96 months) (p = 0.425). In addition, the advice concerning adjustment of refractive correction (p = 0.069), further diagnostics (p = 1.000), and therapy (p = 0.178) did not significantly differ. Waiting time was significantly shorter for the experimental group (22.25 vs. 36.18 minutes; p <.001). People in the experimental group were relatively more often "very satisfied'' than "satisfied'' in comparison with participants in the control group for "attention being paid by the optometrist'' (p = 0.025) and "advice on refractive correction'' (p = 0.047). Conclusions. In diabetic patients, dilating pupils before refraction and visual acuity assessment does not lead to different advice given to patients compared with dilating pupils after refraction and visual acuity assessment, whereas waiting time significantly decreases and patient satisfaction is similar or even better. Increased efficiency is beneficial to both patients and clinicians. (Optom Vis Sci 2013;90:249-256

The role of vitreous cortex remnants in proliferative vitreoretinopathy formation demonstrated by histopathology: A case report

Purpose: The pathogenesis of proliferative vitreoretinopathy (PVR), the most important cause of retinal detachment surgery failure, is still not fully understood. We previously hypothesized a causal link between vitreoschisis-induced vitreous cortex remnants (VCR) and PVR formation. The purpose of this case report is to demonstrate this association by showing the clinical occurrence of PVR in the presence of VCR across the retinal surface, illustrated by histopathological analysis. Observations: A 69-year-old male was referred because of widespread epiretinal membrane formation after treatment of recurrent retinal detachments. During surgery with extensive membrane peeling, a large continuous membrane was peeled from the superior arcade towards the inferior temporal mid-periphery. Histopathological analysis of this membrane revealed areas with different characteristics: paucicellular laminar collagen-rich areas, suggestive for VCR, areas with increased cellularity, and more fibrotic areas with low cellularity. The immunohistochemical analysis identified cell type variety in these areas: collagen-rich areas showed glial cells and hyalocytes, while in areas with high cellularity fibroblasts, macrophages and retinal pigment epithelial cells were found, which have previously been shown to play an important role in the development of PVR as they can transdifferentiate into myofibroblasts, which were seen in the more fibrotic areas. Conclusions and importance: These findings support the theory that VCR have a role in PVR development, where VCR can act as a scaffold for fibrocellular proliferation. We suggest that the presence of VCR over the retinal surface should be qualified as a risk factor for PVR formation. Detection and adequate removal of VCR may improve the success rate of retinal detachment surgery

Carbonate compensation depth (CCD) reconstruction of the equatorial Pacific

Atmospheric carbon dioxide concentrations and climate are regulated on geological timescales by the balance between carbon input from volcanic and metamorphic outgassing and its removal by weathering feedbacks; these feedbacks involve the erosion of silicate rocks and organic-carbon-bearing rocks. The integrated effect of these processes is reflected in the calcium carbonate compensation depth, which is the oceanic depth at which calcium carbonate is dissolved. Here we present a carbonate accumulation record that covers the past 53 million years from a depth transect in the equatorial Pacific Ocean. The carbonate compensation depth tracks long-term ocean cooling, deepening from 3.0-3.5 kilometres during the early Cenozoic (approximately 55 million years ago) to 4.6 kilometres at present, consistent with an overall Cenozoic increase in weathering. We find large superimposed fluctuations in carbonate compensation depth during the middle and late Eocene. Using Earth system models, we identify changes in weathering and the mode of organic-carbon delivery as two key processes to explain these large-scale Eocene fluctuations of the carbonate compensation depth