Badminton-related eye injuries: a systematic review.

OBJECTIVES: To report the nature of badminton-related eye injuries in the published literature. METHODS: A review of the literature with key word and MeSH terms: 'Eye injury', 'Ocular trauma', 'Badminton' 'Shuttlecock' using CENTRAL, MEDLINE, EMBASE and Informit Health Collection databases. Papers were reviewed to assess the circumstances of the injury, patient demographics and clinical data. RESULTS: 19 studies from 1974 to 2020 from 12 countries reported 378 monocular badminton-related eye injuries from 378 patients with a male-to-female ratio of 2.5:1. A closed globe injury was sustained in 97% of eyes and a shuttlecock responsible for 85% of injuries. Doubles play, the shuttlecock and a lack of eye protection were associated with eye injury. CONCLUSION: Vision impairment was associated with the majority of badminton-related eye injuries, and doubles play, the shuttlecock and a lack of eye protection were risk factors.

Retinal Vessel Analysis as a Novel Screening Tool to Identify Childhood Acute Lymphoblastic Leukemia Survivors at Risk of Cardiovascular Disease.

BACKGROUND: Microvascular endothelial dysfunction is central to the pathogenesis of cardiovascular disease (CVD). The eye offers direct access for endothelial health assessment via the retinal microvasculature. The aim of the study was to investigate whether image-based retinal vessel analysis is a feasible method of assessing endothelial health in survivors of childhood acute lymphoblastic leukemia (cALL). MATERIALS AND METHODS: Cardiovascular risk factors (CRFs) were estimated using the 30-year Framingham Risk Score in 73 childhood leukemia survivors (median age: 25; median years from diagnosis: 19) and 78 healthy controls (median age: 23). Radial arterial stiffness was measured using pulse wave analyzer, while endothelial activation markers were measured by soluble intercellular adhesion molecule 1 (sICAM-1) and soluble vascular cell adhesion molecule 1 (sVCAM-1). Retinal fundus images were analyzed for central retinal artery/vein equivalents (CRAE/CRVE) and arteriolar-venular ratio (AVR). RESULTS: cALL survivors had higher CRF (P<0.0001), arterial stiffness (P=0.001), and sVCAM-1 (P=0.007) compared with controls. Survivors also had significantly higher CRVE (P=0.021) while AVR was significantly lower (P=0.026) in survivors compared with controls, compatible with endothelial dysfunction. In cALL survivors with intermediate risk for CVD, CRAE, and AVR are significantly lower, while sVCAM-1 and sICAM-1 are significantly higher when compared with survivors with low CVD risk after adjusting with covariates (age, sex, and smoking status). CONCLUSIONS: cALL survivors have an increased risk of CVD compared with age-matched peers. The survivors demonstrated microvasculopathy, as measured by retinal vascular analysis, in addition to physical and biochemical evidence of endothelial dysfunction. These changes predate other measures of CVD. Retinal vessel analysis may be utilized as a robust screening tool for identifying survivors at increased risk for developing CVD.

The epidemiology of Open Globe Injuries presenting to a tertiary referral eye hospital in Australia.

BACKGROUND: Open globe injuries (OGIs) account for 44% of the cost of ocular trauma within Australia. It is estimated that 90% of ocular trauma is preventable. However, there have been few epidemiological studies within Australia that have identified groups at risk of OGIs specifically. The aim of our study was to review the epidemiology of OGIs presenting to a tertiary referral eye hospital in Australia. METHODS: The Birmingham Eye Trauma Terminology (BETT) system was used to classify injuries as globe ruptures, penetrating eye injuries (PEIs), intraocular foreign bodies (IOFBs) or perforating injuries. Demographic data, past ocular history, mechanism of trauma, ocular injuries, and best-corrected visual acuity (BCVA) before and after treatment were recorded. RESULTS: The 205 OGIs included 80 globe ruptures, 71 PEIs, 48 IOFBs and six perforating injuries. Falls predominated in older age groups compared to the other mechanisms of injury (p<0.0001). A fall was responsible for 33 globe ruptures and 82% of these had a history of previous intraocular surgery. Globe rupture and perforating injuries had poorer visual outcomes (p<0.05), consistent with previous studies. Alcohol was implicated in 20 cases of OGI, with 11 of these due to assault. PEIs and IOFBs commonly occurred while working with metal. BCVA was significantly worse following removal of an intraocular foreign body. We found presenting BCVA to be a good predictor of BCVA at the time of discharge. CONCLUSIONS: The causes of OGI varied in association with age, with older people mostly incurring their OGI through falls and younger adults through assault and working with metal. Globe ruptures occurring after a fall often had a history of intraocular surgery. The initial BCVA is useful for non-ophthalmologists who are unfamiliar with the ocular trauma score to help predict the BCVA following treatment.

Light- and sodium azide-induced death of RGC-5 cells in culture occurs via different mechanisms.

Previous studies have shown that light impinging on the retina in situ has the capacity to kill neuronal and non-neuronal cells in vitro by interacting directly with mitochondrial constituents. A number of fluorophores are associated with mitochondria which can potentially absorb different wave-lengths of light, including cytochrome oxidase. The aim of the present study was to compare the death mechanism of a light insult to RGC-5 cells in culture with that of sodium azide. Sodium azide's main toxic action is in inhibiting the function of cytochrome oxidase in the mitochondrial electron transport chain. Our studies showed that light and sodium azide kill RGC-5 cells via different mechanisms although some similarities do occur. Both inducers of cell death caused the generation of reactive oxygen species (ROS), the expression of phosphatidylserine, the breakdown of DNA and the activation of p38 MAPK, resulting in its translocation from the nucleus to the cytoplasm. However, light-induced cell death occurs via necroptosis, in that it was inhibited by necrostatin-1 and was caspase-independent. This was not the case for sodium azide, where the death process was caspase-dependent, occurred via apoptosis and was unaffected by necrostatin-1. Moreover, light caused an activation of the apoptosis inducing factor (AIF), c-Jun, JNK and HO-1, but it did not affect alpha fodrin or caspase-3. In contrast, sodium azide caused the activation of alpha fodrin and the stimulation of caspase-3 content without influencing AIF, c-Jun, JNK or HO-1. Therefore we conclude that light does not have a specific action on cytochrome oxidase in mitochondria to cause cell death.