Postoperative endophthalmitis.

Endophthalmitis may have devastating consequences for a patient’s vision and therefore should be treated as an emergency. The time from diagnosis to treatment is critical for favourable outcomes. In order to achieve a rapid response, it is important to have an accessible protocol and an endophthalmitis kit at hand for all eye surgeons who see postoperative patients. We have produced a simple protocol of recommended practice collated from a range of sources

Emergency management: acute endophthalmitis

Endophthalmitis can have devastating consequences for a patient’s eye and vision. Prompt recognition and urgent treatment are vital

Endophthalmitis: controlling infection before and after cataract surgery

Endophthalmitis is a rare, but serious, postoperative complication of cataract surgery. It can have a devastating consequence on a patient’s vision: some patients may lose all light perception.The incidence of endophthalmitis has been reported to be between 0.13% and 0.7%.1 The primary source of this intraocular infection is considered to be bacteria from the patient’s ocular surface (cornea, conjunctiva) or adnexa (lacrimal glands, eyelids, and extraocular muscles). The bacteria most frequently isolated are gram-positive coagulase-negative cocci (mainly Staphylococcus epidermidis) which account for 70% of culture-positive cases. Staphylococcus aureus is isolated in 10% of culture-positive cases, Streptococcus species in 9%, Enterococcus species in 2%, and other gram-positive species in 3% of cases. Gram-negative bacteria account for just 6% of culture-positive cases; however, an infection with these bacteria, particularly with Pseudomonas aeruginosa, can lead to a devastating visual outcome

The development of human organotypic retinal cultures for glaucoma research : P2X7 receptor stimulation and interleukin 1B regulation in relation to retinal ganglion cell death

EThOS - Electronic Theses Online ServiceGBUnited Kingdo

The development of human organotypic retinal cultures (HORCs) to study retinal neurodegeneration

Aims To develop human organotypic retinal cultures (HORCs) to study retinal ganglion cell (RGC) death in response to ischaemic and excitotoxic insults, both known to cause loss of RGCs and proposed as mechanisms involved in glaucomatous retinal neurodegeneration. Methods Human donor eyes were obtained within 24 h post mortem. The retina was isolated and explants cultured using two techniques. THY-1 mRNA (assessed by real-time quantitative PCR) and neuronal nuclei (NeuN) (assessed by immunohistochemistry) were used as markers of RGCs. Apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL). Results The distribution of THY-1 mRNA and NeuN-labelling within the human retina was consistent with the expected distribution of RGCs. Gross morphology and retinal architecture remained stable over a 96 h culture period. THY-1 mRNA and NeuN-labelled RGC layer cells decreased over the culture period, and there was an increase in TUNEL-labelling with time, but HORCs cultured in serum-free DMEM/HamF12 medium were useful for up to 48 h in culture. N-methyl-d-aspartate (10 µM) caused a reduction in THY-1 mRNA by 24 h and decreased the numbers of NeuN-labelled RGC layer neurons by 48 h, suggesting that the loss of THY-1 mRNA was a marker of RGC stress prior to death. Simulated ischaemia (60 min oxygen/glucose deprivation) caused a reduction at 24 h in both THY-1 mRNA and the numbers of NeuN-labelled neurons of HORCs. Conclusion HORCs provide a useful model to investigate RGC insult by neurodegenerative mechanisms that may lead to glaucoma in human eyes

Interleukin-1? exacerbates hypoxia-induced neuronal damage, but attenuates toxicity produced by simulated ischaemia and excitotoxicity in rat organotypic hippocampal slice cultures

Using organotypic hippocampal slice cultures we have investigated the actions of Interleukin-1 (IL-1) in a number of injury paradigms. Low concentrations of IL-1 potentiated hypoxia-induced neurodegeneration whilst high concentrations had no effect. In contrast, higher concentrations of IL-1 were strongly neuroprotective in models of combined oxygen/glucose deprivation and N-methyl-D-aspartate toxicity, but no potentiation was observed at low IL-1 concentrations. Both protective and toxic effects of IL-1 were fully antagonized by IL-1 receptor antagonist. These data demonstrate that the effects of IL-1 on neuronal injury are complex, and may be directly related to the injury paradigm studied