Infection is a very important but rare cause of scleritis, occurring in about 5%–10% of all patients presenting with scleral inflammation. However, due to the similarity of its presentation, infectious scleritis is often initially managed as autoimmune, potentially further worsening its outcome. The overall visual outcome in infectious scleritis is generally worse than its autoimmune counterparts, perhaps because of the delay in diagnosis or because of the aggressive nature of associated microbes. Thus, there is a definite need for insight into the diagnostic approach and treatment options for this ocular disease process. Several studies and case reports have been published in recent years that have provided useful information regarding the presenting clinical features and etiologic microbial agents in infectious scleritis. This review summarizes the important findings in the literature that may aid in differentiating infectious scleritis from other etiologies, including predisposing factors, microbe-specific characteristics, diagnostic tools, treatment modalities, and outcomes.

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Macular hole formation after intravitreal injection with ranibizumab is a potential complication that should be considered before treatment, especially in those patients with large subfoveal pigment epithelial detachments and vitreomacular adhesion. Although successful closure may be attained after pars plana vitrectomy, this potential morbidity should be considered when treating these patients. In addition to the already well-described tractional forces of the vitreous overlying the fovea, and the potential contractile nature of a choroidal neovascular complex in response to ranibizumab, a posterior pushing or stretching mechanism of a large pigment epithelial detachment may also contribute to macular hole formation.

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