Over the past decades, the number of patients with dry eye disease (DED) has increased dramatically. The incidence of DED is higher in Asia than in Europe and North America, suggesting the involvement of cultural or racial factors in DED etiology. Although many definitions of DED have been used, discrepancies exist between the various definitions of dry eye disease (DED) used across the globe. This article presents a clinical consensus on the definition of DED, as formulated in four meetings with global DED experts. The proposed new definition is as follows: “Dry eye is a multifactorial disease characterized by a persistently unstable and/or deficient tear film (TF) causing discomfort and/or visual impairment, accompanied by variable degrees of ocular surface epitheliopathy, inflammation and neurosensory abnormalities.” The key criteria for the diagnosis of DED are unstable TF, inflammation, ocular discomfort and visual impairment. This definition also recommends the assessment of ocular surface epitheliopathy and neurosensory abnormalities in each patient with suspected DED. It is easily applicable in clinical practice and should help practitioners diagnose DED consistently. This consensus definition of DED should also help to guide research and clinical trials that, to date, have been hampered by the lack of an established surrogate endpoint.

Most patients with chronic dry eye disease (DED) have episodic flares, which can be triggered by a variety of activities and environmental stresses. These flares are typically associated with rapid exacerbation of discomfort symptoms, followed by prolonged elevation of inflammation. In an acute flare, ocular surface inflammation begins with a nonspecific innate immune response, in some cases followed by a slower but more specific adaptive immune response. At the ocular surface, epithelial cells are central to the innate immune response, and we discuss their role in DED flares alongside the other core components. Epithelial cells and other cells of the innate response (neutrophils, monocytes, macrophages and dendritic cells) trigger flares in response to increased osmolarity, detected via pattern receptors on their cell surface. Ultimately, downstream signaling pathways activate innate and adaptive immune responses, with consequent inflammation and symptoms. In chronic DED, pathogenic T cells have infiltrated the ocular surface tissues. The established adaptive immune response is likely to lead to flare-ups at lower thresholds of stress, with inflammation maintained over a longer period. Increased understanding of the inflammatory cascades activated during a flare may guide management and improve outcomes.

We reviewed 19 cases of delayed-onset pseudophakic endophthalmitis in which diagnostic cultures were performed at one month or more after cataract extraction with posterior chamber intraocular lens implantation. We isolated four different organisms in these 19 cases: 12 Propionibacterium species (63%), three Candida parapsilosis (16%), three Staphylococcus epidermidis (16%), and one Corynebacterium species (5%). Because of the unusual delayed-onset features of these cases and the retrospective nature of this study, a variety of treatment regimens were used. Twelve patients had recurrence of marked inflammation despite an apparent initial cure, and ten of these patients had positive culture results on repeat examination of intraocular fluids. Nine patients continued to be treated with topical corticosteroids postoperatively to suppress low-grade inflammation. Of the 19 patients, 16 had final visual acuity of 20/400 or better. Delayed-onset pseudophakic endophthalmitis had a more favorable visual prognosis, compared to acute-onset endophthalmitis.