Corneal inflammation can be diffuse or localized in particular zones, such as the epithelium or stroma. In addition to the causes listed above, corneal inflammation can also be caused by insufficient tear production, nutritional deficiencies, and infectious agents, such as bacteria, fungi, and viruses. Since the cornea is normally an avascular tissue, stromal neovascularization is a common component of corneal inflammatory lesions. Hyperplasia of the epithelium is also a frequent finding (Figure 1 and Figure 2). In chronic lesions, stromal fibrosis may be seen. While the intact cornea is resistant to most bacterial pathogens, any breach in the epithelium (e.g., from abrasions, penetrating injury, or toxin-induced necrosis) can introduce bacteria, which incite an inflammatory response. Bacteria can also secondarily colonize preexisting areas of inflammation (Figure 3 and Figure 4) and/or ulceration. Anterior chamber inflammation can extend into the adjacent iris, ciliary body, and lens. Inflammatory cells in the anterior chamber can occlude the iridocorneal filtration angle channels and/or the adjacent trabecular meshwork, impeding normal drainage of aqueous humor with resultant elevations in intraocular pressure. Clinically, intracameral accumulations of neutrophils are referred to as hypopyon.
Anterior uveal tract (iris and ciliary body) inflammation can result from various causes, such as infectious agents such as bacteria and viruses, and immune-mediated (allergic) reactions. Iridial and ciliary body inflammation (Figure 7, Figure 8, and Figure 9) often extends into the adjacent anterior and posterior chambers, cornea, and/or choroid. Likewise, inflammation of the choroid, or posterior uvea (Figure 10 and Figure 11), often extends into the anterior uveal tract (ciliary body and iris) and/or into the adjacent retina.
Vitreal inflammation (Figure 12 and Figure 13) is characterized by prominent accumulations of inflammatory cells in the vitreous. Vitreal inflammation can result from trauma (e.g., from intravitreal injections or other penetrating injury) or as a primary effect of intravitreally or systemically administered toxins. It can also occur secondary to other ocular lesions, such as cataracts and retinal inflammation. Chronic inflammatory infiltrates are often accompanied by vitreal fibrosis.
Retrobulbar inflammation (Figure 14 and Figure 15) is most frequently caused by trauma due to retrobulbar bleeding procedures and is typically acute. It is often accompanied by hemorrhage.
In NTP studies, there are five standard categories of inflammation: acute, suppurative, chronic, chronic-active, and granulomatous. In acute inflammation, the predominant infiltrating cell is the neutrophil, though fewer macrophages and lymphocytes may also be present. There may also be evidence of edema or hyperemia. The neutrophil is also the predominant infiltrating cell type in suppurative inflammation, however, in suppurative inflammation, the neutrophils are aggregated and many of them are degenerate (suppurative exudate). Cell debris, both from the resident cell populations and infiltrating leukocytes, proteinaceous fluid containing fibrin, fewer macrophages, occasional lymphocytes or plasma cells, and, possibly, an infectious agent may also be present in within the exudate. Grossly, these lesions would be characterized by the presence of pus. In the tissue surrounding the exudate, there may be fibroblasts, fibrous connective tissue, and mixed inflammatory cells, depending on the chronicity of the lesion. Lymphocytes predominate in chronic inflammation. Lymphocytes also predominate in chronic-active inflammation, but in chronic-active inflammation, there are also a significant number of neutrophils. Both lesions may contain macrophages. Granulomatous inflammation is another form of chronic inflammation, but this diagnosis requires the presence of a significant number of aggregated, large, activated macrophages, epithelioid macrophages, or multinucleated giant cells. Inflammation is differentiated from cellular infiltrates by the presence of other changes, such as edema, hemorrhage, degeneration, necrosis, or other evidence of tissue damage.
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