Follicular conjunctivitis involves redness and new or enlarged follicles (Fig 3-5). Vessels surround and encroach on the raised surface of follicles but are not prominently visible within the follicle. Follicles can be seen in the inferior and superior tarsal conjunctiva and, less often, on the bulbar or limbal conjunctiva. They must be differentiated from cysts produced by tubular epithelial infoldings during chronic inflammation and lymphangiectasis.
Stern G. Chronic conjunctivitis. Focal Points: Clinical Modules for Ophthalmologists. San Francisco: American Academy of Ophthalmology; 2013, modules 11–12.
Figure 3-5 Follicular conjunctivitis. A, Inflammation of the right eye from glaucoma medication. B, Right eye showing follicular conjunctivitis in the inferior fornix. (Courtesy of John E. Sutphin, MD.)
Corneal Signs
Corneal signs of inflammation are described in Table 3-3. The pattern of corneal inflammation, or keratitis, can be described according to the following:
distribution: diffuse, focal, or multifocal
depth: epithelial, subepithelial, stromal, or endothelial location: central or peripheral
shape: dendritic, disciform, etc
The clinician should also note any structural or physiologic changes associated with keratitis, such as ulceration or endothelial dysfunction.
Table 3-3
Punctate epithelial keratopathy (PEK) is a nonspecific term that includes a spectrum of
biomicroscopic changes, from punctate epithelial granularity to erosive and inflammatory changes (Fig 3-6). Punctate epithelial erosions (PEE) are staining lesions of abnormal or degenerated corneal epithelial cells.
Figure 3-6 Punctate lesions of the corneal epithelium. A, Punctate epithelial erosions. B, Punctate epithelial keratitis. C, Slitlamp photograph of punctate epithelial keratitis.
Stromal inflammation may be manifested by the presence of new blood vessels. Inflammatory cells can also enter the stroma from the tear film through an epithelial defect or, less often, from direct interlamellar infiltration of leukocytes at the limbus (eg, after laser in situ keratomileusis [LASIK]). Inflammatory cells enter from aqueous humor in the presence of endothelial injury. In a vascularized cornea, inflammatory cells can emanate directly from infiltrating blood and lymphatic vessels.
Stromal inflammation is characterized as suppurative or nonsuppurative (Fig 3-7). It is further described by distribution (focal or multifocal infiltrates) and by location (central, paracentral, or peripheral). Necrotizing stromal keratitis is a severe form of infiltrate without the liquefaction associated with suppuration. The various morphologic changes of corneal inflammation, categorized by the principal clinical features, aid in differential diagnosis.
Figure 3-7 Inflammation of the corneal stroma. A, Suppurative keratitis. B, Nonsuppurative, nonnecrotizing (disciform) stromal keratitis.
Endothelial dysfunction often leads to epithelial and stromal edema. Swollen endothelial cells called inflammatory pseudoguttae are visible by specular reflection as dark areas of the normal mosaic pattern. Keratic precipitates (KPs) are clumps of inflammatory cells on the back of the cornea that come from the anterior uvea during the course of keratitis or uveitis. The clinical appearance of KPs depends on the composition:
Fibrin and other proteins coagulate into small dots and strands.
Neutrophils and lymphocytes aggregate into punctate opacities.
Macrophages form larger “mutton-fat” clumps.
Inflammation can lead to corneal opacification. Altered stromal keratocytes fail to produce some water-soluble factors and, consequently, make new collagen fibers that are disorganized, scatter light, and form a nontransparent scar. Scarring can also incorporate calcium complexes, lipids, and proteinaceous material. Dark pigmentation of a residual corneal opacity is often a result of incorporated melanin or iron salts.
Corneal inflammation can also lead to neovascularization. Superficial stromal blood vessels originate as capillary buds of limbal vascular arcades in the palisades of Vogt. New lymphatic vessels may also form but cannot be seen clinically. Subepithelial fibrous ingrowth into the peripheral cornea is called a pannus or vascularized pannus (Fig 3-8). Neovascularization may invade the cornea at deeper levels depending on the nature and location of the inflammatory stimulus. Any new vessel tends to remain at a single lamellar plane as it grows unless stromal disorganization has occurred.
Leibowitz HM, Waring GO III, eds. Corneal Disorders: Clinical Diagnosis and Management. 2nd ed. Philadelphia: Saunders; 1998:432–479.