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, paracentral, or peripheral
shape: dendritic, disciform, and so on
The clinician should also note any structural or physiologic changes associated with keratitis, such as ulceration or endothelial dysfunction.
Table 3-3 Corneal Signs
Punctate epithelial keratitis (PEK) is a nonspecific term that encompasses a spectrum of biomicroscopic changes, from punctate epithelial granularity to erosive and inflammatory changes (Fig 3-6). Punctate epithelial erosions (PEE) are lesions of abnormal or degenerated corneal epithelial cells that stain with fluorescein.
Inflammatory cells can enter the stroma from the tear film, through an epithelial defect; less often, they enter by direct interlamellar infiltration of leukocytes at the limbus (eg, after laser in situ keratomileusis [LASIK]). In the presence of endothelial injury, inflammatory cells enter from aqueous humor. Stromal inflammation may be manifested by the presence of new blood vessels. In a vascularized cornea, inflammatory cells can enter the stroma 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). The differential diagnosis for suppurative corneal inflammation or necrotizing stromal keratitis includes microbial keratitis due to bacteria, fungi, or acanthamoeba; retained foreign body; and topical anesthetic abuse. Nonsuppurative stromal keratitis can be caused by reactive arthritis, Cogan syndrome, viral keratitis, congenital or acquired syphilis, Lyme disease, tuberculosis, leprosy (Hansen disease), and onchocerciasis.
Figure 3-6 Punctate lesions of the corneal epithelium. A, Punctate epithelial erosions. B, Punctate epithelial keratitis. C, Slit-lamp photograph from a patient with epithelial keratitis due to herpes zoster.
(Part C courtesy of Robert S. Feder, MD.)
Figure 3-7 Inflammation of the corneal stroma. A, Suppurative keratitis. B, Nonsuppurative, nonnecrotizing (disciform) stromal keratitis. C, Immune ring. D, Peripheral ulcerative keratitis. An ovoid area of thinning (arrow) can be seen in the inferonasal quadrant.
(Parts C and D courtesy of Robert S. Feder, MD.)
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 endothelial mosaic pattern. Keratic precipitates (KPs) are clumps of inflammatory cells that adhere to the back of the cornea and come from the anterior uvea during the course of keratitis or uveitis. The clinical appearance of KPs depends on their composition:
Fibrin and other proteins coagulate into small dots and strands.
Neutrophils and lymphocytes aggregate into punctate opacities.
Macrophages form larger “mutton-fat” clumps.
Corneal inflammation can lead to 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 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.
Figure 3-8 Corneal pannus.
(Courtesy of Kirk R. Wilhelmus, MD.)
Ciralsky J, Lai E, Waring GO III, Bouchard CS. A matrix of pathologic responses in the cornea. In: Mannis MJ, Holland EJ, eds. Cornea. Vol 1. 4th ed. Philadelphia: Elsevier; 2017:46–71.
Leibowitz HM, Waring GO III, eds. Corneal Disorders: Clinical Diagnosis and Management. 2nd ed. Philadelphia: Saunders; 1998:432–479.
Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.