amount of mucopolysaccharide. These changes are accompanied by subconjunctival deposition of fat, which gives the sclera a yellowish appearance. Calcium may also be deposited either diffusely among the scleral collagen fibers in granular or crystalline form or focally in a plaque anterior to the horizontal rectus muscle insertions. These senile plaques are visible as ovoid or rectangular zones of grayish translucency (Fig 12-16) and are sometimes mistaken for a pigmented tumor. Histologically, the midportion of the involved sclera contains a focal calcified plaque surrounded by relatively acellular collagen. The plaques do not elicit inflammation and rarely extrude. If sufficiently dense, they may be visualized on a computed tomography scan.

Figure 12-16 Senile scleral plaque anterior to horizontal rectus muscle insertions. (Courtesy of Robert W. Weisenthal, MD.)

Drug-Induced Deposition and Pigmentation

Ocular medications deposit within the cornea as a result of their concentration within the tear film, limbal vasculature, or aqueous humor or due to a specific affinity of the medication’s chemical properties to corneal tissue. Specific drugs deposit in a characteristic fashion and corneal layer. The deposition of the drug may reduce vision, produce photosensitivity, or cause ocular irritation. Its cessation often eliminates the symptoms and resolves the drug deposits. Most drug-induced deposition is not symptomatic, however, and does not require cessation of the medication (Table 12- 4).

Table 12-4

Corneal Epithelial Deposits

Cornea verticillata

Cornea verticillata, or vortex keratopathy, manifests as a clockwise whorl-like pattern of golden brown or gray deposits in the inferior interpalpebral portion of the cornea (Fig 12-17). A variety of medications bind with the cellular lipids of the basal epithelial layer of the cornea due to their cationic, amphiphilic properties. Amiodarone, an antiarrhythmic, is the most common cause of cornea verticillata, followed by chloroquine, hydroxychloroquine, indomethacin, and phenothiazines. A comprehensive list of systemic drugs associated with cornea verticillata is given in Table 12-4.

Figure 12-17 Cornea verticillata. (Courtesy of Robert W. Weisenthal, MD.)

It is unusual for these deposits to result in reduction of vision or ocular symptoms, although this has occurred in some patients. The deposits typically resolve with discontinuation of the responsible agents. If there is reduced vision with the use of amiodarone or tamoxifen, the possibility of optic neuropathy should be considered. Retinal toxicity associated with the chloroquine family or tilorone hydrochloride can also reduce vision. The differential diagnosis of cornea verticillata should also include Fabry disease, a disorder of sphingolipid metabolism.

Epithelial cysts

Due to the rapid turnover of epithelial cells, drugs that inhibit DNA synthesis may be toxic to the epithelium when used in high doses systemically. Cytarabine, for example, may cause punctate keratopathy and refractile epithelial microcysts that are associated with pain, photophobia, foreignbody sensation, and reduced vision.

Ciprofloxacin deposits

Therapy with topical ciprofloxacin (and less often other fluoroquinolones) can result in the deposition of a chalky white precipitate composed of ciprofloxacin crystals within an epithelial defect. Although white plaques predominate, a crystalline pattern may also be observed. The deposits resolve after discontinuation of the medication.

Adrenochrome deposits

Long-term administration of epinephrine compounds, tetracycline, or minocycline may lead to black or very dark brown deposits in the conjunctiva and cornea. Composed of adrenochrome, an oxidation product of the basic epinephrine compound, these melanin-like deposits can accumulate in conjunctival cysts and concretions in the conjunctiva (Fig 12-18). They may discolor the cornea or