Lubricants, anti-inflammatory agents, antihistamines, and nocturnal patching have been suggested as treatments, although none besides lubrication is a potential long-term solution. If these modalities fail, then surgical excision, conjunctival fixation to the sclera, amniotic membrane grafting, or cauterization of the redundant folds may be required. See Chapter 14 for discussion of surgical procedures used for conjunctivochalasis.

Ward SK, Wakamatsu TH, Dogru M, et al. The role of oxidative stress and inflammation in conjunctivochalasis. Invest Ophthalmol Vis Sci. 2010;51(4):1994–2002.

Conjunctival Vascular Tortuosity and Hyperemia

Conjunctival vascular tortuosity and hyperemia can result from many causes. A differential diagnosis is outlined in Table 12-2.

Table 12-2

Degenerative Changes in the Cornea

For discussion of congenital anomalies of the cornea, see Chapter 9.

Age-Related (Involutional) Changes

As a result of aging, the cornea gradually becomes flatter in the vertical meridian, thinner, and slightly less transparent. Its refractive index increases, and Descemet membrane becomes thicker, increasing from 3 μm at birth to 10 μm in adults. Occasional peripheral endothelial guttae, sometimes known as Hassall-Henle bodies, can form with age (see the discussion later in the chapter). Agerelated attrition of corneal endothelial cells results in a loss of about 100,000 cells during the first 50 years of life, from a cell density of about 4000 cells/mm2 at birth to a density of 2500–3000 cells/mm2 in older adults. The average rate of decrease in endothelial cell density throughout adult life is approximately 0.6% per year.

Epithelial and Subepithelial Degenerations

Coats white ring

A small (1 mm or less in diameter) circle or oval-shaped area of discrete gray-white dots is sometimes seen in the superficial stroma. Referred to as Coats white ring, it represents ironcontaining fibrotic remnants of a metallic foreign body. Once these lesions mature and are free of any associated inflammation, they do not change; hence, therapy with corticosteroids or other antiinflammatory agents is not indicated (Fig 12-5).

Figure 12-5 Coats white ring (arrow) (not to be confused with map-dot-fingerprint dystrophy). (Courtesy of W. Craig Fowler, MD.)

Spheroidal degeneration

Spheroidal degeneration is characterized by the appearance in the cornea, and sometimes in the conjunctiva, of translucent, golden brown, spheroidlike deposits in the subepithelium, Bowman layer, or superficial stroma (Fig 12-6). The condition has been reported under different names, including climatic droplet keratopathy, Bietti nodular dystrophy, and Labrador keratopathy.

Figure 12-6 Spheroidal degeneration. (Courtesy of Cornea Service, Paulista School of Medicine, Federal University of São Paulo.)

In primary spheroidal degeneration, the deposits are bilateral and initially located in the nasal and temporal cornea. With age, they can extend onto the conjunctiva in the interpalpebral zone. The primary degeneration is unrelated to the coexistence of other ocular disease. In rare cases, generally in childhood, the spheroidal deposits extend across the interpalpebral zone of the cornea, producing a noncalcific band-shaped keratopathy. Secondary spheroidal degeneration is associated with ocular injury or inflammation. The deposits aggregate near the area of corneal scarring or vascularization. All cases show extracellular, proteinaceous, hyaline deposits with characteristics of elastotic degeneration; these deposits are thought to be secondary to the combined effects of genetic predisposition, actinic exposure, age, and perhaps various kinds of environmental trauma other than sunlight, such as dust and wind. The composition is not lipid, despite its “oil droplet” appearance. No medical therapy is of much value, although lubrication is recommended to address uneven layering of the tear film over affected areas. In cases of central involvement, superficial keratectomy or

phototherapeutic keratectomy (PTK) using an excimer laser may be indicated. Recurrence after conjunctival resection is common.

Iron deposition

Most iron lines are related to abnormalities of tear pooling due to surface irregularities (Fig 12-7). Often, they can be seen only by using red-free or cobalt blue illumination before instilling fluorescein. A Fleischer ring, representing iron deposition in keratoconus, is one of many corneal iron lines associated with epithelial irregularities (see Chapter 10, Fig 10-27). This sign is extremely useful in the diagnosis of mild or early cases of keratoconus. The Hudson-Stähli line, generally located at the junction of the upper two-thirds and lower one-third of the cornea, is ubiquitous. Iron lines are also associated with keratorefractive surgery. Following radial keratotomy, visually insignificant iron lines are noted centrally in approximately 80% of patients and are commonly characterized as a “tear star.” Common conditions associated with corneal iron lines are listed in Table 12-3.

Palay DA. Corneal deposits. In: Krachmer JH, Mannis MJ, Holland EJ, eds. Cornea. 3rd ed. Vol 1. Philadelphia: Elsevier/Mosby; 2011:289–302.

Figure 12-7 Iron deposition (iron line) (arrow) due to irregularity of the tear film from subepithelial fibrosis. (Courtesy of Robert W.

Weisenthal, MD.)

Table 12-3

Calcific band keratopathy

Calcific band keratopathy is a degeneration of the superficial cornea that involves mainly Bowman

layer. The condition can be idiopathic, but the main known causes are

chronic ocular disease (usually inflammatory) such as uveitis in children, interstitial keratitis, severe superficial keratitis, and phthisis bulbi

hypercalcemia caused by hyperparathyroidism, vitamin D toxicity, milk-alkali syndrome, sarcoidosis, or other systemic disorders

hereditary transmission (primary hereditary band keratopathy, with or without other anomalies) elevated serum phosphorus level with normal serum calcium, which sometimes occurs in patients with renal failure

chronic exposure to mercurial vapors or to mercurial preservatives (phenylmercuric nitrate or acetate) in ophthalmic medications (the mercury causes changes in corneal collagen that result in the deposition of calcium)

silicone oil instillation in an aphakic eye

Band keratopathy may also result from the deposition of urates in the cornea. The urates appear brown, unlike the gray-white calcific deposits, and may be associated with gout or hyperuricemia.

Calcific band keratopathy begins as fine, dustlike, basophilic deposits in the Bowman layer. These changes are usually first seen peripherally in the 3- and 9-o’clock positions. A lucid interval is seen between the limbus and the peripheral edge of the keratopathy. Eventually, the deposits may coalesce to form a horizontal band of dense calcific plaques across the interpalpebral zone of the cornea (Fig 12-8).

Figure 12-8 Band keratopathy.

A workup (eg, serum electrolytes and urinalysis) to rule out associated metabolic/renal disease should be considered. Underlying conditions, such as keratoconjunctivitis sicca or renal failure, should be treated or controlled as much as possible, which may reduce or control the deposition of calcium or at least help reduce the recurrence of band keratopathy. The calcium can usually be removed from Bowman layer by chelation with a neutral solution of disodium ethylenediaminetetraacetic acid (EDTA), which can be warmed to speed up the chemical chelation. (The usual concentration of EDTA, 0.5%–1.5%, is no longer commercially available but can be obtained through a compounding pharmacy.) The epithelium overlying the calcium needs to be removed before the chelating solution is applied. Any cylindrical tube that approximates the corneal diameter (eg, corneal trephine) can facilitate the process by acting as a reservoir to confine the chelating solution to the desired treatment area; however, this is not always necessary. With the reservoir in place, very gentle surface agitation with a truncated cellulose sponge may further