Ординатура / Офтальмология / Английские материалы / Moorfields Manual of Ophthalmology_Jackson_2007

Pterygium

Pterygium

Background Conjunctival overgrowth onto the cornea, typically in young to middle-aged patients, with a male preponderance. There may be history of exposure to high ultraviolet levels, wind, and low humidity, e.g. outdoor work in hot dry climates.

Signs A fleshy triangular growth encroaches a variable distance onto the cornea, with the base arising from the conjunctiva (Fig. 5.27). The lesion is usually on the horizontal meridian, particularly the nasal side, and may be inflamed. There may be subepithelial scarring or iron deposition at the apex (Stocker’s line), and dellen with elevated pterygia. Measure the distance onto the cornea.

Differential diagnosis

■Goldenhar’s syndrome (oculoauriculovertebral dysplasia): page 79.

■Inflammatory pannus : usually less bulky, often not on the horizontal meridian, and often associated with ocular rosacea and underlying corneal thinning.

■Dysplasia : abnormal epithelium arising from the limbus does not have a triangular shape.

Treatment Use sunglasses to reduce exposure to sunlight. Treat ocular irritation with tear substitutes. If inflamed, try G. fluorometholone 0.1% q.d.s. for 1 month. Excise, or avulse, with

conjunctival autografting if symptoms are uncontrolled by conservative therapy or when there is encroachment into the visual axis. Send specimens for histology.

Follow-up If asymptomatic, review as necessary. If on topical steroids, check IOP in 4–6 weeks. Taper by one drop per fortnight when inflammation settles, then see as required.

CORNEA 5 Chapter

Band keratopathy

Band Keratopathy

Background Calcium deposits in the basement membrane, Bowman’s layer, and anterior corneal stroma. Associated with various ocular diseases including chronic low-grade uveitis (10– 50% of juvenile chronic arthritis), corneal dystrophies (posterior polymorphous and CHED), phthisis, silicone oil keratopathy, prolonged glaucoma, and longstanding corneal oedema. Metabolic causes include hypercalcaemia and hyperphosphataemia (Fig. 5.28). Band keratopathy (BK) may also be inherited (juvenile and mature type) or idiopathic.

History and examination BK is a sign not a diagnosis. Take a full ocular and systemic history and examine for underlying causes. The amorphous pale grey deposits are seen peripherally in the anterior cornea, mainly in the palpebral aperture. With time, the central cornea becomes affected. There is a transparent limbal zone.

Investigations Consider serum calium phosphate if there is no obvious ocular disease to account for BK.

Treatment

■Manage the underlying condition.

■Mild irritation : topical lubricants.

■Moderate irritation: bandage contact lens and preservative-free topical lubricants.

■Severe irritation and reduced VA : superficial keratectomy ± ethylene diamino tetra acetic acid chelation (EDTA), or excimer phototherapeutic keratectomy (PTK).

Follow-up Review 3–12 months, depending on the symptoms and underlying cause.

CORNEA 5 Chapter

Corneal degenerations and deposits

Corneal Degenerations

and Deposits

Climatic droplet keratopathy (spheroid degeneration of the cornea, Labrador keratopathy, Bietti’s keratopathy, pearl diver keratopathy) (Fig. 5.29). Occurs mainly in men who work outdoors due to exposure to ultraviolet light. Early on, fine subepithelial yellow droplets form superficially in the peripheral cornea. Later, droplets become central with subsequent corneal clouding and reduced vision. Excimer phototherapeutic keratectomy (PTK) may be necessary.

Terrien’s marginal degeneration See page 164.

Band keratopathy See page 196.

Lipid keratopathy Extracellular lipid deposition from corneal vessels (Fig. 5.30). May be idiopathic or associated with previous keratitis or disordered lipid metabolism (e.g. fish-eye syndrome).

Saltzmann’s nodular degeneration Degeneration of the superficial cornea involving the epithelium, Bowman’s layer, and stroma preceded by chronic corneal inflammation. Patients may complain of red eyes, irritation, and blurred vision. Bluish-white nodules of amyloid result in irregular astigmatism (Fig. 5.31). Treat

Corneal degenerations and deposits

the underlying cause. Consider superficial keratectomy ± PTK. A lamellar graft is rarely required. The disease may recur.

Corneal degenerations and deposits not requiring treatment

Arcus senilis (corneal annulus, anterior embryotoxon) Extremely common, bilateral, benign, peripheral corneal degeneration. Appears as a hazy grey ring ≈2 mm in diameter with a lucent zone between it and the limbus (Fig. 5.32). Caused by lipid droplets in all layers of the cornea, especially the anterior and deep stroma. Check lipids in those under the age of 50; otherwise, no treatment is required.

Kayser-Fleischer ring Copper deposition immediately superficial to Descemet’s membrane, 1–3 mm inside the limbus – usually only visible with gonioscopy. Variable colour: brown, ruby red, bright green, blue, or yellow. Associated with hepatolenticular degeneration (Wilson’s disease) and chronic hepatobiliary disease. Disappears with penicillamine treatment used to treat the systemic disease.

Fleischer ring Accumulation of ferritin within and between basal epithelial cells at the base of a keratoconus cone.

Vortex keratopathy (vortex corneal dystrophy, corneal verticillata of Fleischer, hurricane keratopathy, striate melanokeratosis). Pigmented whorl-shaped lines in the epithelium (Fig. 5.33). Associated with chloroquine, indomethacin, amiodarone, phenothiazine (e.g. chlorpromazine), tamoxifen use and clofazimine toxicity. Seen in Fabry’s disease (X-linked recessive) and asymptomatic female carriers, so examine family members if there is no drug cause.

Hudson-Stähli line Horizontal iron deposition line at the junction of the lower and middle thirds of the cornea

Corneal graft rejection

Corneal Graft Rejection

Background Immunologically mediated graft rejection may occur at any time but most often within 2 years of penetrating keratoplasty (PK). It may affect any part of the graft. Monitor corneal thickness and carefully document all keratic precipitates (KPs). If the cornea thickens, new KPs appear (with or without uveitis), then start treatment as per endothelial rejection (see below). Treat stromal and endothelial rejection as an emergency.

Epithelial rejection A slightly raised linear opacity, confined to the epithelium, starts peripherally and migrates centrally over several days (Fig. 5.34). Mild perilimbal injection may be present but there are usually few symptoms. Complete by 3 weeks postgrafting. No change in treatment or review schedule is required as it seldom leads to endothelial rejection.

Subepithelial rejection May occur up to 1 year following PK. Small, round, subepithelial infiltrates in Bowman’s layer are confined to the graft (Krachmer spots). There may be mild irritation and photophobia, KPs, flare and AC cells, and mild perilimbal injection. Although unlikely to induce endothelial rejection, treat with topical steroids to speed resolution of the infiltrates, e.g. G. prednisolone 0.5% q.d.s., until inflammation is resolved, then taper gradually.

Stromal rejection Only 1–2% of rejections. Rapidly spreading, dense, even infiltrate affecting all stromal layers, but confined to the graft. Vascularization occurs late. Treat as per endothelial rejection.