Corneal Degenerations, Pterygium, Band Keratopathy and Dellen

Separate acquired change from inherited dystrophy

A degeneration is an acquired tissue change associated with age, environment, inflammation or another disorder; a dystrophy is a defined intrinsic corneal disorder, often inherited. The distinction is useful but historical names are not always consistent. Examine symmetry, location, vascularisation, inflammation, family history and progression. A peripheral opaque band in an older patient is not managed like a progressive corneal ectasia or an inherited central stromal deposit.

Corneal arcus is peripheral stromal lipid deposition, usually separated from the limbus by a clear interval. It commonly causes no visual impairment and does not require corneal treatment. In a younger patient, assess systemic lipid risk according to the clinical context. Lipid keratopathy associated with corneal vessels can threaten vision and requires assessment of the vascular or inflammatory cause. Reducing a deposit without addressing that cause may allow recurrence.

Pterygium and its mimics

A pterygium is fibrovascular conjunctival tissue extending across the limbus onto cornea, usually within the interpalpebral area. It can cause irritation, induced astigmatism, visual-axis encroachment and, when severe, restricted movement. A pinguecula is a conjunctival lesion adjacent to the limbus without the same corneal extension. A pseudopterygium is an adhesion after inflammation or injury and can occur at atypical locations. Inspect for an underlying surface lesion rather than assuming all limbal growth is benign.

Document growth, corneal extension, refraction and topography when the optical effect matters. Lubrication and environmental protection can improve symptoms but do not reliably reverse the lesion. Surgery is considered for visual or refractive impairment, documented progression, persistent symptoms or other patient-specific reasons. The visual axis need not already be covered before an optical problem merits treatment.

Bare-sclera excision has substantial recurrence risk. Conjunctival autografting provides surface coverage and is an established approach; amniotic membrane is useful in selected circumstances, including the need to preserve conjunctiva. A randomised mitomycin/autograft trial demonstrated the importance of adjunctive strategies compared with bare sclera in its population. Antimetabolites have potential benefits but can cause serious complications, including delayed healing or tissue melt; concentration and exposure require a validated protocol. Do not present one trial’s recurrence percentage as every surgeon’s expected result.

Superficial nodules and calcium

Salzmann nodular degeneration produces elevated, often bluish-white superficial corneal nodules. Chronic surface inflammation or previous injury may coexist. Nodules can disturb refraction and tear distribution even when peripheral. Manage associated surface disease, then consider superficial keratectomy or selected phototherapeutic keratectomy for significant symptoms or optical distortion. Reassess corneal measurements after surface stabilisation before cataract or refractive planning.

Band keratopathy is calcium deposition mainly in the interpalpebral superficial cornea, often with clear holes and a limbal clear interval. Causes include chronic inflammation, longstanding damaged eyes and systemic calcium/phosphate disturbance. Assess the underlying eye and consider metabolic evaluation when indicated. A painless deposit in a blind stable eye and a painful visually significant band in a seeing eye have different treatment goals.

Chelation with an appropriate EDTA procedure, superficial removal or selected laser treatment can restore a smoother surface. Treatment must account for epithelial healing and recurrent deposition. It does not cure an underlying inflammatory or metabolic process. Do not mistake every peripheral white deposit for calcium: lipid, inflammatory scars and dystrophic deposits have different mechanisms.

Thinning without an epithelial ulcer

Terrien marginal degeneration classically causes slowly progressive peripheral thinning, often superiorly, with an intact epithelium, lipid at the advancing edge and superficial vessels. It can induce astigmatism. Contrast this with peripheral ulcerative keratitis, in which epithelial loss and inflammatory stromal destruction can signal serious systemic immune disease. Some Terrien presentations have inflammatory features, so the distinction is based on the complete examination rather than a rule that all degeneration is painless.

A dellen is local corneal thinning from dehydration beside an elevated surface lesion or conjunctival swelling. Tear-film disruption over that region is the key mechanism. Improve lubrication and tear access and address the adjacent elevation; check for true ulceration, infection or more serious thinning. Escalate promptly if tissue integrity is threatened. A dellen is not simply another name for autoimmune corneal melt.

Applying the distinctions

Before cataract biometry, a peripheral Salzmann nodule or pterygium can alter central measurements. Treating the surface first and repeating stable measurements can be more important than selecting another IOL formula. In a red painful eye with peripheral thinning, confirm epithelial status and systemic risk before calling the lesion a benign degeneration. The examination should lead to a mechanism and management objective, not just recognition of a photograph.