Medical Blog

Megalocornea

Introduction
Background

Megalocornea is a nonprogressive enlargement of the cornea to 13 mm or greater. The cornea and the limbus are enlarged, but the cornea itself is histologically normal. Megalocornea is usually seen as an isolated finding, but it may be associated with other ocular and systemic findings. The additional ocular findings are found in anterior megalophthalmos, which includes an enlarged ciliary ring and crystalline lens in addition to an enlarged cornea. Read more…

Laceration, Corneoscleral

Introduction
Background

A corneoscleral laceration may occur following blunt or penetrating ocular trauma. This eye injury may be sustained at work, during sports, following a motor vehicle accident, from airbag inflation, or in a brawl. The laceration may be the only injury. The uvea, the retina, or the vitreous may prolapse through the wound. Corneal or scleral tissue may be lost. A corneoscleral laceration is more likely to occur in an eye that has undergone a previous surgery, such as radial keratotomy or corneal transplantation. Read more…

Keratopathy, Pseudophakic Bullous

Introduction
Background

Corneal edema occurs for many reasons, but it is often a sequela of intraocular surgery. Corneal edema resulting from cataract extraction is called either pseudophakic bullous keratopathy (PBK) or aphakic bullous keratopathy (ABK). Knowledge of the structure of the cornea and the proper functioning of its layers is fundamental to understanding corneal edema.
Pathophysiology

Bullous keratopathy is caused by changes in the corneal endothelium, which allow the cornea to be in an abnormal state of hydration. As endothelial cells are damaged, the remaining cells rearrange themselves to cover the posterior corneal surface. The remaining endothelial cells become irregularly shaped and enlarged. Any pathologic process that affects the endothelial cells results in cornea guttata due to overproduction of the Descemet membrane.
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Keratopathy, Neurotrophic

Introduction
Background

Neurotrophic keratopathy is a degenerative disease characterized by decreased corneal sensitivity and poor corneal healing. This disease leaves the cornea susceptible to injury and decreases reflex tearing. Epithelial breakdown can lead to ulceration, infection, melting, and perforation secondary to poor healing.
Pathophysiology

The common factor in all cases of neurotrophic keratopathy is corneal hypesthesia. Sensory nerves exert a trophic influence on the corneal epithelium. The sensory neuromediators, acetylcholine, substance P, and calcitonin gene-related peptide, have been shown to increase epithelial cell proliferation in vitro.
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Keratopathy, Band

Introduction
Background

Band keratopathy derives its name from the distinctive appearance of calcium deposition in a band across the central cornea. This corneal degeneration can occur from a variety of causes, both systemic and local.
Pathophysiology
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Keratoconus

Introduction
Background

Keratoconus (KC) is a progressive, noninflammatory, bilateral (but usually asymmetrical) disease of the cornea, characterized by paraxial stromal thinning that leads to corneal surface distortion. Visual loss occurs primarily from irregular astigmatism and myopia and secondarily from corneal scarring.
Pathophysiology

All layers of the cornea are believed to be affected by KC, although the most notable features are the thinning of the corneal stroma, the ruptures in the Bowman layer, and the deposition of iron in the basal epithelial cells, forming the Fleischer ring. Breaks in and folds close to the Descemet membrane result in acute hydrops and striae, respectively.
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Keratoconjunctivitis, Superior Limbic

Introduction
Background

This disorder is characterized as an inflammation of the superior bulbar conjunctiva with predominant involvement of the superior limbus, an adjacent epithelial keratitis, and a papillary hypertrophy of the upper tarsal conjunctiva.

In 1963, Thygeson and Kimura described it as a chronic, localized, filamentary conjunctivitis.1 It was given its name, superior limbic keratoconjunctivitis (SLK), by Theodore, contemporaneously. Five years later, Tenzel and Corwin reported an association with thyroid abnormalities and SLK.2,3 A mimicking disorder has been encountered in soft contact lens wearers, typically with exposure to thimerosal-preserved solutions.
Pathophysiology Read more…

Keratoconjunctivitis, Sicca

Introduction
Background

This condition is characterized by inadequate tear film protection of the cornea because of either inadequate tear production or abnormal tear film constitution, which results in excessively fast evaporation or premature destruction of the tear film.
Pathophysiology
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Keratoconjunctivitis, Atopic

Introduction
Background

Atopic keratoconjunctivitis (AKC) is a relatively uncommon but potentially blinding ocular condition. In 1952, Hogan described AKC as a bilateral conjunctivitis occurring in 5 male patients with atopic dermatitis. Originally described to flare with worsening dermatitis, Foster et al noted that some patients’ ocular involvement evolves independent of dermatitis.1
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Keratitis, Interstitial

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Introduction
Background

Interstitial keratitis (IK) is a broad, descriptive term that has become synonymous with syphilitic disease. Although syphilis remains the leading cause of IK, various bacterial, viral, parasitic, and autoimmune causes of IK exist.
Pathophysiology

By definition, IK is a nonsuppurative inflammation, which is characterized by cellular infiltration of the corneal stroma. In general, no primary involvement of the corneal epithelium or endothelium occurs. Inflammation may be either the direct result of an infectious process or, more commonly, secondary to an immunologic response to a specific foreign antigen. This immunological response may take the form of antigen-antibody complex deposition, complement-mediated disease, or a delayed-type hypersensitivity reaction. Read more…