It is the most anterior and clear layer of the eye, similar to the glass cover on a watch. It is a very specialized tissue designed to refract and transmit light inside the eye. It has 48,33 diopters of convergent power, meaning that it is responsible for most of the eye’s refractive power.

The following are its anatomical relationships: in front, the tear film and the tarsal conjunctiva of the upper lid ; inside, the aqueous humor and the anterior chamber that contains it; and along the perimeter it is in contact with the corneoescleral limbus, the sclera and the bulbar conjunctiva.

The cornea is composed of five layers: epithelium (1), Bowman’s membrane (2), stroma (3), Descemet’s membrane (4) and endothelium (5).

It is a highly organized clear avascular structure, which is quite unique among all the body tissues.

In terms of optics and refractive power, the curvature radius of the anterior central portion of the cornea is ± 7.7 mm (48.83 D). The cornea is steeper at the center than at the periphery and its anterior surface is more like and ellipse. The internal or posterior surface radius is ± 6.8 mm (-5.88D). Corneal thickness is less at the center than at the periphery: ± 530µm central thickness and ± 700µm peripheral thickness. The average horizontal diameter is 12.0 mm.

Epithelium: (a)

It is the outermost layer of the cornea that is in contact with the tear film. It consists of 5-7 cube-shaped cell layers that flatten as they become superficial. The thickness of the corneal epithelium is ± 50 to 52 µm. Like all other epithelial layers, its role is to protect against the environment and prevent the loss of fluid and the penetration of harmful agents. Cells undergo a fast exchange rate over a period of ± 5 to 7 days as they slough off. It reacts very quickly and in a specialized way to aggression. This sensitivity is associated with an exceptional density of nerve endings estimated to be 300 or 400 times greater than in the skin’s epidermis. It is believed that corneal epithelium stem cells are located in the basal cells at the limbus between the corneal epithelium and the conjunctiva.

Bowman’s Membrane: (c)

It is an acellular extra cellular collagen matrix resulting from the coordinated synthesis of the epithelium and the stromal cells. This layer separates stromal collagen from the epithelium.

Stroma: (g)

The stromal layer represents 90% of the corneal thickness. It consists of cross-linked collagen fibers embedded in mucus substances (mucopolysaccarides).

Descemet’s Membrane:

This is the endothelial basement membrane that secretes material throughout life. The average thickness of this layer in young age is 8 µm.

Endothelium:

This innermost layer of the cornea is in contact with the aqueous humor and forms the wall of the anterior chamber. It consists of hexagonal cells distributed in a single layer with an average of 2.500-3.000 cells/mm2. As we age, the number of cells diminishes. This membrane allows the passage of nutrients inside the cornea and controls hydration. Consequently, it is responsible for maintaining a clear cornea. The endothelium has little ability to regenerate, so it is unable to divide and fully repair a defect; the repair mechanism is by cell enlargement and extension.

Alterations in corneal shape, transparency and refractive power resulting from congenital malformations, infections, trauma or metabolic disorders give rise to varying degrees of visual dysfunction that may be treated with drugs. In other instances, surgical repair is required using corneal grafts in order to recover transparency or refractive power and, ultimately, vision.

Because of its physical (absence of blood vessels) and metabolic characteristics, the cornea has a privileged immunological condition that allows for successful grafting in a large percentage of cases.

Keratoconus is a non-inflammatory ectasic disease that affects corneal curvature and thickness leading to bulging and irregularity of the corneal surface. It is relatively frequent with a prevalence of 54.5 for every 100.000 (0.05%). It is found in all ethnic groups, it is bilateral and there is no gender predominance. It occurs more frequently in people living at high altitudes.

Its etiology has not been determined. Six to fifteen per cent of patients with keratoconus have other affected relatives. This condition is associated with a long list of systemic diseases but it occurs sporadically and in an isolated way. It is most frequently associated with compression and rubbing of the eyes leading to chronic mechanical trauma.

It presents during puberty and the rate of progression is usually faster the younger the age of onset. As keratoconus progresses, visual acuity is compromised as a result of the distortion created by the conus and it can even reach the point of causing disability.

Primary:

Fuchs Endothelial Dystrophy, known as cornea guttata because of the warty appearance of the endothelium. Using retroillumination (red reflex), the endothelium looks like embossed silver. It is an inherited progressive familial condition but it takes decades to develop. It produces corneal haziness because of the endothelium’s inability to maintain a state of corneal dehydration.

Dystrophy signs and symptoms become evident after 50 years of age in the form of blurred vision upon awakening that improves throughout the day. As it progresses, the symptoms of blurring last longer until they become permanent.

Primary:

Fuchs Endothelial Dystrophy, known as cornea guttata because of the warty appearance of the endothelium. Using retroillumination (red reflex), the endothelium looks like embossed silver. It is an inherited progressive familial condition but it takes decades to develop. It produces corneal haziness because of the endothelium’s inability to maintain a state of corneal dehydration.

Dystrophy signs and symptoms become evident after 50 years of age in the form of blurred vision upon awakening that improves throughout the day. As it progresses, the symptoms of blurring last longer until they become permanent.

This form of decompensation is spontaneous or induced as a result of accidental or surgical trauma and consists of a reduction in the number of endothelial cells leading to progressive corneal edema and opacification. It is a condition that presents with inflammation, pain and rapid progression.

Hypertonic ointments or eye drops may be used as initial treatment in order to reduce edema. Therapeutic contact lenses are also used to help with discomfort. Full-thickness or endothelial corneal grafting may be eventually required in order to cure the condition.

Full thickness or penetrating keratoplasty:

This procedure is performed when all the corneal layers are involved. The diameter of the grafts ranges between 7.0 y 9.0 mm according to the affected corneal area. It is sutured edge-to-edge with interrupted stitches or with a running polyamide (Nylon) suture. The healing process is slow and sutures are removed between 6 and 12 months after surgery.

Deep lamellar keratoplasty:

This procedure is performed when there is no endothelial involvement. The surgical technique is time-consuming and it requires dissecting layer-by-layer down to Descemet`s membrane in order to place a graft from which the endothelium has been removed. Sutures are removed between 3 to 6 months after surgery.

Queratoplastia Laminar Superficial:

Cuando únicamente el 1/3 anterior de la córnea está comprometida. Se realiza en forma automatizada con Microqueratomo, tanto en el receptor como en el donante. Las suturas pueden retirarse tan pronto como se haya establecido una buena reepitelización: 8-10 días.

Injerto Endotelial:

En este procedimiento únicamente el Endotelio incompetente es cambiado por un Endotelio donante con celularidad normal. Se realiza a través de una incisión pequeña en el limbo córneoescleral. Es una técnica laboriosa y requiere de algunos meses para recuperar la transparencia.

Deep lamellar graft

Sectorial Grafts:

In cases of visual disorders where the lesion does not affect the central area or optic zone, partial or total thickness grafts, eccentric grafts or other grafts of different shapes can be used. An additional surgical procedure may be required in order to correct refraction.

Graft Rejection:

Although the cornea is an immunologically privileged tissue, the graft may become opacified as a result of a rejection response when the body recognizes the tissue as foreign. This immune reaction occurs in 4 to 6% of penetrating surgeries and it is extremely rare with lamellar grafts. This risk is greater in cases of inflammation due to infection, chronic decompensation and congenital malformations, and in those where there is encroachment of blood vessels involving the limbo-corneal transition line (corneoscleral limbus). When grafting is required because of corneal deformation, as is the case in ectasias, avascular leukomas and dystrophies, the probability of obtaining a clear graft is greater than 90%.

Herpes

Herpes Simples viruses are human pathogens capable of causing asymptomatic infections and also active disease involving multiple organs. Human beings are the only natural reservoirs for the Herpes Simplex Virus types 1 and 2. Direct contact is required for transmission because of the instability of the virus and the fact that the main doors for entry are the skin and the mucous membranes.
The ocular involvement is usually caused by the HSV1 that produces one of the most challenging forms of keratitis both in terms of diagnosis as well as treatment. The corneal infection includes epithelial keratitis, neurotrophic keratopathy, necrotizing stromal keratitis, immunological (interstitial) stromal keratitis, and endothelitis.

The most frequent form of herpetic keratitis is a dendritic ulcer consisting of a branching linear lesion with terminal bulbs and inflamed edges containing live viruses. It stains positive with flouresceine, making its diagnosis easier. It involves the epithelium, and in its initial stages it may reach the basement membrane. It produces a foreign-body sensation, tearing and blurred vision.
When the ulcer loses its linear shape, it is known as “geographic ulcer” representing an extended dendritic lesion that is usually associated with prolonged symptoms and prior use of steroids.
A potential sequel of Herpes Simples keratitis is the formation of repair scars in the stroma (leukomas) that give rise to reduced vision.

Despite the conjunctiva’s natural defenses and the protective effect of the tear film against bacteria and other microorganisms, sometimes these adhere to the ocular surface colonizing the cornea and the conjunctiva, giving rise to conjunctivitis and corneal abscesses.

A mild trauma such as an abrasion caused by particles blowing in the wind, a small foreign body in the cornea, contact lenses, eyelashes or conjunctival concretions may create an epithelial erosion though which bacteria may enter the eye.

Immune systemic diseases may be the origin of severe keratitis. Although symptoms vary, the most common are tearing, red eye, foreign-body sensation and ocular pain.

The ulcer is usually round and whitish and the prognosis depends on the extent and the speed with which treatment is instituted and the offending germ.

In very severe case, there may be a corneal perforation and vision may be compromised.

Treatment is designed to eliminate the culprit bacteria and to suppress the inflammatory response.

Epithelial erosion

It may result from contact with any foreign element – paper, contact lenses, plat leave or just the hand, creating a foreign-body sensation, pain and tearing. In most cases, erosions are superficial and heal with no complications within 24 hours. However, it is wise to see a specialist if symptoms are still present after 24 hours, because they may progress to a corneal abscess or actually be a Herpes Simplex infection.

Corneal dystrophies:

These are rare diseases, almost always of autosomal dominant inheritance, although there are some autosomal recessive forms. Presentation and severity may vary among the members of one same family.
Except for “basement membrane dystrophy” (recurrent epithelial erosion) and “Fuchs’ endothelial dystrophy”, The classification of this disorder has become so complex despite the fact that they all have their distinguishing features, that an attempt is being made at a molecular genetic classification based on DNA characteristics.

Corneal dystrophies are primary corneal disorders not associated with inflammation, trauma or underlying systemic diseases. They appear usually during the second decade of life and evolve slowly over a long period of time without symptoms.

Dystrophies affect vision by two mechanisms: a) light diffraction from corneal debris or corneal edema; b) image distortion as a result of an irregular corneal surface and stromal deposits.

Treatment is almost always surgical, consisting of lamellar or penetrating corneal grafting.