Dystrophy (degeneration) of the cornea

Dystrophy (degeneration, keratopathy) of the cornea is a chronic disease, which is based on a violation of general or local metabolic processes.

The nature of corneal dystrophy can be different: family-hereditary factors, autoimmune, biochemical, neurotrophic changes, trauma, consequences of inflammatory processes, etc. The initial link of the lesion may remain unknown. Isolate primary and secondary corneal dystrophy.

[1], [2], [3], [4]

Family-Hereditary Dystrophy of the Cornea

Primary corneal dystrophy is usually bilateral. Among them the main place is occupied by family-hereditary degenerations. The disease begins in childhood or adolescence, very slowly progresses, so that it can go unnoticed for a long period of time. The sensitivity of the cornea gradually decreases, there are no signs of eye irritation and inflammatory changes. In a biomicroscopic study, very delicate opacities in the central part of the cornea, which look like small nodules, spots or strips, are first revealed. Pathological inclusions in the cornea are most often located in the superficial layers of the stroma, sometimes subepithelial. The anterior and posterior epithelium, as well as the elastic membranes of the cornea, do not change. The peripheral parts of the cornea can remain transparent, there are no new vessels. By 30-40 years, the decrease in vision becomes noticeable, the epithelium of the cornea begins to change. Periodic listening of the epithelium causes painful sensations, photophobia, blepharospasm.

Different types of hereditary dystrophies of the cornea differ from each other in the main form and location of focal changes in the cornea. Knot, spotted, latticed and mixed dystrophies are known. The hereditary nature of these diseases was established at the beginning of the last century.

In Ukraine and Russia, this pathology is rare (less often than in other European countries).

Treatment of family-hereditary dystrophies is symptomatic. Prescribe vitamin drops and ointments, preparations that improve corneal trophism: balarpan, taufon, adelon, emoxipin, ethaden, retinol, solcoseryl gel, actovegin; Inside take multivitamins. Conservative treatment does not stop the progression of the disease. If the vision is significantly reduced, layered or through keratoplasty is performed. The best optical result is through corneal transplantation. Family-hereditary dystrophy is the only type of corneal pathology that resumes in the donor transplant. After 5-7 years after the operation, in the transparent transplant, single nodules or patches of tender opacities appear on the periphery, the same as those in the cornea. The number of them slowly increases, gradually deteriorating eyesight. After 10-15 years, it is necessary to perform a corneal transplant, which in most cases is well established, providing a high visual acuity.

[5], [6], [7], [8], [9], [10]

Epithelial (endothelial) dystrophy of the cornea

Epithelial (endothelial) dystrophy of the cornea (synonyms: edematous, epithelial-endothelial, endothelial-epithelial, bullous, deep dystrophy) can be both primary and secondary. For a long time the cause of this disease remained unknown. Currently, no one has doubt about the fact that the primary edematous corneal dystrophy failure occurs when the barrier function of the rear-row layer of epithelial cells caused by degenerative changes in the cells or their critically small amount (less than 500-700 cells per 1 mm ² ) .

Mirror biomicroscopy can reveal subtle initial changes, when the cornea is still transparent and there is no edema. They can be diagnosed with a normal biomicroscopy if you carefully examine the posterior surface of the cornea in a thin light section. Normally, the cells of the posterior epithelium of the cornea are not visible, since they are very small. When the number of cells is significantly reduced, the remaining cells flatten and stretch to cover the entire back surface of the cornea. The cell sizes increase 2-3 times, so they can already be seen with biomicroscopy. The posterior surface of the cornea becomes like a misted glass. This phenomenon is called dropping the cornea (cornea guttata). Currently, there are no ways to radically change this condition, but early diagnosis of harbingers of an impending disease allows you to correctly plan the treatment of concomitant pathology, for example choose a method of extracting cataracts, sparing the back of the cornea, refusing the introduction of an artificial lens (or finding the right model) and, very it is important to instruct the most experienced surgeon to perform the operation. Excluding or reducing the trauma of the cells of the posterior epithelium of the cornea, it is possible to delay the development of edematous degeneration for several months or years.

The presence of the drip corneal symptom does not yet indicate the onset of the disease (the cornea is transparent and non-thickened), but it is an indication that the functionality of the corneal back epithelium cells is close to the limiting ones. It is enough to lose a small number of cells to form uncovered defects. This can contribute to infectious diseases, contusions, injuries, especially cavitary operations.

In those cases when crevices appear between the cells of the posterior epithelium of the cornea, the intraocular fluid begins to impregnate the stroma of the cornea. The edema gradually spreads from the back layers to the entire cornea. Its thickness in the center can increase almost 2 times. This significantly reduces visual acuity due to the fact that the liquid expands the corneal plates, as a result of which their strict order is violated. Later, edematous degeneration extends to the anterior epithelium of the cornea. It becomes rough, inflated in the form of bubbles of various sizes, which easily peel off the Bowman membrane, burst, exposing the nerve endings. There is a pronounced corneal syndrome: pain, foreign body sensation, photophobia, lacrimation, blepharospasm. Consequently, the anterior epithelial dystrophy is the final stage of edematous degeneration of the cornea, which always begins with the posterior layers.

The state of the layer of cells in the posterior epithelium of the cornea is usually the same in both eyes. However, edematous degeneration of the cornea develops first in the eye that was subjected to trauma (domestic or surgical).

Treatment of edematous corneal dystrophy is symptomatic at first. Assign anti-edema drugs in instillations (glucose, glycerin), as well as vitamin drops and products that improve trophic cornea (balarpan, glemocom, carnosine, taufon). When the swelling reaches the epithelium of the cornea, antibacterial agents in the form of drops and ointments, as well as an oil solution of tocopherol, a gel of solcoseryl, actovegin, vitamin ointments that improve the regeneration of the epithelium are necessarily added. Ointment preparations and medical contact lenses serve as a kind of bandage for the cornea, protect the open nerve endings from external irritations, relieve pain.

A good therapeutic effect is provided by low-energy laser stimulation of the cornea by a defocused beam of a helium-neon laser.

Conservative treatment provides only a temporary positive effect, so it is periodically repeated as the corneal condition worsens.

A radical method of treatment is through the subtotal keratoplasty. Donor graft remains transparent in 70-80% of cases, it provides an opportunity to improve visual acuity and has a curative effect on the remaining edema of the cornea, which can be translucent, but the surface becomes smooth, the swelling passes. Already after 1-2 months the corneas of the donor and recipient 'have the same thickness.

Long-existing epithelial (endothelial) dystrophy of the cornea, as a rule, is combined with dystrophic changes in the retina, therefore, even with an ideal transparency of the donor transplant, one can not count on the highest visual acuity: it is in the range 0.4-0.6.

Secondary epithelial (endothelial) dystrophy of the cornea appears as a complication of ocular cavity operations, injuries or burns.

Clinical manifestations of primary and secondary edematous degeneration of the cornea are very similar, but there are also significant differences. One eye usually falls ill. The root cause of the resulting edema is always traced - a household, industrial or surgical trauma. The main difference is that the corneal edema occurs in a limited area according to the place of contact with the traumatizing agent, and around this area there are healthy cells of the corneal back epithelium, capable of replacing the defect.

Through the defect in the layer of cells of the posterior epithelium, the intraocular liquid penetrates into the stroma of the cornea. Local edema gradually reaches the surface layers and anterior epithelium. In those cases where the pathological focus is not in the center of the cornea, visual acuity may decrease slightly. With the appearance of bullous dystrophy of the anterior epithelium, irritation of the eyeball occurs in the sector of the pathological focus, pain, photophobia, lacrimation and blepharospasm.

Treatment is the same as with primary corneal dystrophy. Edema begins to decrease after 7-10 days, when the wound of the cornea heals. In the secondary form of dystrophy, complete healing of the lesion and the disappearance of the edema are possible. This requires a different period of time, from one to several months, depending on the cell density and the area of damage to the posterior epithelium, as well as on the healing speed of the common corneal wound.

In the event that the foreign body, for example the supporting element of the artificial lens, periodically touches the posterior surface of the cornea, the edema increases, and pains increase, despite any therapeutic measures. In this case, you need to either fix the lens (sutured to the iris), or remove, if its design is imperfect.

The fixed (constant) contact of the lens supporting element does not cause edematic dystrophy of the cornea and does not require its elimination, if for this there are no other reasons. With a fixed contact, when the lens support is enclosed in the corneal scar and the iris, no new damage to the corneal back epithelium occurs, unlike the situation with periodically recurring contacts.

Secondary edematous degeneration of the cornea may occur in the eye with an artificial lens, where there is no contact of the lens body or its supporting parts with the cornea. In this case, the removal of the lens does not provide a therapeutic effect, but, on the contrary, will be an additional trauma to the diseased cornea. Do not "punish" the lens, if it is "not to blame" for the onset of corneal edema. In this case, the cause of secondary edematic dystrophy should be sought in the traumatic nature of the operation itself.

Under the influence of the abovementioned medical measures, recovery may occur, however, on the site of edema there is always more or less dense turbidity. In severe cases, when edematic dystrophy captures the entire cornea or its center and conservative therapy does not give a positive result for a long time, it produces through-going subtotal keratoplasty, but not earlier than 1 year after surgery or eye trauma. The smaller the cornea is thickened, the more hope for a favorable outcome of the operation.

[11], [12], [13], [14], [15]

Tenderness degeneration of the cornea

Tenderness degeneration of the cornea is a slowly increasing surface cloudiness in the blind or visually impaired eyes.

The corneal corneal dystrophy develops several years after severe iridocyclitis, choroiditis in the eyes, blinded by glaucoma or severe injuries. Opacification occurs against the background of a changed sensitivity of the cornea, a decrease in the mobility of the eyeball and a decrease in metabolic processes in the eye. With the increasing atrophy of the muscular apparatus, involuntary movements of the eyeball (nystagmus) appear. The opacities are superficial in the region of the Bowman shell and the anterior epithelium. The stroma of the cornea and the posterior layers remain transparent. The changes begin at the periphery of the cornea at the inner and outer edges and, slowly growing, move to the center within the open eye gap in the form of a horizontally located ribbon. From above, where the cornea is covered by the eyelid, it always remains transparent. The opacities are distributed unevenly, there may be islands of the transparent surface of the cornea, but over time they also close. Lenticular degeneration is characterized by the deposition of calcareous salts, so the surface of the cornea becomes dry and rough. For a long time ago such changes, thin plates of cornified epithelium, impregnated with salts, can independently tear themselves away. Exceeding salt outgrowths injure the mucous membrane of the eyelid, so they must be removed.

Rough opacities and salt deposits in the cornea are formed against the background of pronounced common trophic changes in the blind eye, which can lead to subatrophy of the eyeball. There are cases when calcareous deposits were formed not only in the cornea, but also in the course of the vascular tract of the eye. Occurs ossification of the choroid.

Such eyes are subject to removal with subsequent cosmetic prosthetics. In eyes with residual vision, a superficial keratectomy (cutting of turbid layers) is made within the optical zone of the cornea (4-5 mm). The naked surface is covered with an epithelium that grows from the undamaged upper part of the cornea and can remain transparent for several years if the patient regularly digs in droplets that support the cornea trophic and lays ointments that prevent the corneal epithelium.

Corneal corneal dystrophy in children, combined with fibrinoplastic iridocyclitis and cataracts, is characteristic of Still's disease (Still's syndrome). In addition to the triad of eye symptoms, there are polyarthritis, enlargement of the liver, spleen, and lymph glands. After a course of anti-inflammatory treatment for iridocyclitis, cataract extraction is performed. When opacities in the cornea begin to close the central zone, decide on the implementation of keratectomy. Treatment of the underlying disease is performed by the therapist.

Edge degeneration (degeneration) of the cornea

Edge degeneration (degeneration) of the cornea usually occurs on two eyes, develops slowly, sometimes for many years. The cornea becomes thinner near the limbus, a sickle-shaped defect is formed. Neovascularization is absent or is negligible. With a pronounced thinning of the cornea, its sphericity is broken, visual acuity is reduced, and areas of ectasia appear, and there is a threat of perforation. Conventional drug treatment only has a temporary effect. Radical method of treatment is the marginal layer-by-layer transplantation of the cornea.

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