Keratitis

Keratitis and its consequences account for 20-25% of outpatients.

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What causes keratitis?

Causes of keratitis are bacterial fungal flora, viral infections, physical and chemical factors, allergic reactions, and metabolic disorders.

Classification of keratitis by Bolokonenko and Gorbel

Exogenous keratitis:

• corneal erosion;
• traumatic keratitis;
• infectious keratitis of bacterial origin;
• keratitis of viral myology (epidemic keratoconjunctivitis, ulcers in smallpox and chickenpox);
• fungal keratitis - keratomycosis;
• keratitis caused by conjunctivitis, diseases of the eyelids, lacrimal organs, meibolic glands, keratitis in lagophthalmos, meibolic keratitis.

Endogenous keratitis:

• infectious: syphilitic, tuberculosis, malaria, brucellosis, leprosy;
• neurogenic (neuroparalytic, herpetic, recurrent corneal erosion - may occur with burns);
• vitamin - for deficiency of vitamins A, B1, B2, C;
• keratitis of unknown etiology (filamentous keratitis, rosacea keratitis).

Symptoms of keratitis

Inflammatory diseases of the cornea - keratitis. The peculiarities of the structure of the cornea and the absence of vessels can explain a number of subjective and objective symptoms.

When inflammatory processes of various etiologies of both exogenous and endogenous origin develop in it. In response to any irritation, the symptoms are photophobia, lacrimation and blepharosiasm, a sensation of a foreign body under the eyelids. This is the so-called corneal syndrome, which is an important protective mechanism of the eye, in which the pectinates and lacrimal gland participate due to complex innervation.

If the irritation of the cornea is caused by a speck of dirt, then the tear washes away the foreign body, cleans the wound and disinfects it thanks to the lysozyme contained in this liquid.

After removal of the foreign body, lacrimation stops, photophobia decreases, but a sensation of a foreign body may appear, under the eyelid - a defect in the epithelium due to the roughness of the corneal surface.

Complaints about baty in the eye appear with erosion of the corneal surface. They can irradiate over the entire half of the head.

During an objective examination of the affected eye, the following symptoms of keratitis are detected: eye damage (pericorneal injection of vessels), inflammatory infiltration (focal or diffuse), changes in all properties of the cornea in the area of inflammation and ingrowth of newly formed vessels.

Pericorneal vascular injection is an early and constant symptom of corneal inflammation caused by irritation of the deep vessels of the marginal loop network. It appears as a pink-blue halo around the cornea. Redness is always diffuse. Individual vessels are not visible even with biomicroscopy. Depending on the size of the inflammation, pericorneal vascular injection may surround the cornea on all sides or appear only at the site of corneal damage. In severe cases, it acquires a blue-violet color. Pericorneal injection may be accompanied by irritation of the conjunctival vessels, then mixed hyperemia of the eyeball occurs.

The first stage of the inflammatory process in the cornea begins with infiltration and is often focal in nature. Infiltrates can be located in any area and at different depths and can have different shapes (regular rounded outlines in the form of dots, coins, disks or tree branches). Due to swelling of the surrounding tissues in the acute phase of inflammation, the boundaries of the inflammation focus are unclear.

The color of the infiltrate depends on its cellular composition. If the lesion is poorly infiltrated with leukocytes, it is gray. When purulent infiltration increases, the lesion acquires a yellowish tint or yellow color. Normally, the cornea is smooth, shiny, transparent, spherical and highly sensitive. In the area of the inflammatory lesion, all the properties of the cornea change: the surface becomes uneven, rough due to swelling and exfoliation of the epithelium, the mirror shine disappears, and transparency is impaired. In the process of scarring of large corneal defects, the sphericity of the surface is lost. The sensitivity of the cornea decreases, up to complete absence. In toxic-allergic diseases, sensitivity may increase. Changes in corneal sensitivity can be noted not only in the patient, but also in the fellow eye.

A few days after the onset of inflammation, vessels grow towards the infiltrate. At the first stage, they play a positive role, as they promote healing of the cornea. However, subsequently, despite the fact that the vessels partially become empty, they lead to a significant decrease in visual acuity. With superficially located infiltrates, bright red conjunctival vessels cross the border of the limbus, branch like a tree and are directed towards the infiltrate under the epithelium (superficial neovascularization). Inflammatory processes that deeply penetrate the corneal tissues are accompanied by the ingrowth of scleral and episcleral vessels. This is deep neovascularization of the cornea. It has characteristic signs. Deep vessels pass through the middle and deep layers of the stroma, with difficulty extend between the corneal plates, do not branch, and look like threads. The brightness of the color and pattern of the vessels is obscured by a thick layer of edematous corneal plates located above them.

In some cases, superficial and deep vessels grow in - mixed neovascularization of the cornea.

The second stage of the inflammatory process in the cornea is tissue necrosis in the central part of the infiltrate, erosion and ulceration of the surface. The course of the process at this stage depends on its etiology, pathogenicity of the pathogen, the state of the body, the treatment and other factors. In the development of keratitis, the state of general and local immunity is of great importance. In some cases, a corneal ulcer may be limited to the zone of the primary lesion, in others it quickly spreads in depth and width and in a few hours can melt the entire cornea. The bottom of the ulcer may be clean or covered with purulent exudate, the edges of the ulcer - smooth or swollen, infiltrated. The presence of one undermined edge with an overhanging vesicle indicates the progression of the process.

As the necrotic masses are rejected, the bottom and edges of the ulcer are cleared, a period of regression begins, the inflammatory process passes to the third stage: neovascularization of the cornea increases, the edges of the ulcer are smoothed out, the bottom begins to be filled with whitish scar tissue. The appearance of a mirror shine indicates the beginning of the epithelialization process.

The outcomes of keratitis are not the same. The depth of the spread of the inflammatory process is of great importance.

Superficial erosions and infiltrates that do not reach the Bowman's membrane heal without leaving a trace. After the healing of deeper infiltrates, defects in the form of facets of varying size and depth are formed. Their bottom is covered with a connective tissue scar of varying density and depth. Visual acuity depends on the location of the scar. Any clouding does not affect visual acuity and is only a cosmetic defect. Centrally located scars always cause a decrease in vision. There are three types of opacities: a cloud, a spot, a leukoma,

A cloud is a thin, translucent, limited cloudiness of a grayish color, invisible to the naked eye. However, if the cloud is located exactly in the center of the cornea, vision is slightly impaired.

A spot is a denser, limited, whitish opacity. It is visible during external examination. Such opacity leads to a significant decrease in visual acuity.

A leukoma is a dense, thick, opaque, white scar on the cornea. It causes a sharp decrease in visual acuity, up to and including complete loss of object vision, depending on the size of the leukoma and its relationship to the pupil area.

Deep ulcers can melt the cornea down to the internal elastic membrane. It remains transparent, but under the influence of intraocular pressure, it bulges forward in the form of a bubble. Such a hernia of the descement membrane not only interferes with vision, but also poses a risk of corneal perforation. Perforation of the ulcer usually ends with the formation of a coarse leukoma fused with the iris. When the intraocular fluid flows out, the iris shifts to the perforation hole and tamponades it. The anterior chamber is reduced or absent. Fusion of the iris with the cornea is called anterior synechia. Subsequently, they can cause the development of secondary glaucoma. If the iris is pinched in the perforated hole, it can interfere with the formation of a dense scar, resulting in a corneal fistula.

Under the influence of increased intraocular pressure, thinned out opaque spots, fused with the iris, can stretch, forming protrusions above the surface of the cornea - staphylomas.

The consequences of keratitis become more severe if the inflammatory process spreads to the sclera, iris and ciliary body.

Diagnosis of keratitis

Diagnosis of keratitis in most cases does not cause difficulties. The cornea is accessible for examination, so complex studies are not required, in addition, keratitis has characteristic subjective and objective symptoms. It is much more difficult to determine the etiology of the process. For this purpose, special laboratory methods are used to confirm or exclude the cause of the inflammatory process, established on the basis of the characteristics of the clinical course of keratitis.

Pericorneal injection of vessels in combination with corneal syndrome always indicates the presence of inflammation in the anterior segment of the eye. It is necessary to conduct differential diagnostics between keratitis and iridocyclitis. If there are no opacities in the cornea, it is smooth, shiny, spherical and its sensitivity is not impaired, keratitis is excluded. It is more difficult to figure out if there was keratitis in this eye. An old opacification differs from a fresh inflammation focus in that it has clear boundaries, does not bulge, but, on the contrary, can be thinner than the surrounding areas of the cornea, has a smooth, shiny surface, is penetrated by sluggish, semi-deserted vessels, there is no pericorneal injection of vessels.

An important differential diagnostic symptom of keratitis is decreased sensitivity in healthy areas of the cornea and in the fellow eye. This indicates the presence of herpetic or neurogenic keratitis. Keratitis caused by various exogenous factors is characterized by an acute onset with mandatory damage to the superficial layers of the cornea, necrosis of the infiltrate, the formation of erosions and ulcers of the cornea of various depths and lengths, therefore, exogenous keratitis is called superficial in some classifications. Unlike exogenous, endogenous inflammation of the cornea is characterized by a more sluggish and prolonged course. Infiltration can be diffuse or localized, located mainly in the deep layers. The superficial layers do not ulcerate. Such keratitis is called deep.

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