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What causes keratitis?
The causes of keratitis are bacterial fungal flora, viral infections, physical, chemical factors, allergic reactions, metabolic disorders.
Classification of keratitis Bolokonenko and Gorbel
- corneal erosion;
- traumatic keratitis;
- infectious keratitis of bacterial origin;
- keratitis of viral myology (epidemic keratoconjunctivitis, ulcer with natural and varicella);
- fungal keratitis - keratomycosis;
- keratitis caused by conjunctivitis, diseases of the eyelids, lacrimal organs, meibolic glands, keratitis with lagophthalmus, meibolic keratitis.
- infectious: syphilitic, tubercular, malarial, brucellosis, leprosy;
- neurogenic (neuroparalytic, herpetic, recurrent corneal erosion - can be due to burns);
- vitamins - with a deficiency of vitamins A, B1, B2, C;
- keratitis of unexplained etiology (filamentous keratitis, ra betray ulcer, rosacea-keratitis).
Symptoms of keratitis
Inflammatory diseases of the cornea are keratitis. Features of the structure of the cornea and the lack of blood vessels can explain a number of subjective and objective symptoms.
When it develops inflammatory processes of a different etiology of both exogenous and endogenous origin. In response to any irritation symptoms - photophobia, lacrimation and blepharosyazm, the sensation of a foreign body under the eyelids. This is the so-called horny syndrome, which is an important protective mechanism of the eye, in which the pecks and lacrimal glands are involved due to complex innervation.
If the irritation of the cornea is caused by the fallen mote, the tear flushes the foreign body, cleans the wound and disinfects it due to the lysozyme contained in this liquid.
After removal of the foreign body, tearing stops, photophobia decreases, but the sensation of a foreign body may appear, under the eyelid - a defect of the epithelium due to the roughness of the surface of the cornea.
Complaints on bati in the eye appear when the surface of the cornea is eroded. They can irradiate over the entire half of the head.
In an objective examination of the affected eye, the following symptoms of keratitis are found: eye damage (pericorneal vascular injection), inflammatory infiltration (focal or diffuse), changes in all corneal properties in the inflammation zone, and growth of newly formed vessels.
Pericorneal injection of vessels is an early and permanent symptom of corneal inflammation caused by irritation of deep vessels of the marginal loop network. It appears as a pink-cyanotic corolla around the cornea. Redness is always diffuse. Individual vessels are not visible even with biomicroscopy. Depending on the size of the focus of inflammation, pericorneal vascular injection may surround the cornea from all sides or manifest only at the site of the cornea lesion. In severe cases, it acquires a blue-violet color. To pericorneal injection, irritation of conjunctival vessels can join, then there is a mixed hyperemia of the eyeball.
The first stage of the inflammatory process in the cornea begins with infiltration and often has a focal character. Infiltrates can be located on any site and at different depths and can have different shapes (regular rounded outlines in the form of dots, coins, disc or tree twigs). Due to the edema of surrounding tissues in the acute phase of inflammation, the boundaries of the inflammation focus are not clear.
The color of the infiltrate depends on its cellular composition. If the focus is not infiltrated by leukocytes, it is gray. When the purulent infiltration intensifies, the focus becomes yellowish or yellow in color. Normally, the cornea is smooth, shiny, transparent, spherical and highly sensitive. In the area of the focus of inflammation all the properties of the cornea change: the surface becomes uneven, rough due to swelling and sloshing of the epithelium, the mirror shine disappears, transparency is violated. In the process of scarring large defects of the cornea, the sphericity of the surface is lost. The sensitivity of the cornea decreases, until complete absence. In case of toxic-allergic diseases, sensitivity may increase. Changing the sensitivity of the cornea can be observed not only in the patient, but also in the pair eye.
A few days after the onset of inflammation in the direction of infiltration, vessels grow. On the first ethane, they play a positive role, since they contribute to the healing of the cornea. However, later, despite the fact that the vessels are partially emptying, they lead to a significant decrease in visual acuity. With superficially located infiltrates, the bright red conjunctiva vessels cross the border of the limbus, branch out branchily and are sent to the infiltrate under the cover of the epithelium (surface neovacu- larization). Inflammatory processes, deeply penetrating into the corneal tissue, are accompanied by ingrowth of scleral and episcleral vessels. This is a deep neovascularization of the cornea. It has characteristic features. Deep vessels pass in the middle and deep layers of the stroma, with difficulty extend between corneous plates, do not branch, look like strings. The brightness of color and pattern of vessels is obscured by a thick layer of edematous corneal plates located above them.
In some cases, surface and deep vessels grow - a 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 in this stage depends on its etiology, the pathogenicity of the pathogen, the state of the organism, the treatment being administered, and other factors. In the development of keratitis, the state of general and local immunity is of great importance. In some cases, the corneal ulcer may be limited to the zone of primary lesion, in others it spreads rapidly to depth and width and in a few hours can melt the entire cornea. The bottom of the ulcer can be clean or covered with a purulent exudate, the edges of the ulcer - even or swollen, infiltrated. The presence of one dug edge with an overhanging bubble indicates a progression of the process.
As the necrotic masses are torn away, the bottom and edges of the ulcer are cleared, the regression period begins, the inflammatory process passes to the third stage: neovascularization of the cornea increases, the ulcer edges become smoother, the bottom begins to be replaced by a whitish scar tissue. The appearance of a mirror shine indicates the beginning of the epithelization process.
Outcomes keratitis are not the same. The depth of the inflammatory process is of great importance.
Surface erosion and infiltration, not reaching the Bowman shell, heal without leaving a trace. After healing of deeper infiltrates defects are formed in the form of facets of different size and depth. The bottom of them is closed by a connected scar with a different degree of density and depth of occurrence. Visual acuity depends on the location of the scar. Any opacification does not affect the 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 thorn,
A cloud is a thin, translucent, limited cloudiness of grayish color, invisible to the naked eye. However, when the cloud is located exactly in the center of the cornea, the vision deteriorates slightly.
A spot is a denser, limited cloudiness of a whitish color. It can be seen with external examination. This clouding leads to a significant reduction in visual acuity.
Belmo is a thick thick opaque cornea scar of white color. It causes a sharp reduction in the severity of the sight, until the subject's vision is completely lost, depending on the size of the belly and its ratio to the pupillary area.
Deep ulcers are able to melt the cornea up to the inner elastic membrane. It remains transparent, but under the influence of intraocular pressure swells forward in the form of a bubble. Such hernia descetent sheath not only is a hindrance to vision, but the peseta also threatens the perforation of the cornea. The perforation of the ulcer usually results in the formation of a coarse, thorny flesh. With the expiration of the intraocular fluid, the iris is displaced to the perforating opening and swabs it. At the same time, the front camera is shortened or missing. The fusion of the iris with the cornea is called the front synechiae. Subsequently they can cause the development of secondary glaucoma. If there is an infringement of the iris in the perforated hole, it can interfere with the formation of a dense scar, resulting in the formation of a fistula of the cornea.
Under the influence of increased intraocular pressure, thinning belly, fused to the iris, can stretch, forming protrusions over the surface of the cornea - staphylomas.
The consequences of keratitis become more severe if the inflammatory process passes to the sclera, iris and ciliary body.
Diagnosis of keratitis
Diagnosis of keratitis in most cases is not difficult. The cornea is available for inspection, therefore, complex studies are not required, moreover, in keratitis there are 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 clinical course of keratitis.
Pericorneal injection of vessels in combination with corneal syndrome always indicates the presence of inflammation in the anterior part of the eye. It is necessary to conduct differential diagnosis between keratitis and iridocyclitis. If there are no opacities in the cornea, it is smooth, shiny, spherical and its sensitivity is not disturbed, keratitis is excluded. It is more difficult to understand if there was keratitis in this eye. The old cloudiness differs from the fresh inflammation in that it has clear boundaries, does not bulge, but, on the contrary, it can be thinner than the surrounding corneal areas, has a smooth, shiny surface, is perforated by flaccid, half-empty vessels, there is no pericorneal injection of vessels.
An important differential diagnostic symptom of keratitis is a decrease in sensitivity in healthy parts of the cornea and in the paired eye. This indicates the presence of herpetic or neurogenic keratitis. For keratitis caused by various exogenous factors, 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 different depth and extent is characteristic, 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 local, located mainly in deep layers. Surface layers are not ulcerated. Such keratitis is called deep.