Keratitis is a group of inflammatory lesions of the cornea – the anterior transparent membrane of the eye, having different etiologies, causing clouding of the cornea and decreased vision. For keratitis, the so-called corneal syndrome is typical, characterized by lacrimation, photophobia, blepharospasm; sensation of a foreign body of the eye, cutting pains, changes in corneal sensitivity, decreased vision. Diagnosis includes biomicroscopy of the eye, tests with fluorescein, cytological and bacteriological examination of a smear from the conjunctiva and cornea, immunological and allergological tests. When keratitis is detected, etiotropic (antiviral, antibacterial, antiallergic, etc.) treatment is carried out. Microsurgical intervention (keratoplasty) is indicated for corneal ulceration.
Inflammatory diseases of the eye are the most common pathology in ophthalmology. The largest group among them is conjunctivitis (66.7%); inflammatory lesions of the cornea – keratitis occur in 5% of cases. Microflora is constantly present in the conjunctival cavity of the eye, which, even with minimal damage to the cornea, easily causes its inflammation. In half of the cases, the consequence is a persistent decrease in vision, requiring the use of microsurgical techniques to restore the optical properties of the cornea, and in some cases, the course can lead to irreversible blindness. The development of a purulent corneal ulcer with keratitis in 8% of cases is accompanied by anatomical death of the eye and in 17% requires enucleation of the eyeball due to the failure of conservative treatment.
The largest number of cases is associated with viral etiology. In 70% of cases, the causative agents are herpes simplex viruses and herpes Zoster (herpes zoster). Adenovirus infection, measles, chickenpox can also provoke the development of keratitis, especially in children.
The next large group consists of purulent corneal lesions caused by bacterial nonspecific flora (pneumococcus, streptococcus, Staphylococcus, Diplococcus, Pseudomonas aeruginosa, E. coli, Klebsiella, proteus) and specific pathogens of tuberculosis, salmonellosis, syphilis, malaria, brucellosis, chlamydia, gonorrhea, diphtheria, etc.
A severe form is caused by an amoebic infection – the bacterium Acanthamoeba; amoebic keratitis often occurs in people who wear contact lenses, and in the long term can end in blindness. The causative agents of mycotic keratitis (keratomycosis) are fungi fusarium, Aspergillus, candida.
Keratitis can serve as a manifestation of a local allergic reaction with pollinosis, the use of certain medications, worm infestation, hypersensitivity to food or plant pollen. Immune-inflammatory corneal damage can be observed in rheumatoid arthritis, nodular periarthritis, Sjogren’s syndrome, and other diseases. With intense exposure to ultraviolet radiation on the eyes, photokeratitis can develop.
In most cases, the occurrence is preceded by mechanical, chemical, thermal trauma of the cornea, including intraoperative damage to the cornea during eye operations. Sometimes keratitis develops as a complication of lagophthalmos, inflammatory diseases of the eyelids (blepharitis), eye mucosa (conjunctivitis), lacrimal sac (dacryocystitis) and lacrimal tubules (canaliculitis), sebaceous glands of the eyelid (meibomitis). One of the common causes is non-compliance with the rules of storage, disinfection and use of contact lenses.
Among the endogenous factors that favor the development of keratitis, there are exhaustion, lack of vitamins (A, B1, B2, C, etc.), a decrease in general and local immune reactivity, metabolic disorders (diabetes mellitus, a history of gout).
Pathomorphological changes are characterized by edema and infiltration of corneal tissue. Infiltrates formed by polynuclear leukocytes, histiocytes, lymphoid and plasma cells have different sizes, shapes, colors, and fuzzy boundaries. At the stage of resolution of keratitis, corneal neovascularization occurs – the germination of newly formed vessels from the conjunctiva, the marginal loop network or both sources into the shell. On the one hand, vascularization improves the trophism of the corneal tissue and accelerates the recovery processes, on the other hand, newly formed vessels further desolate and reduce the transparency of the cornea.
With severe keratitis, necrosis, microabcesses, corneal ulceration develop. Ulcerative defects in the cornea are further scarred, forming a thorn (leukoma).
Keratitis is classified depending on the etiology, the course of the inflammatory process, the depth of the corneal lesion, the location of the inflammatory infiltrate and other signs.
Depending on the depth of the lesion, superficial and deep keratitis are distinguished. With superficial keratitis, up to 1/3 of the thickness of the cornea (epithelium, upper stromal layer) is involved in inflammation; with deep keratitis, the entire stroma.
According to the localization of the infiltrate, keratitis can be central (with the location of the infiltrate in the pupil zone), paracentral (with infiltrate in the projection of the iris belt), and peripheral (with infiltrate in the limb zone, in the projection of the ciliary iris belt). The more centrally the infiltrate is located, the more visual acuity suffers during the course of keratitis and in its outcome.
According to the etiological criterion, keratitis is divided into exogenous and endogenous. Exogenous forms include corneal erosion, keratitis of traumatic, bacterial, viral, fungal origin, as well as keratitis caused by damage to the eyelids, conjunctiva and meibomian glands (meibomian keratitis). Endogenous keratitis includes infectious corneal lesions of tuberculous, syphilitic, malarial, brucellosis etiology; allergic, neurogenic, hypo- and beriberi keratitis. Endogenous keratitis of unclear etiology includes filamentous keratitis, corrosive corneal ulcer, rosacea-keratitis.
A common manifestation characteristic of all forms of the disease is the corneal syndrome developing with keratitis. At the same time, there are sharp pains in the eye, intolerance to bright daylight or artificial light, lacrimation, involuntary closing of the eyelids (reflex blepharospasm), visual impairment, sensation of a foreign body under the eyelid, pericorneal injection of the eyeball.
Corneal syndrome in keratitis is associated with irritation of the sensitive nerve endings of the cornea by the resulting infiltrate. In addition, due to infiltration, the transparency and gloss of the cornea decreases, its opacity develops, sphericity and sensitivity are disturbed. In neurogenic keratitis, the sensitivity of the cornea and the severity of the corneal syndrome, on the contrary, are reduced.
With the accumulation of lymphoid cells, the infiltrate acquires a grayish hue; with the predominance of leukocytes, its color becomes yellow (purulent infiltrate). With superficial keratitis, the infiltrate can resolve almost without a trace. In the case of a deeper lesion at the site of infiltration, corneal opacities of varying intensity are formed, which can reduce visual acuity to varying degrees.
An unfavorable variant of the development of keratitis is associated with the formation of corneal ulceration. In the future, when the epithelium is exfoliated and exfoliated, surface erosion of the cornea is formed first. The progression of epithelial rejection and tissue necrosis leads to the formation of a corneal ulcer, which has the appearance of a defect with a cloudy gray bottom covered with exudate. The outcome of keratitis with corneal ulcer may be regression of inflammation, purification and epithelization of the ulcer, scarring of the stroma, leading to clouding of the cornea – the formation of a cataract. In severe cases, a deep ulcerative defect can penetrate into the anterior chamber of the eye, causing the formation of descemetocele – a hernia of the descemetal membrane, perforation of the ulcer, the formation of anterior synechiae, the development of endophthalmitis, secondary glaucoma, complicated cataract, optic neuritis.
Keratitis often occurs with simultaneous inflammation of the conjunctiva (keratoconjunctivitis), sclera (keratoscleritis), the vascular membrane of the eye (keratouveitis). Often, iritis and iridocyclitis also develop. Involvement in purulent inflammation of all the membranes of the eye leads to the death of the organ of vision.
In the diagnosis of keratitis, its connection with common diseases, viral and bacterial infections, inflammation of other structures of the eye, microtrauma of the eye, etc. is important. During an external examination of the eye, the ophthalmologist focuses on the severity of the corneal syndrome and local changes.
The leading method of objective diagnosis of keratitis is biomicroscopy of the eye, during which the nature and size of the corneal lesion is assessed. The thickness of the cornea is measured using ultrasound or optical pachymetry. In order to assess the depth of corneal lesion in keratitis, endothelial and confocal microscopy of the cornea is performed. The study of the curvature of the corneal surface is carried out by computer keratometry; the study of refraction is carried out using keratotopography. To determine the corneal reflex, a corneal sensitivity test or estesiometry is resorted to.
In order to detect erosions and ulcers of the cornea, a fluorescein instillation test is shown. When applying 1% sodium fluorescein solution to the cornea, the eroded surface turns greenish.
Bacteriological seeding of the material from the bottom and edges of the ulcer plays an important role in determining the therapeutic tactics for keratitis; cytological examination of the scraping of the conjunctival and corneal epithelium; PCR, PIF, ELISA diagnostics. If necessary, allergological, tuberculin tests, etc. are carried out.
Keratitis treatment should be carried out under the supervision of an ophthalmologist in a specialized hospital for 2-4 weeks. The general principles of keratitis pharmacotherapy include local and systemic etiotropic therapy with the use of antibacterial, antiviral, antifungal, etc. medicines.
With viral keratitis, local instillations of interferon, acyclovir are used to suppress the detected infection; laying ointments (tebrofen, florenal, bonafton, with acyclovir). Parenterally and orally, immunomodulators (thymus preparations, levamizole) are prescribed.
Bacterial keratitis requires the appointment of antibiotics, taking into account the sensitivity of the pathogen to them in the form of eye drops, parabulbar and subconjunctival injections, in severe cases – by parenteral administration of penicillins, cephalosporins, aminoglycosides, fluoroquinolones.
Treatment of tuberculous keratitis is carried out under the guidance of a phthisiologist using anti-tuberculosis chemotherapy drugs. With allergic keratitis, antihistamines, subconjunctival administration and instillation of hormonal drugs are prescribed. In the case of syphilitic or gonorrheal keratitis, specific therapy is indicated under the supervision of a venereologist.
In keratitis of various etiologies, local application of mydriatics (atropine sulfate, scopolamine) is indicated for the prevention of secondary glaucoma; for stimulation of epithelialization of corneal defects – instillation of taurine, application of healing ointments, etc. With a decrease in visual acuity, phonophoresis and electrophoresis with enzymes are prescribed.
Corneal ulceration is the basis for microsurgical interventions: microdiathermocoagulation, laser coagulation, cryoapplication of the defect. In the case of a sharp decrease in vision and due to scarring of the cornea, an excimer laser procedure for removing surface scars or keratoplasty is indicated. With the development of secondary glaucoma against the background of keratitis, laser or surgical treatment of glaucoma is indicated. In severe keratitis, enucleation of the eyeball may be required.
Prognosis and prevention
The outcome and consequences largely depend on the etiology of the lesion, the nature and localization of the infiltrate, and concomitant complications. Timely and rational therapy of keratitis leads to a trace resorption of corneal infiltrates or the formation of light cloud-like opacities. With deep keratitis, especially complicated by corneal ulcers, as well as with paracentral and central location of the infiltrate, corneal opacities of varying severity develop.
The outcome of keratitis can be a thorn, secondary glaucoma, optic nerve atrophy, eyeball atrophy and complete loss of vision. Septic complications in the form of cavernous sinus thrombosis, orbital phlegmon, sepsis are especially life-threatening.
Prevention includes prevention of eye injuries, timely detection and treatment of conjunctivitis, blepharitis, dacryocystitis, somatic diseases, common infections, allergies, etc.