Scleritis is an inflammatory process that affects the entire thickness of the outer connective tissue membrane of the eyeball. It is clinically manifested by hyperemia, injection of blood vessels, edema, soreness during palpation of the affected area or movements of the eyeball. Diagnosis of scleritis is reduced to external examination, biomicroscopy, ophthalmoscopy, visometry, tonometry, fluorescence angiography, ultrasound (Doppler ultrasound) in In-mode, computed tomography. Depending on the form of the disease, the treatment regimen includes local or systemic use of glucocorticoids and antibacterial agents. With purulent scleritis, an opening of the abscess is indicated.
Scleritis is an inflammatory disease of the sclera, characterized by a slowly progressive course. Anterior scleritis is the most common among all forms (98%). The lesion of the posterior sclera is observed only in 2% of patients. Variants of the course of pathology without necrosis prevail over necrotizing ones, which is associated with a favorable prognosis. With rheumatoid and reactive chlamydial arthritis, diffuse variants of the disease are common. In 86% of cases of ankylosing spondylitis, nodular scleritis is diagnosed. In 40-50% of patients, pathological changes in the sclera are combined with joint damage of inflammatory genesis, and in 5-10% of cases, arthritis is accompanied by scleritis. The disease is more common in women (73%). The peak incidence occurs at the age of 34 to 56 years. In children, pathology is observed 2 times less often.
The etiology of scleritis is directly related to systemic diseases in the anamnesis. The triggers of sclera lesions are rheumatoid arthritis, Wegener’s granulomatosis, juvenile idiopathic, reactive chlamydial or psoriatic arthritis, nodular polyarthritis, ankylosing spondylitis and polychondritis, characterized by a recurrent course. Less often, this pathology develops in the postoperative period after surgical removal of the pterygium or traumatic injury. Clinical cases of infectious scleritis in patients with a history of vitreoretinal surgery are described.
The dissemination of the process from the ulceration zone on the cornea often leads to scleritis of infectious etiology. Also, the source of infection may be inflammation of the paranasal sinuses. The most common pathogens of the disease are Pseudomonas aeruginosa, Varicella-Zoster virus and Staphylococcus aureus. In rare cases, scleritis has a fungal origin. Drug–induced sclera damage develops more often when taking mitomycin C. Risk factors are bone and joint forms of tuberculosis in the anamnesis, systemic inflammatory diseases.
From a clinical point of view, ophthalmology distinguishes anterior (non-necrotizing, necrotizing), posterior and purulent scleritis. Non-necrotizing sclera lesion can be diffuse or nodular. Necrotizing may or may not be accompanied by an inflammatory process. In some cases, the course of scleritis is characterized by short-term self-terminating episodes. At the same time, the pathological process in the sclera provokes its necrosis with the involvement of the underlying structures. For this disease, an acute onset is characteristic, sluggish variants are less often observed. With diffuse scleritis, the entire anterior part of the outer connective tissue membrane of the eyeball is involved in the inflammatory process. Nodular lesion is accompanied by a decrease in visual acuity.
Anterior scleritis is characterized by a slowly progressive course. This form is accompanied by binocular damage to the organ of vision. Patients note pronounced soreness when touching the projection area of edema, photophobia. The prolonged course of the disease leads to damage to the sclera along the circumference of the limb (annular scleritis) and the appearance of severe keratitis, iritis or iridocyclitis. With purulent scleritis, the rupture of the abscess membranes is possible, which leads to the development of iritis or hypopion.
With necrotic lesion of the sclera, patients note increasing pain, which later becomes permanent, radiates into the temporal region, the brow arch and the jaw. Pain syndrome is not stopped by taking analgesics. Necrotizing scleritis is complicated by perforation of the sclera, endophthalmitis or panophthalmitis. With the posterior form of pathology, patients complain of soreness during the movement of the eyeball, restriction of its mobility. Postoperative scleritis develops for 6 months after surgery. In this case, a site of local inflammation is formed, which is replaced by necrosis. A decrease in visual acuity is observed only when the inflammatory process spreads to the adjacent structures of the eyeball or the development of secondary glaucoma.
Diagnosis of scleritis includes external examination, biomicroscopy, ophthalmoscopy, visometry, tonometry, fluorescence angiography, ultrasound (Doppler ultrasound) in In-mode, computed tomography. External examination of patients with anterior scleritis reveals swelling, hyperemia and vascular injection. The edema zone has defined boundaries. With palpatory examination, soreness is noted. Carrying out biomicroscopy with “gelatinous” scleritis allows you to identify the zone of overhanging of the chemized conjunctiva over the limb. This area has a red-brown hue and a gelatin-like consistency. Infiltrates with pronounced vascularization can be found on the surface of the cornea. A violation of the physiological radial direction of the vascular pattern is determined by the method of biomicroscopy with a slit lamp with diffuse scleritis. With nodular form, conducting visiometry indicates a decrease in visual acuity.
With purulent scleritis, an external examination reveals purulent infiltration and injection of blood vessels. The lesion of the posterior parts of the sclera is accompanied by swelling of the eyelids, conjunctiva and minor exophthalmos. Ophthalmoscopy is used to determine the perforation of the optic nerve disc, subretinal lipid exudation, detachment of the retina and choroid caused by the accumulation of exudate. Ultrasound in B-mode indicates thickening of the posterior part of the outer connective tissue membrane of the eyeball, accumulation of exudate in the tenon space. The change in the thickness of the sclera can also be confirmed by CT.
With necrotizing scleritis, a convoluted course, areas of vascular occlusion, and avascular zones are determined using fluorescent angiography. Conducting biomicroscopy with a slit lamp allows you to visualize necrotic changes in the sclera, ulceration of the adjacent conjunctiva. An expansion of the necrosis zone is detected in the dynamics. Tonometry in patients with scleritis often reveals an increase in intraocular pressure (more than 20 mmHg).
The treatment regimen for scleritis includes the topical use of glucocorticoid and antibacterial drops for instillation. If the disease is accompanied by increased intraocular pressure, then the therapy complex should be supplemented with topical antihypertensive agents. The course of treatment includes taking nonsteroidal anti-inflammatory drugs. If they are intolerant, it is recommended to prescribe medications from the group of glucocorticosteroids. With scleritis without necrotic lesion, glucocorticoids and antibacterial drugs must be administered in the form of subconjunctival injections. An alternative to this method of administration is the use of prolonged forms of glucocorticoids.
With the development of sclera necrosis, combined therapy with glucocorticosteroids and immunosuppressants is indicated. In cases of an allergic reaction, antiallergic and desensitizing drugs are used in parallel with these drugs. In the purulent form of scleritis, treatment tactics are reduced to conducting massive antibacterial therapy. In this case, oral and subconjunctival routes of administration of drugs from the group of fluoroquinolones, aminoglycosides and semi-synthetic penicillins are used. An additional method of administration is electrophoresis. In the absence of the effect of drug therapy, surgical opening of the abscess is indicated. Also, the treatment regimen should include drugs for the treatment of the underlying pathology, against which scleritis has developed. If the etiological factor is Mycobacterium tuberculosis, anti-tuberculosis drugs for topical use are considered as auxiliary.
Prognosis and prevention
Specific prevention of scleritis has not been developed. Non-specific preventive measures are reduced to timely treatment of the underlying pathology, prevention of inflammation of the paranasal sinuses (sinusitis), compliance with the rules of asepsis and antiseptics during surgical interventions. Patients with a history of systemic diseases need to be examined by an ophthalmologist 2 times a year. The prognosis for life and ability to work depends on the timeliness of diagnosis, the adequacy of treatment, the type of pathogen in infectious lesions and the form of the disease. The most favorable option is diffuse forms of the disease. Scleritis caused by Pseudomonas aeruginosa is more often characterized by an unfavorable prognosis.