Posner-Schlossman syndrome is a paroxysmal benign hypertension of the eye. Characteristic signs of the disease: blurred vision, sudden increase in intraocular pressure (IOP) and the appearance of corneal precipitates. For the diagnosis of the disease, tonometry, biomicroscopy, ophthalmoscopy, gonioscopy, perimetry, electronic tonography are indicated. For immediate relief of signs of hypertension, beta-blockers are prescribed. Pathogenetic therapy is reduced to the use of glucocorticosteroids, antihistamines and nonsteroidal anti-inflammatory drugs.
Posner-Schlossman syndrome was described in detail in 1948 by the American ophthalmologist A. Posner in collaboration with the German pediatrician and biochemist A. Schlossman. Pathology is more common at the age of 30-50 years. In 14.5% of cases, periodic attacks of a sharp increase in intraocular pressure are observed in persons under 30 years of age. The occurrence of symptoms of paroxysmal hypertension of the eye in children may be a consequence of a prolonged course of anterior uveitis. Males are more at risk of developing a crisis than women. The disease is widespread everywhere.
The etiology of the disease is not fully understood. There are two main hypotheses explaining the nature of Posner-Schlossman syndrome. According to the first, the reason for the sudden increase in IOP is allergic edema of the ciliary body. Trigger factors provoking the occurrence of allergies have not been identified. Adherents of the second hypothesis consider it appropriate to consider Posner-Schlossman syndrome as one of the variants of symptomatic uveal hypertension. The leading etiological factor in this case is considered to be inflammation of the vascular membrane of the eyeball.
Allergic edema of ciliary body tissues plays an important role in the mechanism of development of primary Posner-Schlossman syndrome. In response to the action of the allergen, the secretion of immunoglobulin E by plasmocytes increases in the body. During degranulation of mastocytes and basophils, histamine, cytokines, interleukins, leukotrienes and prostaglandins are released. Inflammatory mediators are vasoactive substances that lead to vasodilation. Then neutrophils, lymphocytes, macrophages and eosinophils migrate to the lesion. The consequence of these processes is increased exudation.
With uveal hypertension, intraocular pressure increases due to inflammation of the anterior segment of the vascular membrane of the eye and vasodilation. With the latent course of anterior uveitis, the clinical symptoms of the disease are poorly expressed, so at first glance the eye is intact. However, a slight dilation of the conjunctival vessels and the appearance of “opacities” in front of the eyes indicates a chronic course of uveitis. A large number of attacks of Posner-Schlossman syndrome causes the formation of dystrophic changes on the iris. Due to the decrease in pigment with age, the iris becomes discolored.
The disease is characterized by a unilateral lesion. Patients describe Posner-Schlossman syndrome as the sudden occurrence of a specific attack against the background of complete well-being. The main complaint is the appearance of a “veil” or “fog” in front of the eyes. When looking at a light source, rainbow circles form around its circumference. The feeling of severe discomfort will be replaced by pain syndrome when trying to touch the ocular area or eyelids. Conjunctival redness and pupil dilation are visually determined. Often patients cover the affected eye with their hand to limit its participation in the act of vision.
The duration of one episode can reach 24 hours. After the seizure is stopped, all symptoms disappear. Until the next crisis develops, the patient feels practically healthy. The duration of remission varies widely (from 2-3 weeks to several years). Over the years, such symptoms occur less frequently. Patients note that the color of the eyes in old age becomes lighter. As a rule, Posner-Schlossman syndrome does not lead to complications. However, in patients with a genetic predisposition to primary glaucoma, there is a risk of progression of glaucoma optic neuropathy.
The diagnosis is based on anamnestic information and the results of the examination. It is known from the anamnesis that similar episodes have occurred before. Anatomical and physiological prerequisites for the development of the disease are absent, and changes from the uveal tract are not expressed much. Visual acuity is normal. Specific diagnostic methods for Posner-Schlossman syndrome include:
- Tonometry. At the height of the attack, contactless tonometry is performed: intraocular pressure rises to 40-50 mmHg. After the appointment of beta-blockers, IOP decreases to 30 mmHg. Repeated instillations of antihypertensive agents make it possible to normalize pressure for a short period of time. Electronic tonography allows you to measure IOP and study hydrodynamic parameters. High resistance on the way of outflow of intraocular fluid leads to a decrease in the coefficient to 0.01-0.02. Before performing the diagnosis, instillation of an anesthetic is indicated.
- Inspection of eye structures. When examining the anterior segment of the eyeball by biomicroscopy, signs of precipitation are detected on the posterior surface of the cornea. The precipitates have the form of 2-5 whitish inclusions with clearly defined contours. The cornea is edematous. There is an injection of conjunctival vessels. The direct reaction of the pupils to light is preserved, but there is a delay in the expansion of the pupillary opening. When studying the reverse photoreaction, the changes are weakly expressed. There is moderate mydriasis on the side of the lesion, which indicates anisocoria.
- Inspection of the front camera. According to gonioscopy, in most cases the angle of the anterior chamber of the eye is open. The width of the iris-cornea angle corresponds to the reference values. The depth of the anterior chamber in the central part reaches 3 mm. Watery moisture is transparent, without pathological inclusions.
- Examination of the fundus. With the secondary nature of the disease, the excavation of the optic nerve disc is expanded. The vessels of the fundus look full-blooded. Small foci of hemorrhage are visualized. With an allergic genesis of pathology, ophthalmoscopy does not reveal any changes.
- Definition of visual fields. With a prolonged course of the disease, there is a concentric narrowing of the visual fields. A characteristic manifestation of Posner-Schlossman syndrome is considered to be a narrowing of the field of view to a white object by more than 1 mm. The loading water-dark campimetric test performed within the perimeter is positive.
The disease should be differentiated with iridocyclitis and primary glaucoma. In contrast to an acute attack of glaucoma with a glaucomocyclitic crisis, the pain syndrome is not so pronounced. Changes on the eyeball are stagnant or mixed, which is a differential sign. Paroxysmal hypertension often mimics the clinic of tuberculous lesions of the structures of the uveal tract. To exclude tuberculosis of the eyes, a tuberculin test is carried out. If the information content of the Mantoux sample is low, cytological or histological examination of the biopsy is performed.
Etiotropic therapy has not been developed. In order to quickly reduce intraocular pressure, beta-blockers and carbonic anhydrase inhibitors with a diuretic effect are used once. After 15-20 minutes, it is necessary to re-measure the IOP. If the patient has signs of ophthalmohypertension, it is recommended to re-introduce beta-blockers. Further treatment tactics include:
- Hormonal agents. Pathogenetic treatment is reduced to the appointment of glucocorticosteroids. Medicines of this group make it possible to stop the swelling of the ciliary body and normalize the outflow of intraocular fluid. Instillations should be carried out for 7 days.
- Nonsteroidal anti-inflammatory drugs (NSAIDs). Oral administration of drugs from the group of indoleacetic acid derivatives is recommended for patients. In addition to the anti-inflammatory effect, NSAIDs also have analgesic effect. The duration of the course of treatment is 7 days.
- Desensitizing drugs. Patients are prescribed oral antihistamines. The drugs suppress allergic reactions of the immediate type, preventing the release of inflammatory mediators. The average duration of therapy is 3-5 days.
Prognosis and prevention
The prognosis for glaucocyclitic crisis is favorable, because the pathology is characterized by a benign course. Despite numerous seizures, visual acuity is normal. With age, the number of episodes of Posner-Schlossman syndrome decreases, and secondary changes do not affect visual functions. Specific preventive measures have not been developed. Nonspecific prevention is reduced to periodic monitoring of intraocular pressure indicators. Patients are recommended to undergo a routine examination by an ophthalmologist once every 3 months with a mandatory examination of the fundus, tonometry and biomicroscopy.