LECTURE No. 26. Congenital and secondary glaucoma

1. Congenital glaucoma

There is hereditary congenital glaucoma (about 15% of cases) and intrauterine (about 85% of cases), which occurs as a result of exposure to various pathological factors on the fetal eye, which is a consequence of malformations of the anterior part of the eye. An increase in intraocular pressure occurs due to a violation of the outflow of intraocular fluid due to the closure of the iridocorneal angle of the anterior chamber by unresolved embryonic mesodermal tissue. Less common causes of aqueous humor retention are the anterior attachment of the iris and intratrabecular and intrascleral changes.

Congenital glaucoma manifests itself in three forms: simple (actual hydrophthalmos) with changes in the angle of the anterior chamber of the eye (the most common); congenital glaucoma with anomalies in the anterior part of the eye or the entire eye (aniridia, ectopia of the lens, microphthalmos, etc.); congenital glaucoma with phakomatoses (angiomatosis, neurofibromatosis).

Often, congenital glaucoma appears in newborns or in the first six months of a child's life, as well as in the first year of life. Congenital glaucoma is characterized by a progressive course. There are the following stages of the disease: initial, advanced, advanced, almost absolute and absolute. According to the state of intraocular pressure, it is possible to distinguish compensated, uncompensated and decompensated congenital glaucoma.

The onset of the disease is manifested by photophobia, lacrimation, dullness of the cornea; the length of the sagittal axis of the eye and the diameter of the cornea are normal or slightly enlarged. An increase in the length of the sagittal axis of the eye, the diameter of the cornea and an increase in corneal edema occur in the advanced stage due to further stretching of the membranes of the eyeball. There are ruptures of the Descemet's membrane and clouding of the cornea.

The anterior chamber becomes deeper. Changes occur in the iris in the form of atrophy and stromal hypoplasia, depigmentation. The pupil is dilated. Excavation of the optic nerve head, decreased visual acuity, and narrowing of the field of view on the nasal side to 45-35° are observed (if the child’s age allows them to be examined). The progressive stage of the disease is determined by a sharp increase in the length of the sagittal axis of the eye and the diameter of the cornea. The limbus is stretched. The sclera becomes thinner, and the choroid appears through it in a bluish-bluish color. The anterior chamber is deep. There are degenerative changes in the cornea. The pupil is wide. The optic disc is grayish in color, its excavation increases. There is a sharp decrease in visual acuity, a concentric narrowing of the field of vision, mainly on the nasal side (up to 15°). In the stage of almost absolute and absolute glaucoma, all these phenomena increase, complications often develop (subluxation and dislocation of the lens, intraocular hemorrhages, complicated cataracts, retinal detachment, etc.), vision is reduced to light perception with an incorrect projection, and in the absolute stage complete blindness is observed.

Treatment. Treatment of congenital glaucoma is surgical. In order to eliminate embryonic tissue and improve the outflow of intraocular fluid into Schlemm's canal, in most cases, operations are performed in the area of ​​the anterior chamber angle, as they are the most effective. Despite the age of the child, the operation must be performed urgently. Drug treatment is additional to surgical treatment (before and after surgery). Among medications, a 12% solution of pilocarpine hydrochloride, a 0,055% solution of Armin, a 0,013% solution of phosphacol and a 23% solution of aceclidine, a 0,25% solution of Optimol are prescribed locally. Diacarb or glycerol is taken orally (in doses corresponding to the body weight and age of the child). General strengthening and desensitizing therapy is carried out.

2. Juvenile (juvenile) glaucoma

It develops at a young age due to congenital defects in the structure of the iridocorneal angle of the iris, there is a hereditary transmission of these defects. Usually people older than thirty years are ill. For some patients, changes in the iris are characteristic (hypoplasia, large crypts or their almost complete absence, eversion of the pigment sheet, coloboma), for others, the first symptoms appear in the second decade of life, develop slowly, the cornea is of normal size, the anterior chamber is deep.

In the diagnosis of erased forms, gonioscopic and tonographic studies are important. Many patients with juvenile glaucoma have a remnant of germinal mesodermal tissue in the anterior chamber angle. Topical application of various miotic drugs (pilocarpine, carbacholin, aceclidine, phosphakol, armin), as well as clonidine and optimol, is shown, diacarb is prescribed orally. In the absence of compensation for the glaucomatous process and the deterioration of visual functions, an operation is indicated.

3. Secondary glaucoma

The increase in intraocular pressure that occurs with secondary glaucoma is the result of another disease of the eye (or the whole body) or damage to the eye.

Glaucoma can develop at various times after cataract removal. An increase in intraocular pressure in the early stages after cataract extraction is associated with pupillary block as a result of obstruction of the pupil by the vitreous body, residual lens masses, or air introduced into the eye. The reason for the increase in ophthalmotonus in the later stages after cataract removal may be pupillary or angular blockade, which developed as a result of postoperative complications (iridocyclitis, goniosinechia). Occasionally, glaucoma in an aphakic eye may be a manifestation of primary open-angle glaucoma not identified prior to cataract extraction.

The differential diagnosis is based on the data of tonometric, tonographic studies and gonioscopy of both eyes.

Treatment consists of dilating the pupil, reducing ophthalmotonus, reducing the production of intraocular fluid, eliminating the inflammatory reaction, and also depends on the cause of the increase in intraocular pressure. They use in the form of instillations a 12% solution of pilocarpine hydrochloride, preparations of timolol maleate (0,250,5% timoptik, 0,250,5% ofthimolol, 0,250,5% proxodolol, etc.), combined preparations (fotil, timpilo ), Diacarb is prescribed orally at a dose of 0,1250,25 g 23 times a day. If ineffective, surgical intervention is indicated.

Secondary glaucoma in iridocyclitis and uveitis The causes of this disease are anterior uveitis occurring in the acute period with exudation into the anterior chamber of the eye. The exudate contributes to the closure of the filtering zone of the angle of the anterior chamber and the deterioration of the outflow of intraocular fluid. Changes in the vessels of the uveal tract (expansion of capillaries, blood stasis) associated with the inflammatory process are of great importance. In chronic uveitis, the development of secondary glaucoma occurs as a result of the formation of posterior circular synechia of the pupil, goniosynechia, which are the result of a normal outflow of aqueous humor, which leads to a sharp increase in intraocular pressure. In secondary glaucoma, which is a complication of chronic uveitis, in the light of a slit llama, single precipitates are found on the posterior surface of the cornea, in the corner of the anterior chamber, exudate, goniosinechia.

The diagnosis is made on the basis of tonometry, elastometry, tonography, biomicroscopy and gonioscopy data. Precipitates located on the posterior surface of the cornea distinguish secondary uveal glaucoma from primary.

First of all, the underlying disease is treated. In the acute stage, especially with the formation of posterior synechiae, patients are prescribed applications with a 0,1% solution of adrenaline hydrochloride or a solution of adrenaline is injected subconjunctivally 0,25 ml once a day.

Mydriatic agents are used: 1% solution of homatropine hydrobromide, 0,25% solution of scopolamine hydrobromide, 1% solution of mezatone. Corticosteroid drugs are used locally: 0,52,5% hydrocortisone suspension, 0,3% prednisolone solution, 0,1% dexamethasone solution, Sofradex drops.

To reduce intraocular pressure, diacarb is administered orally at a dose of 0,1250,25 g 23 times a day. A persistent increase in intraocular pressure and the ineffectiveness of medical treatment lead to the need for surgical treatment.

Secondary glaucoma with circulatory disorders in the vessels of the eye, orbit and intraocular hemorrhages

The causes of this pathology are most often thrombosis of the central retinal vein, less often venous circulation disorders in the orbit (inflammatory processes, edematous exophthalmos, etc.), impaired venous outflow in the anterior ciliary veins, intraocular hemorrhages. Pathological changes in the outflow of aqueous humor (development of connective tissue moorings) lead to secondary glaucoma with thrombosis of the central retinal vein. In the case of hemophthalmia, the causes of an increase in intraocular pressure are deposits filling the filtering system in the zone of corneoscleral trabeculae of hemosiderin and other blood decay products due to intraocular hemorrhages. Further, in the corner of the anterior chamber, the formation of connective tissue with newly formed vessels occurs. These changes increase the resistance to the outflow of aqueous humor and are the consequences of a persistent increase in intraocular pressure. Retinopathy of various etiologies can contribute to the development of secondary glaucoma.

The clinical picture is determined by the underlying disease. Secondary hemorrhagic glaucoma with thrombosis of the central retinal vein develops 38 months after the onset of the disease and is characterized by a severe course. Various processes in the orbit can lead to a significant increase in intraocular pressure (up to the development of an attack of glaucoma). The diagnosis is based on the clinical picture of the underlying disease and the data of tonometric, tonographic studies and gonioscopy.

Treatment begins with treatment of the underlying disease. The prescription of miotic drugs is carried out in the absence of newly formed vessels in the iris. Their presence indicates the need to recommend instillation of solutions of adrenaline, clonidine, optimol, and corticosteroids. Medications that promote the resorption of hemorrhages are prescribed: local instillation of a 3% solution of potassium iodide, a 0,1% solution of lidase, lidase and vitreous are prescribed intramuscularly.

Author: Shilnikov L.V.

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