Pigment Dispersion Syndrome

Pigment Dispersion Syndrome (SPD) is a condition in which the pigment is washed out of the pigment epithelium of the back of the iris, its subsidence on various structures of the anterior segment of the eye.

Obstruction and subsequent destruction of the trabecular network can result in increased intraocular pressure and the development of secondary open-angle glaucoma.

[1], [2], [3], [4], [5], [6], [7], [8]

Epidemiology of pigmentary dispersion syndrome

The syndrome of pigment dispersion is more likely to develop in young (20-45 years old) male Europeans suffering from myopia. Approximately 1/3 of patients with pigmented dispersion syndrome develop pigmentary glaucoma.

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Pathophysiology of pigment dispersion syndrome

Currently, it is believed that the release and entry of the pigment into the anterior chamber with the formation of characteristic peripheral defects of the iris seen in transillumination occurs as a result of the contact of the pigment epithelium of the iris and the polar lens fibrils. The pigment can then settle on the structures of the anterior segment of the eye. As a result of blockade and subsequent damage to the trabecular network, the outflow of the intraocular fluid may be disturbed, which leads to an increase in intraocular pressure and subsequent damage to the optic nerve if no timely action is taken.

Symptoms of Pigment Dispersion Syndrome

Often the patient is diagnosed with myopia, and in a family history there are cases of glaucoma. In most cases, there is no symptomatology, but some patients may experience "pigment storms" after intense physical exertion. Exercises associated with stretching or shaking can lead to an extremely massive release of pigment, a "pigment storm," leading to a sudden increase in intraocular pressure. At this point, the patient can complain about blurred vision and headache.

Diagnosis of pigmentary dispersion syndrome

Biomicroscopy

Characteristic features of the pigment dispersion syndrome: Crookenberg spindle (vertically oriented pigment deposition on the corneal endothelium), pigment deposits on the anterior surface of the iris, peripheral iris defects visible in transillumination (best revealed by retroillumination through the pupil using a narrow beam of light), and deposits pigment at the sites of attachment of the zonal fibrils at the equator of the lens.

Gonioscopy

You can observe the deflection of the peripheral part of the iris posteriorly and increase the area of its contact with the lens. Usually the angle of the anterior chamber is very wide, note a moderate or pronounced relatively homogeneous pigmentation along the entire circumference of the angle.

Rear Pole

The characteristic glaucoma atrophy of the optic nerve is observed with prolonged ascent or periodic jumps of intraocular pressure. Patients suffering from myopia (especially with pigment dispersion syndrome) are prone to the formation of peripheral ruptures of the retina, which requires a more thorough examination.

[14], [15]

Treatment of pigmentary dispersion syndrome

The task of treatment is to control intraocular pressure in patients with high intraocular pressure or with glaucoma-specific changes in the optic nerve. Usually, drugs that reduce the formation of intraocular fluid are used. When using myiotics, the release of the pigment decreases, the intraocular pressure decreases. Often in young patients, poor tolerability of these drugs, they can increase the risk of detachment of the retina, and also make it difficult to examine its peripheral parts. When laser peripheral iridotomy is performed, the release of pigment also decreases due to equalization of pressure in the anterior and posterior chambers of the eye and rectification of the iris (elimination of the inverse pupillary block). The method can be used as a prophylaxis for the development of glaucoma in patients in the high-risk group. In the case of insufficient medical compensation for glaucoma, you can use argon laser trabeculoplasty and operations aimed at improving filtration.