Pigment dispersion syndrome.

Pigment dispersion syndrome (PDS) is a condition in which pigment is washed out of the pigment epithelium of the posterior layer of the iris and deposited on various structures of the anterior segment of the eye.

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

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Epidemiology of pigment dispersion syndrome

Pigment dispersion syndrome most often develops in young (20-45 years) European males suffering from myopia. Approximately 1/3 of patients suffering from pigment dispersion syndrome subsequently develop pigment glaucoma.

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Pathophysiology of pigment dispersion syndrome

It is currently believed that the release and entry of pigment into the anterior chamber, resulting in the characteristic peripheral iris defects visible on transillumination, occurs as a result of contact between the iris pigment epithelium and the zonular fibrils of the lens. The pigment may then deposit on structures in the anterior segment of the eye. As a result of the blockage and subsequent damage to the trabecular meshwork, the outflow of intraocular fluid may be disrupted, leading to increased intraocular pressure and subsequent damage to the optic nerve if measures are not taken in a timely manner.

Symptoms of pigment dispersion syndrome

Often the patient is myopic and has a family history of glaucoma. Most cases are asymptomatic, but some patients may experience “pigment storms” after intense physical activity. Stretching or shaking exercises can cause an extremely massive release of pigment, a “pigment storm,” which causes a sudden increase in intraocular pressure. At this point, the patient may complain of blurred vision and headache.

Diagnosis of pigment dispersion syndrome

Biomicroscopy

Characteristic features of pigment dispersion syndrome include Krukenberg spindles (vertically oriented pigment deposits on the corneal endothelium), pigment deposits on the anterior surface of the iris, peripheral iris defects visible on transillumination (best seen on retroillumination through the pupil with a narrow beam of light), and pigment deposits at the sites of attachment of zonular fibrils at the equator of the lens.

Gonioscopy

A posterior deflection of the peripheral part of the iris and an increase in the area of its contact with the lens can be observed. Usually the angle of the anterior chamber is very wide, moderate or pronounced relatively homogeneous pigmentation is noted throughout the circumference of the angle.

Posterior pole

Characteristic glaucomatous optic atrophy is observed with prolonged rise or periodic jumps in intraocular pressure. Patients suffering from myopia (especially with pigment dispersion syndrome) are predisposed to the formation of peripheral retinal breaks, which is why they need a more thorough examination.

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Treatment of pigment dispersion syndrome

The treatment objective is to control intraocular pressure in patients with high intraocular pressure or with optic nerve changes characteristic of glaucoma. Usually, drugs that reduce the formation of intraocular fluid are used. When using miotics, pigment release is reduced, and intraocular pressure is reduced. Young patients often have poor tolerance to these drugs, they can increase the risk of retinal detachment, and also complicate the examination of its peripheral parts. When performing laser peripheral iridotomy, pigment release is also reduced due to equalization of pressure in the anterior and posterior chambers of the eye and straightening of the iris (elimination of reverse pupillary block). The method can be used to prevent glaucoma development in high-risk patients. In case of insufficient drug compensation of glaucoma, argon laser trabeculoplasty and operations aimed at improving filtration can be used.