Glaucoma lens of the masses

Glaucoma of lens masses develops when the integrity of the lens capsule is broken and its cortex and proteins are released into the anterior chamber. This situation occurs after extracapsular extraction of cataracts, lens trauma with a capsule rupture and neodymium IAG laser back capsulotomy, in which free lens particles block the trabecular network, disrupting the outflow of watery moisture. The case of glaucoma of the lens masses after the subluxation of the posterior chamber intraocular lens in a patient with a pseudoexfoliation syndrome was described.

[1], [2], [3], [4]

Pathophysiology of lens mass glaucoma

Increase in intraocular pressure in glaucoma lens material can be caused by:

• obstruction of the trabecular network by lens particles;
• inflammatory cells;
• peripheral front synechiae and angle closure in the development of inflammation;
• pupillary block in the posterior synechiae.

Epstein et al. Perfused the enucleated human eye with a crushed lens substance, as occurs when high-molecular proteins are perfused with soluble proteins in the lens. The outflow of aqueous humor with an increase in the concentration of the substance of the lens decreased in a leap. Not all patients after surgery for cataracts with lens masses in the anterior chamber develop an increase in intraocular pressure, which indicates a dynamic balance between the obstruction of the trabecular network by the substance of the lens and the removal of its particles by phagocytic cells. Phagocytes absorb the lens particles in the trabecular network and purify the outflow pathways. In the contents of macrophages, proteins and lens particles were found. Perhaps in patients with lens glaucoma, the mechanism of cleaning the trabecular network is significantly overloaded, either the phagocytes and the trabecular apparatus are pathologically altered.

Increase in intraocular pressure develops after neodymium IAG laser capsulotomy. Smith established that the outflow of watery moisture decreases after the neodymium of the YAG laser capsulotomy. 1 hour after the laser procedure, the outflow of the intraocular fluid decreases on average by 43%, and the intraocular pressure increases by an average of 38%. To normalize the outflow after the laser operation is necessary from 24 hours to 1 week. After neodymium IAG laser capsulotomy, when examining a patient using a slit lamp, one can see the lens particles consisting of fragments of its capsule and cortical layers. It is assumed that this is one of the mechanisms leading to a decrease in outflow.

Symptoms of glaucoma lens material

Patients are observed to decrease visual acuity due to corneal edema, and with a marked increase in intraocular pressure, complaints of pain appear. Sometimes, there are episodes of a recent trauma, surgical extraction of cataracts, or a laser procedure, but the increase in pressure can develop even years after the cataract removal operation.

Clinical examination

The increase in intraocular pressure observed with glaucoma of lens masses correlates with the amount of lens material circulating in the anterior chamber. Between the release of the lens proteins and the onset of an increase in intraocular pressure, an interval of several days or weeks is possible. Circulating small whitish fragments of the lens cortex appear in the anterior chamber, which are deposited on the corneal endothelium. Increased intraocular pressure leads to corneal edema and inflammation, which is detected by increased brightness and cellular suspension. A hypopion may appear. First, when the gonioscopy angle is open, then peripheral anterior sinuschi can appear.

Special tests

The diagnosis is based on the detection of freely circulating lens particles in the anterior chamber and increased intraocular pressure. In an atypical picture or a small number of lens particles, one can take a sample of the intraocular fluid for the histological identification of the lens material.

Treatment of glaucoma lens material

Depending on the degree of elevation of intraocular pressure, the medicinal antiglaucomatous drugs mentioned above for the treatment of phacolitic glaucoma are used. To prevent the development of posterior synechia, cycloplegics are used. Use and local glucocorticoids, but completely suppress the inflammatory process should not be, because there will be a delay in the processing of lens particles. If the drug is ineffective, the lens substance is removed by aspiration. When delaying surgical treatment, a persistent inflammatory process leads to the formation of peripheral anterior synechia, the pupillary block and the appearance of inflammatory membranes that propagate posteriorly and cause retinal traction. At this stage, the membranes and the lens material are removed by instruments for vitrectomy.

To control the intraocular pressure and the process of inflammation, surgical aspiration of the lens substance is sufficient.