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Crystalline lens glaucoma

 
, medical expert
Last reviewed: 08.07.2025
 
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Lens mass glaucoma develops when the integrity of the lens capsule is disrupted and its cortex and proteins are released into the anterior chamber. This situation occurs after extracapsular cataract extraction, lens trauma with capsule rupture, and neodymium YAG laser posterior capsulotomy, in which free lens particles clog the trabecular meshwork, disrupting the outflow of aqueous humor. A case of lens mass glaucoma after subluxation of the posterior chamber intraocular lens in a patient with pseudoexfoliation syndrome has been described.

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Pathophysiology of lenticular mass glaucoma

Increased intraocular pressure in glaucoma of lens masses can be caused by:

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

Epstein et al. perfused an enucleated human eye with crushed lens material, as occurs when high-molecular proteins are perfused with soluble lens proteins. The outflow of aqueous humor decreased abruptly with an increase in the concentration of lens material. Not all patients with lens masses in the anterior chamber experience an increase in intraocular pressure after cataract surgery, which indicates a dynamic balance between the obstruction of the trabecular meshwork by lens material and the removal of its particles by phagocytic cells. Phagocytes engulf lens particles in the trabecular meshwork and clear the outflow pathways. Proteins and lens particles were found in the contents of macrophages. It is possible that in patients with lens mass glaucoma, the trabecular meshwork clearance mechanism is significantly overloaded or the phagocytes and trabecular apparatus are pathologically altered.

Increased intraocular pressure also develops after neodymium YAG laser capsulotomy. Smith found that the outflow of aqueous humor decreases after neodymium YAG laser capsulotomy. One hour after the laser procedure, the outflow of intraocular fluid decreases by an average of 43%, and intraocular pressure increases by an average of 38%. It takes from 24 hours to 1 week to normalize the outflow after laser surgery. After neodymium YAG laser capsulotomy, when examining a patient using a slit lamp, particles of the lens can be seen, 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 of crystalline masses

Patients experience decreased visual acuity due to corneal edema, and with a marked increase in intraocular pressure, complaints of pain appear. Sometimes there is a history of recent trauma, surgical cataract extraction, or laser procedure, but increased pressure can develop years after cataract surgery.

Clinical examination

The increase in intraocular pressure seen in lens mass glaucoma correlates with the amount of lens material circulating in the anterior chamber. There may be an interval of days or weeks between the release of lens proteins and the onset of the rise in intraocular pressure. Small whitish fragments of lens cortex appear to circulate in the anterior chamber and are deposited on the corneal endothelium. The increase in intraocular pressure leads to corneal edema and inflammation, which is detected by increased brightness and cellular suspension. Hypopyon may appear. At first, the angle is open on gonioscopy, then peripheral anterior synechiae may appear.

Special tests

The diagnosis is made based on the detection of freely circulating lens particles in the anterior chamber and increased intraocular pressure. If the picture is atypical or the number of lens particles is small, a sample of intraocular fluid can be taken for histological identification of the lens substance.

Treatment of glaucoma of crystalline masses

Depending on the degree of intraocular pressure increase, the medicinal antiglaucoma drugs mentioned above for the treatment of phacolytic glaucoma are used. Cycloplegic agents are used to prevent the development of posterior synechiae. Local glucocorticoids are also used, but the inflammatory process should not be completely suppressed, since this will delay the processing of lens particles. If drug treatment is ineffective, the lens substance is removed by aspiration. If surgical treatment is postponed, the persistent inflammatory process leads to the formation of peripheral anterior synechiae, pupillary block, and the appearance of inflammatory membranes that spread posteriorly and cause retinal traction. At this stage, the membranes and lens material are removed with vitrectomy instruments.

Surgical aspiration of the lens substance is sufficient to control intraocular pressure and the inflammatory process.

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