Facial glaucoma or glaucoma of lens proteins
Last reviewed: 23.04.2024
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Pathophysiology of facial glaucoma
With phacolitic glaucoma, high-molecular proteins (more than 150x10 6 daltons) block outflow from the trabecular network, leading to an increase in intraocular pressure. Based on the detection of macrophages in the intraocular fluid and in the trabecular apparatus of patients with phacolitic glaucoma, it was believed that an increase in pressure causes solely blockade of outflow by macrophages. However, Epstein (Epstein) et al. Suggested that obstruction of the trabecular network is caused by proteins with a large molecular weight.
- When examining samples of the intraocular fluid of patients with phacolitic glaucoma, Epstein detected an excess of high molecular weight proteins, the concentration of which increased as cataract maturation.
- Perfusion in vitro of cadaveric eyes with soluble high-molecular proteins after 1 hour resulted in a 60% reduction in outflow.
- High-molecular proteins were present in the watery moisture of patients with phacolitic glaucoma in sufficiently high concentrations, causing an outflow disturbance.
- In some samples with phacolitic glaucoma, a small number of macrophages were detected.
Lens proteins are capable of inducing the migration of blood monocytes and macrophages that may function as purifiers, removing the soluble proteins of the lens and fragments from the anterior chamber and the trabecular apparatus.
Symptoms of facial glaucoma
With mature or overripe cataract, patients complain of a gradual decrease in vision, pain due to inflammation and an increase in intraocular pressure.
Clinical examination
Facial glaucoma develops with mature or overripe cataracts. In such patients, intraocular pressure rises sharply, redness and pain appear. The outbreak of clinical manifestation is associated with soluble proteins that have emerged from the lens with mature cataracts. The cellular response is an accumulation of mostly macrophages and cells that are larger in size and more transparent than lymphocytes. Hypopion is not typical. On the surface of the lens, white areas can be seen which are considered aggregates of macrophages phagocytizing the lens proteins in the places of their infiltration from the anterior capsule. With gonioscopy, the angle of the anterior chamber is open. In some cases, retinal perivascular activity is observed.
Special tests
In the samples of intraocular fluid concentrated with the filtration of Milpore (MilHpore), macrophages and an amorphous substance corresponding to the lens protein substance are detected. Diagnosis is usually established only on the basis of clinical studies.
Treatment of phacolitic glaucoma
Treatment of phacolithic glaucoma should begin with drug therapy to reduce increased intraocular pressure. The basis of drug therapy - beta-adrenoblockers, prostaglandin analogs, a-adrenergic drugs and inhibitors of carbonic anhydrase. Local glucocorticoids are also used to reduce the activity of inflammation, cycloplegic drugs to stabilize the blood-watery moisture barrier and reduce soreness. The drug treatment partially reduces the pressure, but the final treatment is only the extraction of cataracts.