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Corneal endothelial changes in primary acute angle-closure glaucoma

F Bigar, R Witmer

    Ophthalmology
    |June 1, 1982
    PubMed
    Summary
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    Acute angle-closure glaucoma significantly damages corneal endothelial cells, reducing density by 33%. Cell loss correlates with pressure duration, increasing risks for corneal degeneration post-surgery.

    Area of Science:

    • Ophthalmology
    • Corneal Science
    • Glaucoma Research

    Background:

    • Acute angle-closure glaucoma (AACG) can cause corneal edema due to elevated intraocular pressure (IOP).
    • The long-term effects of AACG on corneal endothelium are not fully understood.
    • Corneal guttata, an indicator of endothelial dysfunction, may be linked to AACG.

    Purpose of the Study:

    • To assess corneal endothelial cell damage following AACG.
    • To investigate the correlation between IOP duration and endothelial cell loss.
    • To determine the incidence of bilateral cornea guttata in AACG patients.

    Main Methods:

    • Specular microscopy was performed on 20 AACG patients before surgery.
    • Intraocular pressure and its duration were recorded.

    Related Experiment Videos

  • Endothelial cell density was compared between affected and unaffected eyes.

    • Main Results:

    • Mean IOP was 55 mm Hg, lasting an average of 47 hours.
    • Endothelial cell density decreased by 33% in affected eyes (1534 cells/mm²) compared to unaffected eyes (2243 cells/mm²).
    • A significant correlation was found between the duration of elevated IOP and endothelial cell loss; 35% of patients had bilateral cornea guttata.

    Conclusions:

    • AACG causes significant corneal endothelial cell loss.
    • The extent of cell loss is dependent on the duration of IOP elevation.
    • Pre-existing or induced endothelial dystrophy (cornea guttata) following AACG contributes to corneal degeneration, particularly after cataract surgery.