Abstract

Breakdown of the blood-aqueous barrier (BAB) resulting in protein and cells in the aqueous humor of humans and many animals has been documented.¹ This breakdown occurs during uveitis, and following surgery and paracentesis. BAB breakdown occurs following these initiating insults because endothelial cells contract in the ciliary body, causing protein leakage from the vascular system which results Jn dysjunction of the epithelial layers, further vascular damage and protein leakage.^2,3 These changes are mediated by prostaglandins, leukotrienes, free radicals, neurostimulators (such as in the anti-dromic reflex) and mechanical disruption.^3,4,5,6 Sequelae to the BAB breakdown can be severe and include hypopyon, cataract, synechia, vitreal opacities, glaucoma, blindness and occasionally phthisis bulbi.

© 1991 Optical Society of America