Clinical Implications of Breakdown of the Blood–Aqueous Barrier
The blood–aqueous barrier may be disrupted in a number of conditions, including ocular trauma (mechanical, chemical, or physical), infection or inflammation, and ischemia, as well as with use of pharmacologic agents (eg, prostaglandin analogues, cholinesterase inhibitors). With compromise of the blood–aqueous barrier, the levels of inflammatory mediators, immunoglobulins, fibrin, and proteases rise, and the balance among the various growth factors is disrupted. The protein content of the aqueous humor increases, possibly as much as 10–100 times normal, especially in high-molecular-weight polypeptides.
The clinical sequelae include fibrinous exudate (with or without a macrophage reaction and formation of cyclitic membranes) and synechiae formation (peripheral and posterior), as well as an abnormal neovascular response, which further exacerbates breakdown of the blood–aqueous barrier. Chronic disruption of this barrier is implicated in the abnormal hyperplastic response of the lens epithelium, corneal endothelium, trabecular meshwork, and iris, and in the formation of complicated cataracts. Degenerative and proliferative changes may occur in various ocular structures as well. The use of anti-inflammatory steroidal and nonsteroidal drugs, cycloplegics, protease activators or inhibitors, growth factor and anti–growth factor agents, and even surgical intervention may be necessary to combat these events.
Excerpted from BCSC 2020-2021 series: Section 2 - Fundamentals and Principles of Ophthalmology. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.