Dave Soham D., Zeppieri Marco, Meyer Jay J.
College of Physician and Surgeons
University Hospital of Udine, Italy
Glaucoma is a progressive optic neuropathy generally associated with elevated intraocular pressures, leading to visual field loss. In its advanced stage, it has the potential to culminate in total blindness. Angle-closure glaucoma occurs due to the narrowing or closure of the anterior chamber angle, typically responsible for facilitating the drainage of aqueous humor. Acute angle-closure glaucoma is a condition that occurs when there is a gradual narrowing of the anterior chamber angle, which obstructs the drainage of aqueous humor, leading to elevated intraocular pressure and subsequently damaging the optic nerve. Chronic angle-closure glaucoma occurs when a portion of the angle is intermittently obstructed, resulting in subsequent scarring and narrowing of the angle further over time. Characteristic features of chronic angle-closure glaucoma include the gradual formation of peripheral anterior synechiae (PAS) and irreversible iridotrabecular adhesions, which impede aqueous outflow, leading to elevated intraocular pressures. In all forms of angle-closure glaucoma, iridotrabecular contact occurs, wherein the iris is observed to make contact with the anterior chamber angle, either at the posterior pigmented trabecular meshwork or more anterior structures. Angle-closure glaucoma can be classified as either primary or secondary. Primary angle-closure (PAC) glaucoma is attributed to a physiological predisposition and is not associated with any other ocular condition or eye disease. In contrast, secondary angle-closure glaucoma is associated with one or more additional ocular conditions. In PAC, the lens is positioned too far forward, pressing against the iris and causing the peripheral iris to bulge due to increased pressure in the posterior chamber. Certain factors such as iris neovascularization, trauma, and uveitis can push the iris or ciliary body forward or deform the iris, leading to its retraction into the angle and resulting in secondary angle-closure glaucoma. Individuals with PAC glaucoma are predisposed to this condition, whereas those with secondary angle-closure glaucoma have an underlying condition that contributes to the narrowing of the anterior angle. Acute angle-closure glaucoma is characterized by decreased visual acuity, headache, severe eye pain, nausea and vomiting, and halos around lights. This condition is considered a medical emergency and requires swift treatment to prevent permanent vision loss. Chronic angle-closure glaucoma can manifest with or without symptoms and may later cause potential damage to the optic nerve. Intraocular pressure gradually increases with chronic angle-closure glaucoma, leading to the designation of "silent" angle-closure glaucoma. This condition primarily involves iridotrabecular contact, resulting in synechiae formation and subsequent angle closure, and it is also referred to as "creeping" angle-closure glaucoma.
青光眼是一种进行性视神经病变,通常与眼内压升高有关,可导致视野缺损。在晚期,它有可能导致完全失明。闭角型青光眼是由于前房角变窄或关闭引起的,前房角通常负责房水的引流。急性闭角型青光眼是指前房角逐渐变窄,阻碍房水引流,导致眼内压升高,进而损害视神经的一种病症。慢性闭角型青光眼是指部分房角间歇性受阻,随着时间的推移,导致后续瘢痕形成和房角进一步变窄。慢性闭角型青光眼的特征性表现包括周边前粘连(PAS)的逐渐形成和不可逆的虹膜小梁粘连,这会阻碍房水流出,导致眼内压升高。在所有形式的闭角型青光眼中,都会出现虹膜小梁接触,即观察到虹膜与前房角接触,接触部位可以是后色素性小梁网或更靠前的结构。闭角型青光眼可分为原发性或继发性。原发性闭角型(PAC)青光眼归因于生理易感性,与任何其他眼部疾病无关。相比之下,继发性闭角型青光眼与一种或多种其他眼部疾病有关。在原发性闭角型青光眼中,晶状体位置过于靠前,压迫虹膜,导致后房压力增加,周边虹膜膨隆。某些因素,如虹膜新生血管形成、外伤和葡萄膜炎,可使虹膜或睫状体向前移位或使虹膜变形,导致虹膜向后房角退缩,从而引起继发性闭角型青光眼。原发性闭角型青光眼患者易患此病,而继发性闭角型青光眼患者则有导致前房角变窄的潜在病因。急性闭角型青光眼的特征是视力下降、头痛、眼剧痛、恶心呕吐以及灯光周围出现光晕。这种情况被视为医疗急症,需要迅速治疗以防止永久性视力丧失。慢性闭角型青光眼可能有症状,也可能没有症状,后期可能对视神经造成潜在损害。随着慢性闭角型青光眼的发展,眼内压会逐渐升高,导致“安静型”闭角型青光眼的出现。这种情况主要涉及虹膜小梁接触,导致粘连形成和随后的房角关闭,也被称为“渐进性”闭角型青光眼。