Havens Shane J, Gulati Vikas
Dev Ophthalmol. 2016;55:196-204. doi: 10.1159/000431196. Epub 2015 Oct 26.
Neovascular glaucoma (NVG) is a secondary ocular pathological condition resulting from a myriad of ocular and systemic conditions with retinal ischemia as a mediator in over 95% of cases. NVG is caused by the growth of a fibrovascular membrane secondary to a local angiogenic stimulus over the trabecular meshwork obstructing aqueous outflow. This results in an initial secondary open-angle glaucoma stage that may be amenable to intraocular pressure (IOP)-lowering medications and modulation of the underlying ischemic process, often in combination with panretinal photocoagulation and adjunctive use of vascular endothelial growth factor inhibitors. In the more advanced stages of neovascularization, connective tissue myofibroblasts associated with new vessel growth contract causing progressive synechial closure of the anterior-chamber angle. Elevation of IOP, once significant secondary angle closure is established, tends to be refractory to topical and oral IOP-lowering medications and often requires glaucoma surgical interventions.
新生血管性青光眼(NVG)是一种继发性眼部病理状况,由多种眼部和全身疾病引起,在超过95%的病例中以视网膜缺血为介导因素。NVG是由小梁网局部血管生成刺激继发的纤维血管膜生长所致,该纤维血管膜阻碍房水流出。这会导致最初的继发性开角型青光眼阶段,此时可能适合使用降低眼压(IOP)的药物并调节潜在的缺血过程,通常联合全视网膜光凝和血管内皮生长因子抑制剂的辅助使用。在新生血管形成的更晚期阶段,与新血管生长相关的结缔组织肌成纤维细胞收缩,导致前房角逐渐发生粘连性关闭。一旦形成明显的继发性房角关闭,眼压升高往往对局部和口服降眼压药物难治,通常需要进行青光眼手术干预。