Neovascular glaucoma (NVG)


Potentially blinding secondary glaucoma, characterized by the development of neovascularization of the iris, elevated intraocular pressure (IOP) and, in most instances, poor visual prognosis.

NVG also defined as presence of iris and anterior chamber (AC) angle neovascularization with elevated IOP (>>21 mmHg)

History:

In 1963, Weiss and colleagues, proposed the term NVG. Coats first described the histological findings of new vessels on the iris on a patient with central retinal vein occlusion. With the introduction of clinical gonioscopy, the visualization of new vessels in the angle was possible and the origin of elevated IOP was explained by the closure of the iridocorneal angle.


Aetiology

Pathophysiological basis of NVG is retinal capillary nonperfusion, retinal ischemia, or uveal capillary insufficiency caused by various primary or secondary diseases, such as:

  • Proliferative diabetic retinopathy (PDR) (M/C cause)
  • Ischemic retinal venous obstruction (RVO)
  • Ocular ischemic syndrome (OIS)
  • Central retinal artery/vein obstruction
    • NVG has been called ‘90-’ or ‘100-day glaucoma’ in the past due to its typical development 3 months after the onset of CRVO
  • Uncommon ocular causes: Uveitis, ocular tumours, and miscellaneous retinal diseases

Pathophysiology

Posterior segment ischemia → Neovascularization

Rubeosis iridis
(Iris NV (INV) without elevated IOP)

Aqueous humor outflow obstruction → ↑ IOP

NVG

Development of a fibrovascular membrane on the anterior surface of the iris and iridocorneal angle of anterior chamber. Invasion of the anterior chamber by a fibrovascular membrane initially obstructs aqueous outflow in an open-angle fashion and later contracts to produce secondary synechial angle-closure glaucoma with high IOP. Iris and angle neo-vessels almost invariably develops before the intraocular pressure rises.


Clinical features

  • Development of a fibrovascular membrane on the anterior surface of the iris and the iridocorneal angle of AC
  • Followed by the development of:
    • Progressive anterior synechiae
    • Angle closure
    • Acute precipitous rise of IOP

Management

Refractory to both medical management and surgical intervention.

IOP-lowering agents:

Suppress aqueous production and possibly increasing uveoscleral outflow
  • Topical β-adrenergic antagonists
  • Topical α-2 agonists
  • Topical/oral carbonic anhydrase inhibitors

Panretinal photocoagulation (PRP)

Mainstay in controlling the neovascular drive
  • Treatment of choice

Vascular endothelial growth factor inhibitors:

Stifle the neovascularization process secondary to retinal ischemia

Surgical management:

Cases of peripheral anterior synechia formation and angle closure
  • Trabeculectomy with antimetabolites
  • Glaucoma drainage devices
  • Cyclophotocoagulation

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