Neovascular Glaucoma

Updated: Aug 01, 2016
  • Author: Hemang K Pandya, MD; Chief Editor: Hampton Roy, Sr, MD  more...
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Overview

Background

Neovascular glaucoma (NVG) is classified as a secondary glaucoma. First documented in 1871, historically, it has been referred to as hemorrhagic glaucoma, thrombotic glaucoma, congestive glaucoma, rubeotic glaucoma, and diabetic hemorrhagic glaucoma. Numerous secondary ocular and systemic diseases that share one common element, retinal ischemia/hypoxia and subsequent release of an angiogenesis factor (eg, vascular endothelial growth factor [VEGF]), cause NVG. These angiogenesis factors causes new blood vessel growth from preexisting vascular structure. Depending on the progression of NVG, it can cause glaucoma either through secondary open-angle or secondary closed-angle mechanisms. This is accomplished through the growth of a fibrovascular membrane over the trabecular meshwork in the anterior chamber angle, resulting in obstruction of the meshwork and/or associated peripheral anterior synechiae.

NVG is a potentially devastating glaucoma, where delayed diagnosis or poor management can result in complete loss of vision or, quite possibly, loss of the globe itself. Early diagnosis of the disease, followed by immediate and aggressive treatment, is imperative. In managing NVG, it is essential to treat both the elevated intraocular pressure (IOP) and the underlying cause of the disease. [1]

It is essential that primary care physicians refer all patients with diabetes, including those with sudden vision loss, to their local ophthalmologists for a dilated fundus examination. In addition, as neovascular glaucoma may present with severe pain, emergency medicine physicians should become proficient with slit-lamp examination to evaluation for iris neovascularization.

Ophthalmologists should remain cautious when managing patients with diabetic and retinal vein occlusion. They should keep a low threshold for referring patients to their local retina specialists for further management.

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Pathophysiology

Retinal ischemia is the most common and important mechanism in most, if not all, cases that result in the anterior segment changes causing NVG. Various predisposing conditions cause retinal hypoxia and, consequently, production of angiogenesis factors.

Several angiogenesis factors have been identified as potential agents causing ocular neovascularization. Recent studies suggest that vascular endothelial growth factor (VEGF) might play a central role in angiogenesis. [2]

Once released, the angiogenic factor(s) diffuses into the aqueous and the anterior segment and interacts with vascular structures in areas where the greatest aqueous-tissue contact occurs. The resultant growth of new vessels at the pupillary border and iris surface (neovascularization of the iris [NVI]) and over the iris angle (neovascularization of the angle [NVA]) ultimately leads to formation of fibrovascular membranes. The fibrovascular membranes, which may be invisible on gonioscopy, accompany NVA and progressively obstruct the trabecular meshwork. This causes secondary open-angle glaucoma.

As the disease process continues, the fibrovascular membranes along the NVA tend to mature and contract, thereby tenting the iris toward the trabecular meshwork and resulting in peripheral anterior synechiae and progressive synechial angle closure. Elevated IOP is a direct result of this secondary angle-closure glaucoma.

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Epidemiology

Frequency

United States

Incidence of NVG is rare.

Mortality/Morbidity

Treatment of NVG is difficult. Maintaining visual acuity in patients with NVG also is difficult.

Age

NVG is more prevalent in elderly patients.

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Prognosis

Owing to retinal ischemia and intraocular pressure damage to the optic nerve, visual prognosis is often poor. As with most of medicine, prevention is the primary goal in patients with vasculopathy.

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