History
A careful and detailed ocular and systemic history is imperative in diagnosing both neovascular glaucoma (NVG) and the underlying problem causing it.
Physical
A complete ocular examination of both eyes, particularly of the posterior segment, will almost certainly provide the etiology of neovascularization. Of the 3 most common causes of NVG, ocular ischemic syndrome presents as a diagnostic dilemma and, thus, deserves special mention.
The typical clinical presentation of NVG is the same regardless of the underlying cause. The typical clinical presentation can be divided into the following 2 stages: the early stage and the advanced stage. These stages generally follow each other in progression, and the early stage is subdivided further into rubeosis iridis and secondary open-angle glaucoma.
Early stage (rubeosis iridis)
Findings of rubeosis iridis may include the following:
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Normal IOP
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Presence of tiny, neovascular, dilated capillary tufts at pupillary margin
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High magnification on slit lamp (to view earliest finding in NVG)
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NVI (irregular, nonradial vessels usually not in the iris stroma)
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NVA (can occur with or without NVI)
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Careful gonioscopy in all eyes at high risk for NVG even without pupillary and iris involvement
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Poorly reactive pupil
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Ectropion uvea
Early stage (secondary open-angle glaucoma)
Findings of secondary open-angle glaucoma may include the following:
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Elevated IOP
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NVI continuous with NVA
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Proliferation of neovascular tissue over the angle
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Fibrovascular membranes (develop circumferentially across the angle, blocking the trabecular meshwork)
Advanced stage
In this stage, secondary angle-closure glaucoma is characterized by some or all of the following:
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Acute severe pain, headache, nausea, and/or vomiting
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Photophobia
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Reduced visual acuity (counting fingers to hand motion)
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Elevated IOP (≥ 60 mm Hg)
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Conjunctival injection
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Corneal edema
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Plus/minus hyphema
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Aqueous flare
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Synechial angle closure
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Severe rubeosis
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Distorted, fixed, mid-dilated pupil and ectropion uveae
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Retinal neovascularization and/or hemorrhage
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Optic nerve cupping (possibly)
Ocular ischemic syndrome
Ocular ischemic syndrome occurs in the presence of more than 90% of patients with carotid artery stenosis, but it can occur as a result of aortic arch disease (eg, syphilis, Takayasu arteritis, dissecting aneurysm), in which case the presentation may be bilateral.
Symptoms include a dull periocular/periorbital pain that can be secondary to the ischemia and/or NVG.
Signs include the following:
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Vision can vary from 20/20 to no light perception.
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Midperipheral intraretinal hemorrhage (in contrast to diabetic retinopathy and CRVO where the hemorrhage is mostly situated in the posterior pole)
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IOP can be elevated secondary to NVG, decreased secondary to ciliary body hypoperfusion, or normal as a result of both processes.
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Other signs include corneal decompensation, iritis, iris atrophy, cataract, and spontaneous pulsations of the central retinal artery.
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Intravenous fluorescein angiogram will demonstrate prolonged choroidal filling and increased arteriovenous transit time.
Causes
Relatively frequent causes of NVG include the following:
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Carotid artery occlusive disease (CAOD)
Less frequent causes of NVG include the following:
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Intraocular tumor
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Chronic retinal detachment
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Secondary to intraocular lens (uveitis-glaucoma-hyphema [UGH] syndrome)
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Chronic or severe ocular inflammation
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Sickle cell retinopathy
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Radiation retinopathy
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Eales disease
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Coats disease
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Carotid-cavernous fistula
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Ocular ischemic syndrome/carotid insufficiency
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Anterior segment ischemia (ie, previous extraocular muscle surgery)
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Trauma
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Metastatic intraocular malignant lymphoma [3]
Complications
Complications include uncontrolled glaucoma, hyphema, and loss of vision.
