Description, Causes and Risk Factors:
Neovascular glaucoma is devastating ocular disease, often seen as an end-stage complications of retinal ischemia. Its pathogenesis is associated with neovascularization of the iris (NVI) and neovascularization of the anterior chamber angle (NVA) with resultant proliferation of fibrovascular tissue in the anterior chamber. The fibrovascular membrane eventually obstructs the trabecular meshwork and contract to produce progressive angle closure with broad peripheral anterior synechiae. The IOP (intraocular pressure) become significantly elevated and difficult to control, resulting in advanced glaucomatous optic neuropathy and irreversible visual loss.
Although NVG primarily effects the front part of the eye (anterior chamber), its cause usually is associated with a lack of oxygen to the retina in the posterior region (vitreous chamber). The technical term for this lack of oxygen is retinal hypoxia.
Conditions leading to retinal hypoxia include diabetic retinopathy and central retinal vein occlusion (CRVO). These two diseases account for about two-thirds of all NVG cases. The predisposing condition for diabetic retinopathy obviously is diabetes. With respect to CRVO, predisposing conditions include elevated intraocular pressure (IOP) and systemic hypertension (high blood pressure).
Less-common causes may include:
Carotid artery obstructive disease.
Rhegmatogenous retinal detachment (a tear in the retina with fluid accumulating underneath that can further separate the pigment layer from other layers).
Choroidal melanoma beneath a retinal detachment.
Carotid-cavernous fistula (an abnormal communication between the arterial and venous systems within a specific area [cavernous sinus] of the skull).
Central retinal artery occlusion (CRAO).
NVG is more prevalent in elderly patients.
Neovascular glaucoma remains a therapeutic challenge. Early detection of neovascularization and prophylactic treatment with PRP (panretinal photocoagulation) directed at the ischemic retina are key elements in preventing a visually devastating outcome of this disease. Randomized, prospective clinical trials are needed to compare the three main surgical modalities: filtration surgery, aqueous drainage implants and cyclodestruction. Current research on ocular angiogenesis and the advent of new pharmacological agents with activity against vascular endothelial growth factors may increase our treatment options for combating this serious disease.
Patients with neovascular glaucoma (NVG) may be asymptomatic, but more typically present with a chronically red, painful eye which often has significant vision loss. Further, there will be significant concurrent vascular disease such as diabetes, hypertension, carotid artery disease, or giant cell arteritis (GCA). There frequently is an antecedent history of a retinal vessel occlusion or chronic uveitis.
There will be visible neovascularization of the iris (NVI) and angle (NVA). Only rarely will NVA develop without NVI. The patient typically has significant corneal edema and elevated intraocular pressure, often exceeding 50-mmHg. There may be a shallow anterior chamber. Gonioscopically, there will be total or near-total angle closure. Funduscopically, there typically will be evidence of retinal vessel occlusion (either artery or vein), ocular ischemic syndrome or diabetic retinopathy.
In patients with associated ocular conditions who areat high risk of developing NVG, clinicians should perform a comprehensive ocular evaluation with particularattention to the pupillary margin of the iris.A complete ocular examination of both eyes, particularly of the posterior segment, will almost certainly provide the etiology of neovascularization.
Imaging studies may include:
Optical coherence tomography- Images observed per grade of neovascular glaucoma.
Intravenous fluorescein angiogram and electroretinography (ERG) to assess retinal ischemia.
The goal of the treatment include to lower intraocular pressure to prevent damage to the optic nerve and to eliminate neovascularization.
Medications designed to decrease the amount of aqueous humor produced by the ciliary body in the anterior chamber may include carbonic anhydrase inhibitors, such as acetazolamide (Diamox), which is taken orally in pill form, and beta-blockers, such as Timolol (Timoptic, Betimol), levobunolol (Betagan, AKBeta), betaxolol (Betoptic), and carteolol (Ocupress), which are administered as eye drops.
Neovascularization is obtained through a procedure called panretinal photocoagulation (PRP), also known as scatter coagulation, PRP seeks to reduce oxygen demand in the retina by decreasing the number of retinal cells through multiple laser burns (ablations). Ophthalmologists usually do this in two treatments that are separated by a few weeks. The macula, which is responsible for central vision, does not receive this treatment. PRP controls the hypoxia and helps to return the VEGF-PEDF (vascular endothelial growth factor-Pigment epithelium-derived factor) balance back to normal, thereby eliminating neovascularization.
In the majority of patients with NVG secondary to PDR (proliferative diabetic retinopathy), wherein retinal ischemia is the underlying etiology, the ablation of the peripheral retina is first-line therapy to counter the angiogenic cascade. In most instances, PRP (proliferative retinopathy photocoagulation) with the argon laser is the treatment of choice.
NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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