NEOVASCULAR GLAUCOMANeovascular glaucoma is an example of a secondary glaucoma, meaning that it is caused by other health conditions. Learn here about risk factors, causes, and treatments for this disease. Neovascular glaucoma (NVG) is a special type of angle-closure glaucoma, in which abnormal, new blood vessels obstruct the normal flow of of a fluid called aqueous humor in the front part (anterior chamber) of the eye. When fully developed, NVG presents with aberrant blood vessel growth in the iris (called neovascularization), a closed anterior chamber angle, and elevated intraocular pressure. Early detection of the neovascularization and its causes can prevent the angle closure from occurring and reduce the need for surgery. Although several eye diseases can cause neovascular glaucoma, there are two main ones.
WHAT IS NEOVASCULARIZATION? Neovascularization refers to the proliferation of blood vessels in areas where they do not belong. It starts with a process called angiogenesis,
Blood vessels generated through neovascularization have different qualities than normal ones. These vessels, called neovessels, have walls that are fragile, which means that blood easily can seep through them. The technical term for this is that the neovessels have increased permeability. The following eye problems are associated with neovascularization.
CAUSES OF NEOVASCULAR GLAUCOMA? 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 and systemic hypertension (high blood pressure). The remaining one-third of NVG cases have less-common causes. Among these are:
A causative condition for NVG that is not associated with retinal hypoxia, is chronic anterior uveitis (irritation of the middle layer of the eye).
I mentioned earlier that neovascular glaucoma has its origins in the back of the eye and that it effects structures in the anterior chamber. But how does this happen? How does it result in glaucoma? Retinal hypoxia (loss of oxygen to the retina) is the triggering mechanism. This sets into motion a cascade of events that can lead to neovascular glaucoma.
Oxygen and other nutrients are transported to cells through the blood. This is accomplished through a complex network of blood vessels called arteries and veins. Hypoxia signifies that this normal process has been disrupted in some way. For example, in the figure to the right of the back of the eye, central retinal vein occlusion (CRVO) Lack of sufficient oxygen supply to the cells of the retina stimulates release of a number of chemical signals that instruct the body to create new blood vessels. Primary among these are vascular endothelial growth factor (VEGF) and pigment epithelium-derived growth factor (PEDF). VEGF is a proangiogenic chemical (promotes new vessel growth) and PEDF is an antiangiogenic chemical (restricts new vessel growth). Knowing a lot about these technical terms is not necessary in order for you to understand the process. The important thing to know is that VEGF and PEDF normally are maintained in a delicate balance. Unfortunately, in most of the causes of neovascular glaucoma listed above, an imbalance exists in which levels of VEGF are higher than normal and PEDF levels are lower. Loss of the VEGF-PEDF equilibrium causes the activation, proliferation, and migration of endothelial cells, which in turn results in the formation of new, fragile, and leaky blood vessels. Some of these cells move into the anterior chamber of the eye, lodge in the structures there, and proliferate. Thus, the mechanism of neovascular glaucoma could be explained in terms of a normal response by the body to correct a serious emergency situation (lack of oxygen) that itself develops into an abnormal condition (neovascularization).
The creation of new endothelial cells and their subsequent migration and proliferation into the anterior chamber of the eye results in neovascularization. When this occurs in the iris (the colored part of the eye), it is called rubeosis iridis. Progression to neovascular glaucoma is characterized by three main stages. Pre-glaucoma Stage. Rubeosis iridis is present but intraocular pressure remains within normal range. It first appears as a thin ring of vessels surrounding the pupil of the eye. As further proliferation of vessels occurs, neovascularization is observable in the anterior chamber angle through gonioscopy . This appears as blood vessel trunks growing out of the iris and reaching across the scleral spur and branching into the trabecular meshwork. Open-angle Stage. Rubeosis iridis with subsequent proliferation into the anterior chamber angle is more prominent. Intraocular pressure is now elevated. New vessels can be seen stretching across the iris and may be associated with inflammation and bleeding (hemorrhage). The anterior chamber angle remains open and there is the appearance of a fibrovascular membrane on the iris surface and in the anterior chamber angle. Advancement of the fibrovascular membrane into the anterior chamber angle is believed to cause obstruction of aqueous humor flow into the trabecular meshwork, resulting in elevated intraocular pressure. Damage to the optic nerve can occur during this stage. Closed-angle Stage.
Angle closure
at this stage can result in progressively higher and higher increases in intraocular pressure, which in turn can result in severe damage to the optic nerve. The anterior chamber angle closes because the fibrovascular membrane contracts, causing a condition called peripheral anterior synechia (adhesion of the iris to the cornea) with pupillary block (pupil is frozen in one position and cannot open or close). This makes elevated intraocular pressure more difficult to control.
WHO IS AT RISK FOR NEOVASCULAR GLAUCOMA? The following conditions can lead to poor blood flow to the eye and place a person at risk for developing NVG.
Having high blood pressure or hypertension, where the force exerted by your blood against the internal walls of your arteries is consistently above the normal range, is a risk factor for central retinal artery occlusion (CRAO), central retinal vein occlusion (CRVO), and the subsequent development of neovascular glaucoma. High blood pressure also significantly raises your risk for the development of coronary heart disease. Hypertension is a serious medical condition that must be treated and controlled in order for you to remain healthy.
CLINICAL MANAGEMENT OF NEOVASCULAR GLAUCOMA When I treat patients with neovascular glaucoma, I have two goals in mind. The first of these is to lower intraocular pressure as soon as possible in order to prevent damage to the optic nerve. To accomplish this, I prescribe medications designed to decrease the amount of aqueous humor produced by the ciliary body in the anterior chamber. Examples of these medications are carbonic anhydrase inhibitors, such as acetazolamide (Diamox), which is taken orally in pill form, and beta-blockers, such as Timolol (Timoptic), levobunolol (Betagan, AKBeta), betaxolol (Betoptic), and carteolol (Ocupress), which are administered as eye drops.My second goal is to eliminate neovascularization. In cases where it is diagnosed early and drainage through the trabecular meshwork is not entirely blocked, this is especially important. I may be able to preserve portions of the trabecular meshwork that can continue to drain aqueous humor and maintain intraocular pressure within normal limits. I accomplish this 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). I 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 balance back to normal, thereby eliminating neovascularization.Panretinal photocoagulation has benefits and drawbacks. Although the burns from the laser control neovascularization, they also cause some loss of peripheral vision. Nevertheless, by sacrificing some peripheral vision, I am able to preserve as much central vision as possible.
Although diabetic retinopathy is an eye disease that can lead to neovascular glaucoma, not all people with it develop this sequela. A sequela is a pathological condition that develops from a prior disease or injury. Diabetic retinopathy is classified in stages that correspond to the appearance of certain signs and the presence of new vessels in the retina. For example, if a patient shows evidence of new vessels in the retina, it is classified as proliferative diabetic retinopathy. This means that there is sufficient hypoxia in the retina to induce neovascularization. If the problem goes untreated, neovascularization can migrate to effect the iris and anterior chamber angle. A person with proliferative diabetic retinopathy should receive proper treatment to prevent permanent sequelae, such as retinal detachment, severe involvement of the macula, or the development of neovascular glaucoma. All of the above can lead to blindness. Diabetic retinopathy is the cause of 35% of cases of neovascular glaucoma
Not necessarily. Other factors can cause NVG and it is important that your ophthalmologist identifies the specific problem in your case. Nevertheless, it is true that one of the primary causes of neovascular glaucoma is diabetic retinopathy. On average, diabetic retinopathy usually develops after a patient has had diabetes mellitus for ten years or more and whose blood glucose (sugar) levels have been persistently high for an extended period. This means that the person does not have good control of his or her diabetes. Common symptoms of diabetes mellitus are:
The best way to know if you have diabetes is to visit a doctor who will perform a series of tests to arrive at a diagnosis.
Return from Neovascular Glaucoma to Types of Glaucoma
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How does oxygen get to the retina in the first place?
exhibits a number of symptoms; among these are venous engorgement and twisting (yellow arrows), abnormal accumulation of fluid (edema) in the fovea (green circle), yellowish-white exudate (black arrows), optic disc swelling (white circle), and feather- or flame-shaped bleeding called nerve-fiber-layer hemorrhaging (blue arrow). 
