In contrast to primary open angle glaucoma, secondary open angle glaucomas are diagnosed when glaucoma occurs as a consequence of another eye problem. There are numerous ocular problems that may yield glaucoma.
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Uveitis is the term for intraocular inflammation. Inflammation is one of the body’s most important normal functions. Healing and tissue repair are part of the inflammatory process. However, sometimes the inflammatory process causes unwanted side effects. Inside the eye, uveitis may cause formation of scar tissue that damages intraocular structures. Scar formation may block the normal flow of fluid inside the eye from the pump to drain. Inflammation may decrease the function of the pump and the drains themselves. Ultimately, this process may cause high intraocular pressure and optic nerve damage from glaucoma. Often, anti-inflammatory medicines called corticosteroids are used to treat uveitis. Unfortunately, as a side effect, these medicines may cause elevated intraocular pressure independent of the uveitis they are used to treat. Therefore, in some cases both the problem, uveitis, and the treatment, corticosteroids, cause glaucoma.
Problems with circulation of the eye affect its blood flow. Circulatory problems occur more commonly in people with diabetes mellitus and atherosclerosis. When the eye is starved of blood, it calls out for more nutrients and oxygen. In response to this call, new blood vessels sometimes grow inside the eye. This process of new blood vessel growth is called neovascularization. The new blood vessels may grow in places that are undesirable. One of the common locations for neovascularization is in the anterior chamber angle where they may cause scar formation that blocks outflow of fluid through the eye’s drainage apparatus. This leads to high intraocular pressure and optic nerve damage from glaucoma. This type of secondary glaucoma is called neovascular glaucoma.
Pseudoexfoliation syndrome is the most common type of secondary open angle glaucoma. A structural change in membranes within cells ultimately leads to the buildup of white flakes on structures inside the eye. These flakes are called pseudoexfoliation material. Over time, nearly 50% of people with pseudoexfoliation syndrome will also develop glaucoma. In addition to glaucoma, pseudoexfoliation may lead to poorly dilating pupils and weakness of lens zonules, which hold the lens in place. As a result, cataract surgery to remove the lens when it becomes cloudy with age is more complicated in patients with pseudoexfoliation syndrome.
The iris, the colored structure in the front of the eye, is composed of many tiny pigment granules. In everyone some these pigment granules become dislodged from the iris over time. In pigment dispersion syndrome, an abnormally large amount of pigment granules are liberated from the iris. These granules travel on fluid currents inside the eye and ultimately rest on many different intraocular structures. People with pigment dispersion syndrome have a higher likelihood of developing glaucoma.
Traumatic injury of the eye and treatment of eye injuries may lead to glaucoma. Both blunt force trauma and penetrating ocular trauma may damage structures that are critical for proper regulation of intraocular fluid flow and intraocular pressure. As well, bleeding and inflammation caused by trauma may result in elevated intraocular pressure. Glaucoma is most likely to develop within months of a traumatic injury, but may also occur many years later. Interestingly, there is a greater likelihood of glaucoma in the seemingly unaffected fellow-eye of patients with traumatic glaucoma in one eye.