There are numerous other types of glaucoma

Post-Traumatic Glaucoma

Glaucoma that develops after an eye has sustained trauma is called post-traumatic glaucoma or traumatic glaucoma. Traumatic glaucoma can be a secondary open angle glaucoma or a secondary angle closure glaucoma depending on the type of injury sustained by the eye. For example, if the angle closes up because of the inflammation and bleeding caused by the ocular trauma this causes a secondary angle closure glaucoma. Another example of traumatic glaucoma happens when the angle structures are torn from their proper attachments. This causes a specific type of traumatic open angle glaucoma called angle recession glaucoma.

Traumatic glaucoma is treated by correcting the inciting cause if possible. For example, if the glaucoma is caused by blood filling the anterior chamber then removing the blood is the first treatment step. After the immediate cause of the traumatic glaucoma has been treated (if possible), the next treatment steps in traumatic glaucoma follow the same IOP lowering methods as the primary glaucomas.

Sometimes, traumatic glaucoma can manifest months or years after the initial injury. Some people who have sustained an eye injury may need periodic check-ups for the rest of their lives so that a newly developing glaucoma can be caught early.

Neovascular Glaucoma

Neovascular glaucoma is a severe type of secondary glaucoma that can develop in eyes that have poor blood flow to the retina, a condition called ischemia. This is most commonly due to diabetic retinopathy or due to occlusion of one of the major retinal blood vessels which can happen in those with diabetes or hypertension. The prefix “neo“ means new and “vascular” refers to blood vessels. Neovascular glaucoma occurs when the ischemic retina produces chemicals that stimulate new blood vessel growth. These abnormal and fragile new vessels tend to occlude the anterior chamber angle and cause a glaucoma that is very difficult to treat.

Because the diseases that cause neovascular glaucoma tend to occur in both eyes, especially diabetic retinopathy, it is important that the patient’s other eye be monitored closely to watch out for the development of either the predisposing disease or neovascular glaucoma itself. Prevention and early treatment are the best means of treating neovascular glaucoma because of the poor outcome of treatment when the disease process has already taken hold. Neovascular glaucoma can be prevented if the initial retinal condition is diagnosed promptly, monitored regularly, and if treatment is instituted as soon as it becomes necessary.

The first step in treating neovascular glaucoma is to stop the retina from producing more chemicals. This is usually achieved by using laser treatment on the diseased retina but, in rare instances, it can also be achieved by restoring blood flow to the retina (e.g. in cases of occlusion of the carotid artery). The next step is to lower the IOP by whatever means possible. It is usually very difficult to lower the IOP in neovascular glaucoma because the condition does not respond well to the usual treatments such as medication and conventional glaucoma surgery. Partially destroying the ciliary body, the eye’s fluid producer, or inserting a special glaucoma drainage implant may be necessary to control the IOP.

Even if the IOP is successfully lowered, the visual outcome after treatment is usually poor because of both the original disease that caused the neovascular glaucoma, the damage caused by high IOP, and the side effects of treatment.

Steroid-Induced Glaucoma

Steroids are an important part of the treatment of inflammatory disease affecting various parts of the body. Steroids are regularly used as tablets, skin creams, nasal sprays, eye drops, injections and inhalers. Unfortunately, steroids have many side effects, one of which is increased intraocular pressure (IOP). The effect of steroids on IOP depends on the duration of treatment, the route of administration, and the susceptibility of the individual. Eye drops, injections and oral steroids, because they are given directly in the eye or because of the high dose given, have the greatest potential to induce increased IOP. Usually, it takes at least two weeks of use for a person to develop an IOP response to steroid eye drops and longer for those taking steroids via other routes. Not all people treated with steroids over the long term will develop increased IOP and, consequently, glaucomatous optic nerve damage. People who are highly susceptible to increased IOP due to steroid use are called “steroid responders”.

There is no way to tell in advance if a person is a steroid responder. The only way to know is to see how they respond to being treated with steroids. Prolonged use of steroid-containing eye drops without being seen by the ophthalmologist is a common cause of steroid-induced glaucoma. Thus it is important to see the doctor regularly when being treated with steroids over a prolonged period.

Childhood Glaucoma

Children can also be affected by glaucoma due to defects in the development of the eye’s fluid drainage pathway during the pre-natal period, infancy, and early childhood. Practically all cases of childhood glaucoma involve high intraocular pressures unlike adult glaucoma where a significant proportion of patients have normal IOPs. Just like adult glaucoma, childhood glaucoma cases can have either open or closed angles.

Childhood glaucoma can occur alone, in combination with other eye defects, or in combination with congenital defects in other parts of the body. The specific defect that causes the intraocular pressure rise varies depending on the type of childhood glaucoma. One of the most noticeable signs of childhood glaucoma is an enlarged eyeball. This occurs because young children’s eyes are still relatively elastic and the high eye pressure can easily stretch the eyeball. Other signs include tearing, sensitivity to bright light (photophobia), tightly squeezing the eyelids shut (blepharospasm), and haziness of the cornea.

Surgery is the usual first choice treatment for the childhood glaucomas because the open angle types of childhood glaucoma respond well to surgery and because the closed angle types of childhood glaucoma usually cannot be controlled with the few medications that can be safely used in children.

Inflammatory Glaucoma

When the eye becomes inflamed due to uveitis (intraocular inflammatory disease), trauma, or surgery, increased intraocular pressure can result. The increased IOP can occur during the active phase of the inflammation even though the angles remain open because of inflammatory products clogging up the meshwork. When the inflammation has subsided, the intraocular pressure can remain high if the drainage structures of the eye have become damaged or scarred by the inflammation. This can result in either an open angle type or closed angle type of glaucoma.

The main treatment method for inflammatory glaucoma is to reduce inflammation to prevent further damage to the drainage angle. Medications are used initially to lower the IOP but laser or surgery may be needed later on if the high IOP persists after the inflammation has subsided.

Lens-Induced Glaucoma

The eye’s natural lens, called the crystalline lens, is located just behind the iris. There are several types of secondary glaucoma that can develop due to the lens.

As we get older our lenses naturally become thicker. In some eyes, the thickness of the lens reaches the critical point where it is now able to block the flow of fluid from behind the iris to the front of the iris. This is called phacomorphic glaucoma and is treated by removing the lens.

As we age our lenses become thicker and cloudier, eventually forming a cataract. If the cataract is left too long in the eye and it becomes overly mature it can start to leak lens proteins into the anterior chamber. The lens proteins then clog the trabecular meshwork causing a secondary open angle type of glaucoma called phacolytic glaucoma. This is treated by removing the lens and all of the leaked proteins in the anterior chamber.

When the lens capsule is ruptured due to trauma or surgery the lens particles now become exposed to the anterior chamber. An immune response may form against the lens particles and the resulting inflammation can clog the trabecular meshwork. This is called phacoanaphylactic glaucoma. Treatment is by anti-inflammatory and IOP lowering medications and surgical removal of the lens material if necessary.

References:

1. Kass et al. The Ocular Hypertension Treatment Study: A randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Archives of Ophthalmology 2002; 120:701-713.
2. Ritch R, Shields MB, Krupin T (Eds). The Glaucomas, 2^nd Edition. St. Louis, Missouri, USA, 1996, Mosby-Year Book, Inc.
3. Epstein DL, Allingham RR, Schuman JS (Eds). Chandler and Grant’s Glaucoma, 4^th Edition. Baltimore, Maryland, USA, 1997, Williams & Wilkins.
4. South East Asian Glaucoma Interest Group. Asia-Pacific Glaucoma Guidelines. Sydney, Australia, 2003-2004, SEAGIG.
5. European Glaucoma Society. Terminology and Guidelines for Glaucoma 2^nd Ed. Savona, Italy, 2003, EGS.