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To help you better understand the
following discussions on specific glaucoma topics you may need to first read
the FAQs on glaucoma found at
www.eye.com.ph/glaucoma.htm.
This information is provided for
your convenience and to help you understand your condition or procedure. It
is not meant to serve as a substitute for a discussion with your doctor
about the specifics of your condition, treatment, or procedure.
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:
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.
Ritch R, Shields MB, Krupin
T (Eds). The Glaucomas, 2nd Edition. St. Louis, Missouri, USA,
1996, Mosby-Year Book, Inc.
Epstein DL,
Allingham RR, Schuman JS (Eds).
Chandler and Grant’s
Glaucoma, 4th Edition. Baltimore, Maryland, USA, 1997, Williams &
Wilkins.
South East Asian Glaucoma
Interest Group. Asia-Pacific Glaucoma Guidelines. Sydney, Australia,
2003-2004, SEAGIG.
European Glaucoma Society.
Terminology and Guidelines for Glaucoma 2nd Ed. Savona, Italy,
2003, EGS. |
