Glaucoma is the Name for a Group of Eye Diseases That Damage The

8/2/2019 Glaucoma is the Name for a Group of Eye Diseases That Damage The

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Glaucoma is the name for a group of eye diseases that damage the optic nerve . The optic

nerve, which carries information from theeyeto thebrain, is in the back of the eye. When the

nerve is damaged, you can lose yourvision.

At first, people with glaucomalose side (peripheral) vision. But if the disease is not treated,

vision loss may get worse. This can lead to total blindness over time.There are three types of glaucoma.

Open-angle glaucoma is the most common form in the United States. In this type of

glaucoma, the optic nerve is damaged bit by bit. This slowly leads to loss of eyesight.

One eye may be affected more than the other. Sometimes much of your eyesight may

be lost before you notice it.

Closed-angle glaucoma is less common. About 10% of all glaucoma cases in the

United States are closed-angle. In this type of glaucoma, the colored part of the eye

(iris) and the lens block movement of fluid between the chambers of your eye. This

causes pressure to build up and the iris to press on the drainage system of the eye. (See

a picture of the iris and lens .) A related type is sudden (acute) closed-angle

glaucoma. It is often an emergency. If you get this acute form, you will need medical

care right away to prevent permanent damage to your eye.

Congenital glaucoma is a rare form of glaucoma that some infants have at birth. Some

children and young adults can also get a type of the disease.

Finding and treating glaucoma early is important to prevent blindness. If you are at high risk

for the disease, be sure to get checked by an eye specialist (ophthalmologist) even if you have

no symptoms.

Your risk for glaucoma rises after age 40. Race is also a factor. Blacks are more likely than

whites to get the disease. You are also at risk if you have diabetes or if a close family memberhas had glaucoma.

What causes glaucoma?

Damage to the optic nerve is often caused by increased pressure in the eye (intraocular

pressure). This can happen when extra fluid builds up in the eye, such as when the eye makes

too much fluid or does not drain well. But some cases of glaucoma aren't caused by increased

pressure. In these cases, the cause may not be found.

You can get glaucoma after an eye injury, after eye surgery, or because of an eye tumor. Some

medicines (corticosteroids) that are used to treat other diseases may cause glaucoma.

What are the symptoms?

If you have open-angle glaucoma, the only symptom you are likely to notice is loss of vision.

You may not notice this until it is serious. Thats because, at first, the eye that is not affected

makes up for the loss. Side vision is often lost before central vision.

Symptoms ofclosed-angle glaucoma can be mild, with symptoms like blurred vision that last

only for a short time. Severe signs of closed-angle glaucoma include longer-lasting episodes of

blurred vision or pain in or around the eye. You may also see colored halosaround lights, have

red eyes, or feel sick to yourstomach and vomit.

In congenital glaucoma, signs can include watery eyes and sensitivity to light. Your baby may

rub his or her eyes, squint, or keep the eyes closed much of the time.
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HISTORY

A 70-year-old woman was referred to me with neovascular glaucoma.Her medical history was significant for hypertension and asthma. She was taking Vasotec

(enalapril maleate, Merck), Advair (fluticasone propionate and salmeterol, GlaxoSmithKline)

and albuterol. She had an ocular history of cataract extraction with posterior chamber IOL

implantation in 1987 and argon laser trabeculoplasty in both eyes in 1994. The patient had

scarring of her right cornea from a corneal ulcer in 2006.

In 2008, the patient developed a central retinal vein occlusion in her right eye. Shortly

thereafter, vascularization of the iris could be visualized. The referring ophthalmologist

performed panretinal photocoagulation, which was incomplete because of the poor view into

the eye. The referring ophthalmologist also gave an Avastin (bevacizumab, Genentech)

injection to the affected eye. The IOP was temporarily controlled with these maneuvers alongwith Azopt (brinzolamide ophthalmic, Alcon) twice daily in both eyes, Lumigan (bimatoprost

ophthalmic solution 0.03%, Allergan) in both eyes every night at bedtime and Alphagan

(brimonidine 0.1%, Allergan) twice daily in both eyes. However, the IOP elevated with time.

When I saw the patient, the IOP was 68 mm Hg and the patient was in pain. The patient also

experienced a decrease in vision from counting fingers to hand motion. The cornea, iris and

angle had vascularized and there was blood in the angle. There was a very poor view into the

eye due to corneal scarring, edema and poor dilation from iris synechiae. Gonioscopy was

difficult but revealed impressive vessels in the angle. The posterior chamber IOL was in good

position, but with white lens material barely visible just posterior to the lens optic. The view of

the retina was hazy because of the cornea and small pupil, and there was a mild vitreoushemorrhage. Panretinal photocoagulation could not be performed.

Surgical course

After discussing the treatment options with the patient, I performed an endoscopic pars plana

vitrectomy with endolaser of the retina and of the ciliary body. The view was not clear enough

to visualize the retina through the cornea, so an endoscopic approach was necessary.

The endoscope with the endolaser cyclophotocoagulation (ECP) system (Endo Optiks) is ideal

to assist with this type of vitrectomy. It can be performed through an opaque cornea and avoids

having to stretch and dilate a rubeotic pupil. I used the 23-gauge vitrectomy system (Alcon). A

23-guage infusion port was placed in the inferior temporal quadrant and a 23-gauge sleeve was

placed in the superior temporal quadrant. A larger 19-gauge sclerostomy was made in the

superior nasal quadrant. A 19- to 20-gauge port is necessary to insert the endoscopic laser.

With the infusion on in the inferior port, the straight endoscope was placed through the 19-

gauge opening. The Occutome (Alcon) was placed in the superior temporal port and a complete

vitrectomy was performed (Figure 2). As the vitreous base was removed, several pieces of

white lens material fell onto the macula. The lens remnants were located with the endoscope

and removed with the Occutome. At times, the endoscopic probe tip was used to help move and

crush the lens material into the Occutome.

The endoscope was invaluable in locating and manipulating the lens material. Subsequently,the retina, pars plana, and lens-ciliary body complex could be viewed with the curved


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endoscope in its entirety. A complete panretinal photoablation was easily done with the ECP

settings of 600 mW to 800 mW. After this, attention was turned to the ciliary body. A 180

cyclophotoablation of the ciliary body was performed as well as treatment of the processes to

pars plana (Figure 3). An intravitreal injection of dexamethasone was given at the end of the

case.

Glaucoma Treatment

Glaucoma treatment cannot cure the condition, but it can dramatically slow or temporarily halt

its progress. Glaucoma can be treated with either medication or surgery. Both of these

treatments are aimed at lowering intraocular pressure (IOP), or pressure within the eye. In the

United States, medications are usually the first-line of glaucoma treatment. If this fails, then

glaucoma surgery is the next treatment considered.

Glaucoma Medication

Glaucoma medications are either oral or topical. Topical medications such as eye drops, eye

ointments, or inserts (strips of medication inserted in the corner of the eye) work to reduce IOP

either by increasing the outflow of fluid from the eye or by reducing the amount of fluid

produced by the eye. To learn more about the condition, examine the risk

factors and symptoms of glaucoma. It is important to tell all of your doctors about any

glaucoma medications that you are using. In order for these medications to work, you must take

them regularly and continuously as they were prescribed.

DocShop can help you find an eye care specialist in your area today.

Topical Glaucoma Medications

There are five types of topical glaucoma medications, each achieving different purposes:

Miotics increase the outflow of fluid. These include Isopto Carpine, Ocusert,

Pilocar, and Pilopine.

Epinephrines increase the outflow of fluid. These include Epifrin and Propine.

Beta-blockers reduce the amount of fluid. These include Betagan, Betimol,

Betoptic, Ocupress, Optipranalol, and Timoptic.

Carbonic-anhydrase inhibitors and alpha-adrenergic agonists reduce the amount of

fluid present. These include Alphagan, Iopidine, and Trusopt.

Prostaglandin analogs increase the outflow of fluid through a secondary drainage

route. These include Lumigan, Rescula, Travatan, and Xalatan.

Oral Glaucoma Medications

Your ophthalmologist can also prescribe oral medications to treat glaucoma. Carbonic

anhydrase anhibitors are the oral medications most commonly used in the treatment of

glaucoma. These include Daranide, Diamox, and Neptazane.

Patients will be started on one medication or a combination of drugs. If a patient does not

respond to one type of drug, he or she can be switched to another until all possibilities have

been exhausted. Once this happens, the ophthalmologist may recommend glaucoma surgery.
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Glaucoma Surgery

For patients who still have an elevated IOP after attempting glaucoma treatment through

medication, an ophthalmologist may recommend either laser or conventional surgery.

Glaucoma Laser Surgery

There are three types of glaucoma laser surgery that can be performed in the doctors office:

Trabeculoplasty

Trabeculoplasty uses a laser to burn tissue from the trabecular meshwork, a structure within the

eye that controls the flow of fluid. This procedure increases the aqueous outflow in the area

surrounding the laser spot, relieving pressure within the eye. Pressure is reduced in 60 to 70

percent of the patients in whom a laser trabeculoplasty is performed. This type of glaucoma

laser surgery is used to treat patients with open-angle glaucoma.

Iridotomy

Closed-angle glaucomaoccurs when the angle between the iris and the cornea in the eye is too

small. This causes the iris to block fluid drainage, increasing inner eye pressure. Iridotomy

glaucoma laser surgery makes a small hole in the iris, allowing it to fall back from the fluid

channel so fluid can drain.

Cyclophotocoagulation

Cyclophotocoagulation uses a laser to burn ciliary tissue, which decreases the production of

fluid in the eye. The procedure, performed under local anesthesia, has only recently become

available to glaucoma patients to reduce the intraocular pressure. This type of glaucoma laser

surgery is used to treat patients who have failed to respond to other types of glaucoma surgery.

Many patients will require more than a single treatment. The procedure appears to have

significant success and relatively low risk.

Conventional Glaucoma Surgery

If laser surgery fails to lower IOP, the surgeon may recommend conventional glaucoma

surgery, known as trabeculectomy or filtering surgery. This is an outpatient procedure

involving the removal of a tiny piece of the eye under the eyelid. This conventional glaucoma

surgery creates a new drainage path that increases the outflow of fluid from the eye.

Locate a Doctor for Glaucoma Treatment

Preventive glaucoma diagnosis, medication, and treatment are crucial to safeguarding yourvision against this debilitating condition. DocShop can help you find a glaucoma specialistin

your area who is trained in conventional or laser glaucoma surgery.

Outcome

The following day, the patient was pain-free and IOP measured 17 mm Hg and her vision was

hand motion. The patient was placed on prednisolone acetate 1% and moxifloxacin. These

medications were tapered over 4 weeks. Over the course of the next 3 months, the eye pressure

rose to 28 mm Hg and brimonidine 0.1% was started. At 4 months the IOP decreased and the

patients IOP is 16 mm Hg with no glaucoma medication. The patient feels as though she has

some useful vision in this eye. The patient is especially grateful since the primary open-angle
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glaucoma has progressed in the other eye and requires a trabeculectomy with mitomycin C,

seton or ECP.

Discussion

Neovascular glaucoma is a serious complication of systemic and retinal disease. The IOP can

rise rapidly, often resulting in extremely high IOP with irreversible and severe loss of vision.Early panretinal photocoagulation for neovascularization is necessary to ameliorate the

devastating sequelae from neovascular glaucoma. Unfortunately, all too often the synechiae

between the iris and the lens prevent adequate dilation of the pupil for treatment with panretinal

photocoagulation.

Today there is no substitute for panretinal photocoagulation. Transscleral diode laser

cyclophotocoagulation is an option for treatment, but it is very destructive to the eye and

vision. Usually vision is lost after this type of treatment and hypotony can ensue.

I have found that ECP has tremendous results in patients with vascular glaucoma. A complete

panretinal photocoagulation can be performed as well as ablation of the ciliary body at thesame time. It avoids the poor visualization issues with a standard vitrectomy and allows for

extensive panretinal photocoagulation. ECP in neovascular glaucoma can prevent the need for a

glaucoma implant or a trabeculectomy. A 180 ablation of the ciliary body is usually enough to

control the IOP without creating hypotony. In vascular glaucoma, the ciliary processes are

already damaged and 180 treatment of the ciliary body is usually all that is needed. Other

glaucomas usually require at least 270 treatment.

When ablating the ciliary body through the pars plana, it is best to treat all the way to the pars

plana because these structures also produce aqueous fluid. Treat the ciliary process until it

whitens, shrinks and contracts, but avoid gas bubble formation and audible popping. The

intensity of the treatment can be adjusted by the distance from the probe to the ciliary body.

The closer the probe is to the target, the more intense the treatment. I use 200 mW to 250 mW

of laser power. An intravitreal injection of dexamethasone at the end of the case is useful to

reduce postoperative inflammation. Dexamethasone is short-lived and usually will not raise the

IOP when given in this setting.

In cases of vascular glaucoma, I have not found the need to perform a trabeculectomy or place

a glaucoma implant if the ciliary body can be adequately treated with ECP. If the IOP is too

high after the first treatment, additional ECP can be performed. A trabeculectomy can be

performed as well as placement of a glaucoma implant if necessary. In patients who have

conjunctiva that is scarred and vascularized, a trabeculectomy or placement of a glaucoma

implant may be difficult. Such cases occur in patients who have had multiple eye surgeries,

trauma or chemical burns. Patients with vascular glaucoma usually have such conjunctivaltissue. The best choice in many of these cases would be ECP.

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