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Module 42 |
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Module 42: |
Glaucoma, Part 2 |
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Types of glaucoma
Open-angle glaucoma is subdivided into primary open-angle glaucoma (POAG) and secondary open-angle glaucoma. |
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| POAG is also called chronic open-angle glaucoma (COAG). As the name suggests, in this disease the anterior chamber angle is open. The aqueous has open access to the trabecular meshwork, but for some unknown reason the drainage of aqueous from the meshwork onward is slowed, the IOP is raised, and damage to the nerve fiber layer occurs. |
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Secondary open-angle glaucoma occurs when an otherwise open angle structure is clogged mechanically by cells or by a disease process. Examples include neovascularization and cell blockage (pigment, red blood cells, macrophages). This type of glaucoma is discussed in more detail in another section of this module.
Primary open angle glaucoma is the most common type of glaucoma. It is usually bilateral, but does not usually affect each eye at the same rate. In the early stages it is without symptoms, meaning the patient has no pain, no discomfort, and no noticeable vision loss. Vision loss occurs from the periphery inward toward the central vision, and a substantial percentage of the visual field can be lost before the patient notices a problem with his/her vision. The only way to diagnose the disease is with a complete eye examination. Intra-ocular pressure screening exams are useful in identifying people at high risk.
As discussed in Module 41, there is no single, absolute diagnostic test for POAG. The eye doctor weighs the IOP readings, the appearance of the anterior chamber angle, the appearance of the optic nerve head, the thickness of the nerve fiber layer, and the automated perimetry results when deciding if and how to treat the eye. There is no cure for POAG. Once vision is lost to glaucoma, it cannot be regained. The goal is to stop or to slow vision loss. This is accomplished by lowering the IOP with medical (drops) or surgical treatment.
Blacks have a 3-4x greater chance of developing POAG than whites. There is an increased risk of glaucoma in those over 40 years old. Glaucoma affects more myopes than hyperopes. Other risk factors include diabetes, hypertension, and smoking. Those with higher IOP readings are at greater risk than those with lower IOP readings. A family history or glaucoma is a significant risk factor for developing POAG. It is helpful to know who the relative is (was), because first degree relatives are genetically more significant. It is also helpful to know what kind of treatment the relative received, and whether or not the person became blind from the disease. |
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Ocular Hypertension The "normal" IOP range is between 10 and 21 mmHg. Some people have consistent IOP readings at or above 22 mmHg, but they have no other definitive signs of glaucoma. These people are said to have "ocular hypertension". Even though they will not receive treatment for the above normal pressure readings, they must be followed with regular exams for developing signs of glaucoma. |
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The flip side of the ocular hypertensive is the patient with "normal tension glaucoma" (NTG). This patient has had IOP readings in the normal range all along, even without treatment, but the other signs of glaucoma (optic nerve head cupping, nerve fiber thickness loss, and visual field loss) are there. Just as with regular POAG, the goal of treatment will be to lower the IOP, but the IOP target for the NTG patient will be much lower. |
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The primary goal of any treatment for glaucoma is to preserve what vision the eye has. Unlike cataract surgery, treatment for glaucoma will not restore vision that has been lost. Damaged retinal nerve fibers do not regenerate. All current treatments are aimed at lowering the IOP as a means of stopping nerve fiber damage and vision loss. When treatment begins, the eye doctor has a "target" IOP in mind, which may be a single number or a pressure range. The target is based upon the present condition of the eye and the risk factors the patient has that are associated with glaucoma. The physician will begin with a conservative treatment. If the target IOP is reached, then the patient will be monitored on that treatment until there are signs of deterioration in terms of optic nerve head cupping, loss of nerve fiber thickness, loss of visual field, or a combination of the factors. The target IOP may be adjusted and a more aggressive treatment may be started. If the target IOP is not reached, and the eye shows signs of glaucomatous deterioration, then again a more aggressive treatment is begun. The treatment process is one of continuous monitoring for deterioration, and adjustment in treatment to halt the deterioration. |
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Non-compliance is a major issue in the medical treatment of glaucoma. Non-compliance means that the patient is not using the eye drops as prescribed. To compound the problem, the patient may be dishonest when asked about compliance and claim that the drops are being used on schedule when in actuality they are not. One study reported that patients who claimed 100 % compliance were only using the drops 76% of the time. Of the glaucoma patients in the study, 40% were not using their drops 90% of the time.
There are many reasons for this. The patient may be forgetful. The patient may run out of drops and not get re-supplied in a timely manner. The patient may miss the eye when using the drop. The patient may try to save money by not using the drop as prescribed. The patient may not think that using the drops on schedule is important. The patient may perceive no benefit from using the drop because there are no short term symptoms that the medication is relieving.
Non-compliance makes it more difficult for the eye doctor to manage the disease. If the patient is losing vision to glaucoma, is it because the drops being used are ineffective, or is it because the patient is not using the drops as prescribed?
There are some ways to combat non-compliance:
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Most of the medications used to treat glaucoma are drops that work by either increasing the outflow of aqueous from the eye, or by decreasing the production of aqueous. Glaucoma drugs are classified or typed according to how the drugs work. All glaucoma medications have side effects that are particular to the drug type. The doctor must find a drug, or a combinations of drugs, that will achieve the target pressure and have acceptable side effects for the particular patient. Convenience, in terms of how many times a day the drop is used, is sometimes a factor, and cost is sometimes a factor. |
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| All of the drops listed below can cause stinging, burning, and itching when instilled. Localized allergic reaction can include redness and swelling of the conjunctiva and lids. The list of side effects for each class is not a complete list. For more information about each drug, see the insert that comes with the drug, or consult the PDR. | |||
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Beta blocker drops decrease the production of aqueous. This class includes the following:
Side effects can include shortness of breath in patients with asthma or other respiratory disorders. Beta blocker drops have an additive effect with beta blockers taken for heart disease and blood pressure problems. Beta blockers reduce blood pressure and lower the heart rate They also reduce cardiac response during exercise. They are contraindicated for some patients with heart disease. |
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Carbonic Anhydrase Inhibitors decrease the production of aqueous. This class includes:
The first two drugs are drops. Acetazolamide (250mg tab, or 500mg sequel) and methazolamide (25mg and 50mg tabs) are pills that are usually used short term to speed the lowering of a spike in the IOP, typically after an intra-ocular procedure. Acetazolamide can also be administered intravenously for faster effect. Side effects include tingling in the extremities, nausea, memory problems, depression, and frequent urination. If used long term, acetazolamide and methazolamide can cause kidney stones. Acetazolamide and methazolamide should not be given to a patient with a sulfa allergy. |
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Alpha agonists work by decreasing aqueous production and increasing outflow:
Side effects include drowsiness, fatigue, headache, and dryness of mucous membranes. An important drug contraindication for alpha agonists occurs with monamine oxidase inhibitors, which are used to treat depression. The alpha agonists should not be used if the patient has taken a monoamine oxidase (MAO) inhibitor such as isocarboxazid (Marplan), phenelzine (Nardil), or tranylcypromine (Parnate) in the last 14 days. These drugs should not be given to children under the age of 6. |
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Prostaglandin analogs work by increasing the outflow of aqueous:
Side effects include increased brown pigmentation of iris, growth of eyelashes, and darkening of the skin around the eyes. |
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This combination drop has a carbonic anhydrase inhibitor and a beta blocker, which both decrease the production of aqueous.
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Cholenergic (Miotic) drops work by increasing the outflow of aqueous:
Miotics make the pupil size smaller. This side effect can be a blessing or a curse depending upon how much light is available. On a bright sunny day outside, vision can be improved by the pinhole effect. In a dimly lit interior, vision is worse because not enough light is going through the small pupil. The patient can experience a brow ache when first staring these drops. Miotics are not used anymore as a frontline glaucoma treatment for POAG, but they are used in the treatment of angle-closure glaucoma. |
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This cholinesterase Inhibitor works by increasing the outflow of aqueous:
This drug has the same side effects as the above listed miotics, plus numerous systemic side effects, and it is associated with an increased incidence of retinal detachment. For these reasons, this drop is not a frontline glaucoma treatment. |
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Surgical treatment of glaucoma is not usually recommended unless medical treatment has failed to stop vision loss. As is the case with medical treatment, vision that has already been lost cannot be restored. The goal of surgical treatment is to lower the IOP. |
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Argon Laser Trabeculoplasty (ALT)
The argon laser is used to make a number (50-100) of small burns in the trabecular meshwork in the angle of the eye. In about 75% of the patients treated, this method works to significantly lower the IOP by increasing the outflow of aqueous, although it is not understood exactly how this treatment works to lower the IOP. For about half the patients, the pressure lower effect lasts less than 5 years. |
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| The eye is not dilated for this procedure, so that there is a clear view into the angle. A gonioscopy lens is placed on the anesthetized cornea and a slit lamp biomicroscope is used to aim the laser beam into the angle by reflection on one of the gonio mirrors. |
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The complete circle of the angle (360 degrees) is available for treatment. Treatment of half the angle (180 degrees) may be done in one session in order to judge the response of the eye before the other half is done on another day. The ALT treatment can only be repeated one time. The patient typically will still need to use drops to control the IOP.
The treatment is painless and takes less than 15 minutes. The IOP is checked about an hour after the procedure, before the patient is sent home. The patient may be given a steroid drop to use for a few days to reduce post-operative inflammation. |
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Selective Laser Trabeculoplasty (SLT)
SLT works by using a short pulsed laser of a specific wavelength to target only the melanin-containing cells in the trabecular meshwork. Non-pigmented trabecular meshwork cells are not damaged. This treatment is thought to release cytokines that trigger macrophage recruitment and other changes that lead to IOP reduction. ALT can only be repeated once, but SLT can be repeated several times.
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Filtering Microsurgery (Trabeculectomy)
When medical therapy and laser therapy fail to adequately control the IOP, an alternate drainage route can be made surgically. The procedure is called a trabeculectomy, or a "trab" for short. A small opening, called a sclerostomy, is made in the sclera at the limbus. The opening is connected to the peripheral anterior chamber. |
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The hole is covered by conjunctiva and the aqueous passes through the opening into the subconjunctival space where it is absorbed. When the trab is working correctly, a small blister or "bleb" is formed. The opening is placed such that the bleb is hidden by the upper eyelid. The figure to the right shows the approximate size and position of the bleb from a front view and and a side view. The surgery is done on a outpatient basis under local anesthesia. |
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The most common complication is failure due to scarring and closure of the opening. Drugs (5-FU and mitomycin-C) can be used to inhibit scarring. Other possible complications include bleeding, infection, chronic inflammation, cataract formation, and hypotony (the IOP is too low). |
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The Tube-Shunt
In an eye that is not suitable for the filtering procedure, or the filtering procedure has failed, a drainage implant can be used. A small tube is surgically inserted onto the anterior chamber. The tube connects to a small plate that is inserted next to the sclera and is covered by the conjunctiva. |
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Two such devices are the Baerveldt Tube (baerveldt.com) and the Ahmed Valve (ahmedvalve.com). Both websites have good animations depicting how the valves are inserted.
Possible complications include the tube coming into contact with the cornea, blockage of the tube by the iris, choroidal hemorrhage, hypotony, infection, and chronic inflammation. |
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Ciliary Body Ablation (destruction of the ciliary body)
These treatments are only used in cases of refractory glaucoma. The term "refractory" means "resistant to treatment". Medical and other surgical treatments have failed to sufficiently lower the IOP.
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Primary Angle-Closure Glaucoma
The mechanism of primary angle-closure glaucoma is very different than that of primary open-angle glaucoma. As you might guess, the big difference is that one involves an open angle and the other involves a closed angle. In POAG, the access (the angle) to the drainage mechanism is open, but the filtering tissue (the trabecular meshwork) is not allowing aqueous to drain fast enough. In angle-closure glaucoma, the trabecular meshwork may be operating normally, but access (the angle) to the meshwork is blocked.
There are several anatomical factors that can cause the problem. The anterior chamber of the eye may be shallow. This can be caused by hyperopia (the eye is shorter than normal), or the lens may be larger than normal. The peripheral area of the iris may have a convexity. The space between the pupil and the lens may be blocked, causing the iris to bow forward. |
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| Anatomy of an angle closure: (1) Notice that the anterior chamber is shallow. (2) The pupil dilates, the angle is blocked by the peripheral iris, and the iris bows forward. |
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| The angle can be partial
closed, or totally closed. A partially closed angle will cause a
proportional rise in the IOP. A totally closed angle causes a
sudden, very high elevation in the IOP (40-90mmHg) that constitutes an
ocular emergency. Pressures associated with POAG (24-35mmHg) do
not cause eye pain. The high pressure of angle-closure glaucoma
causes severe eye pain with associated nausea and vomiting. The
eye becomes red and inflamed. The high pressure causes corneal
edema and the patient sees halos around lights. The pupil becomes
fixed and mid-dilated. If the pressure remains high for an
extended period, or if the eye suffers repeated episodes, then permanent
damage to the nerve fibers can result. The terms "primary angle-closure" and "acute angle-closure" are often used interchangeably. Some doctors argue that the term "acute angle-closure" should be reserved for an eye that has had an attack, as described above. Some also argue that the term "glaucoma" should not be used unless there has been vision loss due to the condition. |
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The short term treatment of an angle closure attack involves using medications to rapidly bring the pressure down:
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| The long term treatment for angle-closure glaucoma is a laser peripheral iridotomy (LPI, or PI), sometimes called a laser peripheral iridectomy. An "ectomy" is a removal of tissue and an "otomy" is a hole made in the tissue. Before the laser came into use, a piece of the iris was surgically removed (surgical peripheral iridectomy, pictured to the right, upper). The laser is now used to make a full thickness hole in the peripheral iris (pictured to the right, lower). The hole creates an alternative passage for the aqueous from the posterior chamber to the anterior chamber. Angle-closure attacks are usually unilateral, but the other eye is usually at risk for an attack. For this reason an LPI is usually performed in the fellow eye as well to prevent future angle-closure. |
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A laser gonioplasty can be used if a laser iridotomy is not possible. The laser beam is used in the angle to shrink the peripheral iris away from the trabecular meshwork. |
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A full blown angle-closure attack may be preceded by one or more shorter duration episodes with symptoms of eye pain and blurry vision that may be precipitated by dilation of the pupils. Dim light, emotional distress, and some medications (e.g. muscle relaxants, tranquilizers, antihistamines) can cause dilation of the pupils.
A patient who is suspected to be at risk for angle-closure glaucoma can be examined by the eye doctor with a gonioscopy lens to view the angle of the eye and confirm the problem. The eyes can then be treated prophylactically with a laser peripheral iridectomy. |
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| Above left: The three mirror gonioscopy lens. Above right: The view into the angle. | |||
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A secondary glaucoma is glaucoma caused by some other condition or disease. Glaucoma can be secondary to another eye disease, condition, or trauma. Glaucoma can also be secondary to a systemic disease or to a medication that the patient is or has taken. If possible, treating the primary disease or condition may reduce or eliminate the rise in the IOP.
As is the case with POAG, a moderate rise in IOP (<35 mmHg) probably will not be symptomatic with the patient. As is the case with angle closure glaucoma, IOP above 35 mmHg may cause eye pain, decreased vision, nausea and vomiting.
The following is a discussion of some of the secondary glaucomas that you may hear of. It is not a complete list.
Inflammatory (Uveitic) Glaucoma
Chronic inflammation in the eye can be caused by trauma, disease, or even surgery. Inflammatory cells in the anterior chamber and/or synechiae can cause the IOP to rise. A synechia is an adhesion of the iris to either the lens (posterior) or to the cornea (anterior). An IOP rise can also be exacerbated by corticosteroid treatment of the inflammation.
Treatment involves using steroids to decrease the inflammation and cycloplegia (atropine, homatropine, cyclopentolate) to put the uvea at rest. Beta blockers and carbonic anhydrase inhibitors may be used to lower the IOP. These patients are followed closely until the inflammation subsides. |
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Neovascular Glaucoma
Neovascularization is the abnormal growth of new blood vessels. It is the response of the eye to decreased oxygen flow in certain tissues. Instead of providing more oxygen, neovascularization on the angle causes a web of neovascular tissue that blocks the meshwork. The neovascularization is most often caused by either a central retinal vein occlusion, or by diabetic retinopathy.
Treatment is aimed at preventing neovasularization to form in the angle, by means of laser panretinal photocoagulation. If neovascularization is established in the angle, treatment is difficult. A tube-shunt may be needed to try and save the eye. |
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Hemolytic Glaucoma
Material from an anterior or posterior chamber hemorrhage can block the trabecular meshwork, causing the IOP to rise. If standard glaucoma treatment is not successful at lowering the IOP, then a paracentesis (removal of fluid) with irrigation of the anterior chamber may be required. |
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Pigmentary Glaucoma
Pigment floating in the anterior chamber becomes clogged in the trabecular meshwork. The pigment is thought to come from the posterior iris rubbing against the zonules.
Upon examination with a slit-lamp, the pigment can be seen deposited on the surface of the lens and on the endothelium of the cornea (Krukenberg's spindle). The pigment can be seen in the angle with a gonio lens. If enough pigment is lost from the iris, light may transilluminate through the "holes" in the iris when a slit beam is used to illuminate the retina through the pupil (see images below).
Treatment may include the use of drops, laser peripheral iridotomy (PI), and argon laser trabeculoplasty (ALT). |
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In the photo directly above, notice that the slit lamp beam is directed from an acute angle, almost perpendicular, directly through the pupil. This transillumination technique illuminates the retina. The orangish light from the retina can then be seen shinning through the holes and thin places in the iris. Notice the area that the arrow is pointing to. The pigment has been rubbed off here and the iris is thin, allowing the light to come through. If you look at the photo above that is not transilluminated, it is difficult to see any difference in this area from the surrounding iris tissue.
At first glance it looks like the surgeon went crazy, creating multiple iridectomies in this iris, but the holes to the right and the left are related to the fit of the anterior chamber IOL in this eye. If you look closely, you can see the haptics of the IOL poking through the holes. |
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Pseudoexfoliation Glaucoma
Pseudoexfoliation material is a fibrillar material associated with an abnormality in the basement membrane of epithelial cells in various parts of the body. In the eye it is thought that it can be produced by the epithelium of the iris, ciliary body, or anterior lens. The material floats in the aqueous and becomes deposited on the structures of the anterior chamber. The material can block the trabecular meshwork, causing a rise in the IOP. The terminology differentiates it from exfoliation syndrome which is a "peeling off" of the anterior lens capsule caused by heat and infra-red radiation, as was experienced by glassblowers.
Using a slit-lamp, the material can be seen deposited on the anterior surface of the lens. With a gonio lens, the material may be seen in the lower trabecular meshwork. Treatment options may include drops, ALT, or a filtering procedure. |
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Some other causes of secondary glaucoma:
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Glaucoma in children is rare. Glaucoma present at birth is called congenital glaucoma. Glaucoma that develops from birth to age three is called infantile glaucoma, and glaucoma in a child older than three is called juvenile glaucoma.
Glaucoma in children may be secondary to another problem and may be associated with systemic conditions such as Sturge-Weber syndrome, neurofibromatosis, congenital rubella, Marfan's syndrome, and others. Congenital eye problems associated with glaucoma include include aniridia, persistent hyperplastic primary vitreous (PHPV), nanophthalmos, and microcornea. Isolated congenital glaucoma results from an abnormal development of the trabecular meshwork. |
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Because the sclera of an infant is very elastic, the eye will enlarge noticeably in response to a significant increase in IOP. The glaucomatous enlargement is called "buphthalmos" (cow eye). If there is a difference in IOP between eyes, the eyes may appear to be different sizes. The cornea may be opaque, and the eye may be tearing and photophobic, and there my be blepharospasm (eyelids squeezed closed).
The baby is examined under general anesthesia if congenital glaucoma is suspected. Under anesthesia the IOP can be measured, and gonioscopy and ophthalmoscopy can be performed. The cornea is measured and would normally be less than 10.5mm in an infant eye. Pachymetry can be used to confirm corneal edema and A-scan biometry can be used to confirm axial distention of the eye. |
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The primary treatments for congenital glaucoma are surgical. The procedures mechanically open the angle to increase outflow. The success rate is about 80% and the procedures can be repeated.
Standard medical and surgical glaucoma treatments may be needed after these procedures to control the pressure. |
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Chronic Angle-Closure Glaucoma (CACG)
CACG is a complicated type of glaucoma that involves an anterior chamber angle that has sections permanently closed by peripheral anterior synechiae (PAS). Subtypes of CACG include combined mechanism glaucoma, mixed mechanism glaucoma, plateau iris, and miotic-induced glaucoma. Discussion of CACG is beyond the scope of this module, but this type is mentioned so that you are aware of the terminology.
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