Maria Theresa Villaluz-Heyrosa M.D. VillaluzEye Diseases, Laser and Eye MicroSurgery Specialist 09200920-9093989

What is Glaucoma ?
‡ gradual death of the optic nerve, often associated with high intraocular pressure.

What causes glaucoma?
‡ Two of the main theories are: 1) increased intraocular pressure (pressure inside the eye) causing compression of the optic nerve or compressing its blood supply 2) vascular abnormalities causing lack of blood flow to the optic nerve.

How common is glaucoma? glaucoma?
‡ In 2000, an estimated 90.8 million people worldwide were affected with glaucoma. ‡ According to the Third Philippine National Survey of Blindness it is the third leading cause of bilateral blindness (after cataract and error of refraction) and the leading cause of irreversible bilateral blindness in the Philippines. ‡

Who are likely to develop glaucoma?
major risk factors: ‡ increased age, ‡ race ‡ a family history of glaucoma ‡ increased intraocular pressure.

Who are likely to develop glaucoma?
Other risk factors ‡ diabetes and hypertension, ‡ extreme myopia (near-sightedness) or hyperopia (far-sightedness), ‡ previous eye trauma ‡ prolonged use of steroids whether as eye drops, oral, nasal spray or inhaled. ‡ Smoking has also been implicated a risk factor for glaucoma (and other serious eye diseases as well) due to its deleterious effects on the blood vessels.

The Aqueous Pathway
1. Aqueous is first produced at the ciliary body, a ring of muscle behind the iris that produces aqueous and also controls the lens shape by pulling on zonules. Aqueous then fills up the posterior chamber (the area immediately in front of the lens and behind the iris). It then flows forward through the pupil into the anterior chamber. The anterior chamber is then filled and the fluid moves into the angle (the angle formed by the iris and cornea) and drains out the trabecular meshwork into the canal of Schlemm blood vessels.


3. 4.

Important Eye Findings to Dx Glaucoma
‡ elevated eye pressures ‡ optic disk changes ‡ repeatable visual field loss patterns.

Normal Eye Pressure
‡ usually considered 10 to 21 mmHg. ‡ many people with pressures of 22-28 that we describe as ocular hypertension who don¶t seem to manifest any glaucoma damage. ‡ there are many people with pressures under 21 who develop glaucoma. ‡ look at the ³big picture´ when determining if an eye pressure is ³normal.´

What causes increased intraocular pressure?
‡ Fluid circulates inside the front part of the eye (anterior chamber) in order to nourish certain structures and to wash away toxins. ‡ This fluid is constantly being produced and constantly being drained.

What causes increased intraocular pressure?
‡ Sometimes the fluid drainage pathway located in the anterior chamber angle malfunctions or becomes blocked. ‡ Despite this fluid production continues as usual. This causes fluid to build up within the eye and the intraocular pressure to increase.

most accurate way to measure IOP
‡ Goldman applanation tonometer

we measure how much force it takes to flatten a 3mm area of corneal surface.

‡ Goniolens: which is a special glass lens with mirrors on its sides, to look directly at the angle.


Diagrammatic representation of angle grading.
‡ A. The iris completely occludes the chamber angle. ‡ B. Although the lens-iris diaphragm is forward, the angle is still open to 10° (grade 1). ‡ C. A more open angle, though still occludable under certain circumstances (grade 2). Angles that are grade 2 or lower are considered capable of closure. ‡ D. A wide-open angle. The anterior chamber is deep and the iris flat, with no forward bowing (grade 3 or 4). These angles are judged to be incapable of closure. This is the most common anatomic appearance, best exemplified in a young, normal patient.

Composite cross-section and gonioscopic crossview of angle structures.


Optic Disc Changes

Visual Loss:
‡ can be followed by automated perimetry (machines that map out the peripheral vision). ‡ late stage patients may have 20/20 central vision, but be otherwise legally blind because of peripheral blindness.

Visual Field Changes

OpenOpen-angle glaucoma
‡ occurs from decreased aqueous drainage caused by an unidentified dysfunction or microscopic clogging of the trabecular meshwork. ‡ leads to chronically elevated eye pressure, and over many years, gradual vision loss. ‡ With prolonged high pressure, the ganglion nerves in the retina (the same nerves that form the optic nerve) atrophy.

Open Angle Glaucoma
‡ major risk factors are family history, age, race, high eye pressure, and large vertical nerve cupping, thin-corneas ‡ ³sneaky thief of sight´ because the visual loss occurs so slowly that many patients don¶t realize they have the disease until it is far advanced.

Symptoms of Open Angle Glaucoma
‡ At first, vision stays normal, and there is no pain; however, as the disease progresses, a person with glaucoma may notice his or her side vision gradually failing. ‡ That is, objects in front may still be seen clearly, but objects to the side may be missed. ‡ As glaucoma remains untreated, miss objects to the side and out of the corner of their eye. ‡ Without treatment, people with glaucoma will slowly lose their peripheral (side) vision and seem to be looking through a tunnel. ‡ Over time, straight-ahead vision may decrease until no vision remains. Glaucoma can also develop in one or both eyes.

ClosedClosed-angle glaucoma
- ³acute glaucoma,´ which occurs when the angle between the cornea and iris closes abruptly. -With this closure, aqueous fluid can¶t access the drainage pathway entirely, causing ocular pressure to increase rapidly. -This is an ophthalmological emergency and patients can lose all vision in their eye within hours.

Acute glaucoma
‡ most common mechanism is pupillary block. ‡ This occurs when aqueous fluid movement is hindered while moving forward through the pupil. ‡ This resistance produces a pressure gradient across the iris that forces the iris to move anteriorly. ‡ When the iris moves forward, the irido-corneal angle closes, blocking the trabecular meshwork. ‡ Without an exit pathway, aqueous fluid builds up, eye pressure increases rapidly, and the retina is damaged from stretching and decreased blood supply.

Acute glaucoma
‡ people with naturally shallow anterior chambers such as hyperopes (far-sighted people with small eyes) and Asians are predisposed to developing angle closure. ‡ One inciting condition that is typical in acute glaucoma is pupil dilation ² many patients describe onset of their symptoms occurring while in the dark or during stressful situations. ‡ When the iris dilates, the iris muscle gets thicker and the irido-corneal angle becomes smaller, making it more likely to spontaneously close. ‡ Along those lines, medications that dilate the eye, such as over-the-counter antihistamines and cold medications, also predispose angle closure.

Symptoms of Angle Closure Glaucoma
‡ ‡ ‡ ‡ Blurred vision Severe eye pain Headache Rainbow haloes around lights ‡ Nausea and vomiting

‡ Since IOP is the only risk factor we can treat, the primary treatment of glaucoma focuses on decreasing eye pressure to less than 20 mm Hg or even lower depending upon the severity of disease. Treatment may be either medical or surgical.

Medical Treatment
‡ Topical beta-blockers are the traditional therapy ‡ Beta-blockers work by decreasing aqueous humor production at the ciliary body. ‡ systemic side effects can occur from nasal absorption, making it especially important to ask your patients about history of asthma, COPD, and cardiac problems. ‡ topical CAIs, alpha-agonists, and prostaglandin analogues for first-line therapy, as they have fewer systemic side effects.

Surgical Treatment
Trabeculectomy: ‡ where an alternate drainage pathway is surgically created. A small hole is cut through the superior limbus, creating a drainage tract from the anterior chamber to a space under the conjunctiva. Laser procedures ‡ Argon laser trabeculoplasty (ALT) can be used to burn portions of the trabecular meshwork itself. The resulting scarring opens up the meshwork and increases outflow. ‡ used to burn away part of the ciliary body to decrease aqueous production


Nd: YAG laser iridotomy performed superiorly

Neovascular Glaucoma
‡ This can occur in diabetic patients or those with an old retinal vascular occlusion. ‡ VEGF production from areas of ischemic retina can float forward through the pupil and promote neovascularization of the iris. ‡ At later stages of neovascularization, the new vessels actually pull the iris forward and cause a closed angle glaucoma that is essentially irreversible.

Pigment Dispersion Syndrome (PDS)
‡ Occurs when the pigmented back-surface of the iris rubs against the radial zonules supporting the lens. ‡ Little flecks of pigment are shed into the aqueous and end up clogging the trabecular meshwork drain. ‡ can see pigment in the TM via gonioscopy and you can also find trans-illumination defects in the thin iris itself. ‡ Some of the pigment will stick to the innercorneal surface, and because of convection currents in the aqueous, form a vertical line of pigment on the inner corneal surface called a Krukenberg spindle.