Contents:

Title	Date	Author
Good News for Macular Degeneration Patients	May 2007	Andrew Henrick, M.D.
Accommodative Intraocular Lens Implants	Nov 2005	Andrew Henrick, M.D.
South Coast Eye Care Centers Offers Excellence in Laser Vision Correction	Oct 2005	Paul Prendiville, M.D.
Laser Vision Correction in 2005	Jan 2005	Holly Spanggord, M.D.
Dry Eye Syndrome: Treatment Options for A Complex Condition	Jan 2005	Holly Spanggord, M.D.
Lose Those Wrinkles!	July 2004	Andrew Henrick, M.D.
New Developments in Macular Degeneration Research	Mar 2004	James R. Brinkley, Jr., M.D.
Vision Improvement After Cataract Surgery	Oct 2003	Andrew Henrick, M.D.
Diabetic Retinopathy	Jul 2003	James R. Brinkley, Jr., M.D.
The Nature and Treatment of Cataractous Visual Loss	Apr 2003	Paul Prendiville, M.D.
New Laser Vision Correction Procedures for Very Near-Sighted Patients	Jan 2003	Holly M. Spanggord, M.D.
A Revolution in Glaucoma Treatment? Perhaps Not!	Oct 2002	James R. Brinkley, Jr., M.D.
Dr. Holly Spanggord to Join South Coast Eye Care	Jul 2002
What's New In Glaucoma Treatment	Apr 2002	Andrew Henrick, M.D.
New Procedure Adds Refractive Surgical Option	Jan 2002	Paul Prendiville, M.D.
Important News for Macular Degeneration Patients	Oct 2001	James R. Brinkley, Jr., M.D.
Dr. Henrick Elected President of California Academy of Ophthalmology	Oct 2001
Dr. Brinkley Honored by U.S.C.	Jul 2001
New Advances in Contact Lenses	Apr 2001	Cathy Hull, C.O.T.
What Can I Do About My Droopy Eyelids?	Jan 2001	Andrew Henrick, M.D.
South Coast Eye Care Centers Using a New Laser Vision Correction Facility	Oct 2000	Paul Prendiville, M.D.
Colored Contact Lenses	Apr 2000	Denise Levin, C.O.M.T.
The Mid-Face Lift	Jan 2000	Andrew Henrick, M.D.

July, 2004

Return to Top

New Developments in Macular Degeneration Research
by
James R. Brinkley, Jr., M.D.

Age Related Macular Degeneration (ARMD or AMD) is the leading cause of legal blindness in our nation in people over the age of 65. As the baby boomers approach senior citizen status, ARMD is rapidly becoming a major public health crisis. Consequently, a great deal of effort and money is being invested in investigating potential cures and/or preventions.

The retina is the lining inside the back of the eye, analogous to the film in a camera. However, although the film in a camera is uniform, the retina has a very small, specialized area in the center called the macula. Its full name is macula lutea, which means yellow spot. It is yellow because it contains lutein. I’ll have more to say about lutein later.

The macula has one of the highest metabolic rates of any tissue in the body and therefore has a high demand for oxygen, nutrients, and the removal of waste products. Although the cause of ARMD is unknown, there is speculation that it may be due to a failure of the microcirculation that supplies the macula. It is well known that cigarette smoking, which causes damage to small blood vessels throughout the body, is a very high risk factor for ARMD. Even former smokers have a much higher risk than non-smokers, although quitting does significantly reduce the risk compared to that of current smokers. There may be a genetic predisposition as well, although certain epidemiological studies have failed to prove this.

There are two main types of ARMD: atrophic and exudative, popularly known as “dry” and “wet.” Wet refers to the fact that there is either bleeding or leakage of fluid (serum) from abnormal blood vessels beneath the macula. Dry means there is no such fluid or blood present. The dry (atrophic) type usually has the better prognosis, progressing slowly and only occasionally reducing vision to the level of legal blindness. The wet type of ARMD, however, often causes a sudden dramatic loss of vision, usually in one eye at a time.

At the present time the only approved treatment for dry (atrophic) ARMD is a specific combination of vitamins and minerals, shown in the Age Related Eye Disease Study (AREDS) to slow the progression of the disease in certain very specific types of dry and wet macular degeneration. This combination is available commercially as Ocuvite Preservision. Lutein was not included in this study and we do not yet know if taking supplemental lutein might be beneficial. It has been suggested that taking supplemental lutein might block the absorption of natural lutein from the digestive tract. Therefore I advise my patients not to take it but instead to eat fruits and vegetables rich in lutein. These include corn, kiwi fruit, red seedless grapes, zucchini squash, and spinach. Egg yolks are also high in this nutrient.

There are two approved treatments for exudative (wet) ARMD. Traditional LASER (Light Amplification by Stimulated Emission Radiation) can sometimes be used to destroy abnormal blood vessels beneath the macula. This treatment cannot be used if the vessels are under the center of the macula (called the fovea) because the visual cells (photoreceptors, also called cones and rods) are destroyed as well. A newer type of laser, called photodynamic therapy (PDT) or Visudyne Therapy can be used in a limited number of cases to slow the progress of the disease when the abnormal blood vessels are beneath the center of the fovea. Unfortunately, even these two therapies can offer help to only a very small number of people with wet ARMD.

Fortunately, there are some exciting new advances under investigation. Some of these may be approved for general use within the next few years. Investigational therapies for atrophic (dry) ARMD include laser prophylaxis of drusen, intra-ocular telescopes, retinal implants, and retinal transplants.

Drusen are yellowish deposits beneath the macula, which are often the first sign of macular degeneration. One type of drusen, called soft drusen, is often a predictor of the development of exudative (wet) ARMD with possible sudden loss of vision. In an effort to prevent the progression of dry ARMD with soft drusen to wet ARMD, researchers are trying to destroy the drusen with a laser. This treatment is called laser prophylaxis of drusen. Initial studies a few years ago showed that while the drusen were destroyed, the incidence of progression to wet ARMD actually increased. Now some scientists believe this happened because the energy used in the laser treatments was too high. Current studies are attempting to use lower laser energy, called sub-threshold laser. Initial results are very promising with not only a reduction in the number of drusen but also with an actual improvement in vision.

Several of my patients have sent me forms to fill out so that they might enroll as subjects in a trial of intra-ocular telescopes. In this study, a lens (similar to the lens implant used in cataract surgery but of much higher power) is surgically placed inside the eye. In conjunction with another lens mounted in an eyeglass frame, a telescope is created. While this sounds like a good idea, whenever I am asked about it I discourage my patients from enrolling in this study. The problem with the concept is that while the telescope magnifies things so that they may be more easily seen, it also drastically reduces peripheral vision, often making it difficult to walk, let alone perform more complex tasks. This concept was actually tried over twenty years ago and failed for this same reason.

Retinal implants are tiny computer chips inserted into the eye surgically. They are designed to bypass the function of the diseased retina by capturing incoming light and converting it to electrical impulses. These in turn are passed to the optic nerve to be carried to the brain. The concept shows initial promise but the technology required for useful sight is still probably at least a decade or two away.

Retinal transplants were long thought to be impossible but of course, nothing is impossible. Recently, retinas have been successfully transplanted in experimental animals. The transplanted retinas actually survive in the host. The problem has been that so far, researchers have been unable to establish connections between the transplanted retinas and the optic nerve, so no visual signals are actually sent to the brain.

Investigational therapies for exudative (wet) ARMD include Transpupillary Thermotherapy (TTT), Feeder Vessel Therapy, Rheotherapy, Drug Therapy, Gene Therapy, Radiation Therapy, and innovative surgical procedures.

In Transpupillary Thermotherapy, a low power diode laser is used to heat the abnormal blood vessels beneath the macula without actually coagulating them, therefore sparing the overlying rods and cones. Initial results are promising, although much work remains to be done. In feeder vessel therapy, a complicated device called a Scanning Laser Ophthalmoscope is used to try to identify the single blood vessel of origin feeding all the other abnormal vessels. If such a vessel is found, a laser can close it, cutting off the blood supply to the abnormal tissues. Although there have been some successes, unfortunately this technology is extremely expensive and difficult to use. In rheotherapy, the patient’s blood is actually removed form the body, cleansed of high molecular weight proteins, and then replaced. This is done using equipment very similar to that used in renal dialysis for patients with kidney failure. The idea is that the large proteins accumulate in the blood, blocking the transport of nutrients to the macula and the transport of waste products away from it.

Gene Therapy for wet ARMD sounds like science fiction but the first human clinical trial is actually underway in Oregon. Drug therapy may also sound far-fetched but several very promising drugs are in development. Some of these are designed for injection into the eye and some are actually being developed in oral (pill) form! Radiation therapy has been shown in the past not to be helpful and in fact, even to accelerate the progression of wet ARMD. However, new studies, using different types and doses of radiation, are currently underway.

Aggressive and complicated surgical procedures have been designed in recent years to treat exudative (wet) ARMD. Unfortunately, these are extremely complex, very expensive, and have a very low rate of success. However, since a few individuals have benefited from this approach, some clinical trials are still in progress.

In summary, there is aggressive ongoing research into the treatment of ARMD on many fronts. Some of this research should begin to result in available therapies within the next few years. Meanwhile, we recommend that everyone over 65 should have yearly eye examinations with an ophthalmologist, stop smoking, and if your ophthalmologist says you are a candidate, consider taking the nutritional supplements studied in AREDS. Please continue to check our web site for new developments.

Return to Top

A cataract is the clouding of the natural lens of the eye, which focuses light onto the back of the eye. When cataract surgery is performed, the cataractous lens is removed. If it were not for lens implants, the vision after cataract surgery would be very blurred because of the absence of a focusing lens. An intraocular lens (IOL) is a focusing lens made of a synthetic, inert material that is implanted into the eye at the time of cataract surgery. It is placed permanently inside the eyeball in the approximate position occupied by the natural lens. Except in very rare instances, the implant never needs to be replaced.

Many patients ask, "Will I need to wear glasses after my cataract surgery with lens implant?" The answer depends on a number of factors, but in general, glasses will be necessary at least part-time for best vision. Most lens implants available today are single focus. That means that they are focused at some predetermined distance, usually far distance. In this case, near vision will be blurred without additional reading glasses. When cataract surgery is performed on both eyes, most people opt to have both lens implants focused for distance so that driving and sports don’t require additional use of glasses. Reading glasses are then worn for near tasks such as reading, crafts, and computer work. Patients who spend a large part of their day doing near work may decide to have both eyes focused at near and wear glasses for distance vision only. Some people may be comfortable with monovision, one eye focused at distance and the other at near. Then glasses need not be worn at all but there may be some visual confusion. Additionally, people with pre-existing astigmatism (an irregular curvature of the cornea, the clear front part of the eye, which results in blurred vision) will not have clear vision without glasses since most lens implants do not correct for this condition. If astigmatism is present after cataract surgery, laser vision correction (LASIK) may be considered to eliminate this condition.

New lens implants are being developed that compensate for some of the shortcomings of current vision rehabilitation following cataract surgery. But as so often happens, one problem is solved only to have a new one surface! Here is a listing of some new developments:

• IOLs that correct for astigmatism. These lenses must be aligned precisely inside the eye. Unfortunately they don’t always stay put and rotate inside the eye as the healing process takes place. The result is blurred vision necessitating another operation to reposition the lens.
  
• Bifocal IOLs. These lenses are a good idea but don’t work like bifocal glasses where the eye looks through a different lens for distance and near by shifting position. Since the IOL does not move inside the eye, both near and distance powers are placed in the center of the lens. The patient thus looks through both lenses simultaneously. Both near and distance images are focused onto the back of the eye and the brain must choose which one to concentrate on. Some patients have difficulty adjusting to this arrangement and may even see halos around lights, making night driving difficult. Some people have even undergone second surgeries to replace the bifocal IOL with a conventional one!
  
• IOLs that can change focus inside the eye. Very flexible lenses are being developed that can move inside the eye ever so slightly when the internal focusing muscles of the eye contract, allowing the lens to focus near, far, and in between as the need arises. Sounds promising but the jury is still out on this one.
  

No IOLs exist that can correct for both astigmatism and focusing. With any of these new lenses, glasses might still need to be worn for some situations. The current standard of practice is to use single focus IOLs. For selected patients, one of these new technology lenses may be appropriate. It is best to discuss the choice of IOL with your ophthalmologist when cataract surgery is contemplated. But in any case, it is prudent to expect to wear glasses at least some of the time following cataract surgery.

Return to Top

July 2003

Prior to the development of insulin in 1922, Type I diabetes was a fatal disease. Even today it is fatal in many third world nations, where insulin is not readily available. Because diabetics did not live long, severe diabetic complications in the eye, the kidney, and other target organs were rare. In addition, since most diabetics did not live into their reproductive years, the diabetic gene pool was limited. There are now 150 million people with diabetes worldwide. This number is expected to grow to 300 million by 2025. 90% are Type II diabetics, virtually unknown until the twentieth century.

Today diabetic retinopathy is the leading cause of blindness among working age people in the United States. While Type I diabetics are more at risk for totally blinding ocular complications, Type II diabetics can also suffer severe visual loss, often to the point of legal blindness.

The retina is the inner lining of the back of the eye, analogous to the film in the camera. It converts incoming light into signals that travel along the optic nerve to the brain, allowing us to see. Damage to the retina from diabetes is called diabetic retinopathy. There are two major types of diabetic retinopathy, as well as an intermediate type.

Non-Proliferative Diabetic Retinopathy (NPDR), sometimes called Background Diabetic Retinopathy, includes the first signs of eye damage from diabetes. Weak spots in the tiny capillaries of the retina appear as tiny red dots. These capillary weak spots are called microaneurysms. Some of them rupture and bleed, producing small "dot and blot" hemorrhages in the retina. These hemorrhages alone do not cause visual loss but they do indicate that the diabetes may not be under optimal control.

As more capillary damage occurs, serum begins to leak from the capillary walls. This serum collects in between the cells of the retina. When serous fluid collects in the interstitial (between the cells) space in living tissue, the resultant swelling is called edema. The central portion of the retina, responsible for our sharp central vision, is called the macula. Consequently, swelling of the macula from the accumulation of serum in the interstitial space is called macular edema. Macular edema is one way that diabetic retinopathy reduces vision. It can occur in anyone with diabetes but it is more common in Type II diabetics.

When macular edema occurs, a diagnostic test called a fluorescein angiogram can determine exactly which capillaries are leaking and where. Then a laser can be used to seal these leaks. Once the leaks have been sealed , the serous fluid is slowly absorbed, the edema reduced, and in some cases, vision is restored. Unfortunately, sometimes lipid material in the serum precipitates out and accumulates in the macula, causing permanent damage to the visual cells (rods and cones). Although sealing of capillary leaks with the laser can lead to absorbtion of the exudates; cellular damage, and therefore vision loss, is often permanent.

When the capillary damage becomes severe enough, the retina becomes ischemic, meaning severely deficient in oxygen. The tissue responds by elaborating a chemical called Vascular Endothelial Growth Factor (VEGF), which stimulates the growth of new blood vessels called neovascularization. Since new vessels are proliferating, this is called Proliferative Diabetic Retinopathy or PDR. It might seem that the growth of new blood vessels would be a good thing. Unfortunately, these vessels are abnormally fragile. They have a tendency to rupture, producing large hemorrhages that can fill nearly the entire eye. These are referred to as vitreous hemorrhages, because they fill the vitreous cavity. Vitreous hemorrhage is the second way diabetes can cause blindness. This problem can occur in anyone with diabetes but it is far more common in Type I diabetics.

Once neovascularization occurs, it can be halted, and even made to regress, with a laser treatment called pan-retinal photocoagulation or PRP. In this treatment a large number of laser burns (often as many as 2,000) are placed in the peripheral retina. These burns are absorbed by the layer under the retina, which is called the Retinal Pigment Epithelium (RPE). The RPE subsequently becomes thinner allowing more oxygen to reach the retina from the choroid, the vascular layer beneath the RPE.

If the neovascularization is not discovered in time and a vitreous hemorrhage occurs, it usually will clear. However, if there is repeated bleeding, eventually the eye remains filled with blood and the vision is lost. In such a case, an operation called vitrectomy allows the blood, along with the vitreous gel, to be removed from the eye and vision to be restored.

Whenever new blood vessels grow within the eye, they are accompanied by a sheet of supporting tissue. This is fibrous tissue. Fibrous tissue is similar to scar tissue and over time, it always shrinks. When the fibrous tissue accompanying retinal neovascularization shrinks, it can tug on the retina and eventually cause a traction retinal detachment or TRD. TRD can also be repaired using vitrectomy surgery. After the vitreous gel (and any old blood) is removed, the attachments of the fibrous tissue to the retina can be severed, allowing the retina to settle back into place.

Sometimes, there is an intermediate stage between NPDR and PDR, called pre-proliferative diabetic retinopathy. This is when the retina can be shown to be severely lacking in oxygen supply by demonstrating large areas of capillary death (dropout) on a fluorescein angiogram. In this situation, the eye is at very high risk of developing neovascularization and the patient must be seen more frequently so that laser treatment can be carried out as soon as significant new blood vessel growth appears. If the capillaries in the macula drop out (die), the visual cells in the macula also die from lack of blood supply and vision is lost. In this situation, there is nothing that can be done to restore it.

In summary, diabetic retinopathy can reduce vision in four ways: macular edema, hemorrhage from new blood vessel growth, traction retinal detachment, and loss of the blood supply to the macula. We have treatments for the first three and new treatments are on the horizon. Drugs that inhibit VEGF are being developed that may be injected into the eye or even taken in pill form. Gene therapy is in the very early stages of development. Some day we may have a cure for the diabetes itself or even a way to prevent it.

For now, prevention of the retinopathy is the best approach. It has been conclusively demonstrated that rigid control of the blood sugar can prevent sight threatening diabetic retinopathy. This involves very hard work on the part of the diabetic individual. Rigid adherence to diet, weight loss, exercise, frequent testing of blood sugar, and adjustment of medication dosage in response to the test results are all necessary to achieve the rigid blood sugar control required to prevent diabetic retinopathy from progressing. For many, this means multiple blood tests and even multiple insulin injections daily. For some, an insulin pump is required. However, the results are well worth the effort: a long, healthy life with all the joys of normal sight, our most precious resource.

April 2003

A cataract is an opacity in the natural lens with which we are born. Cataract is the leading cause of mild visual loss in this country and fortunately is correctable with safe, highly effective surgery. The removal of a cataract is the most commonly performed out-patient surgery, and technological advances have made surgery much less disruptive to patients.

Visual loss due to cataract is characterized by blurring. The earliest symptoms may include difficulty with night vision, glare, and/or halos around lights. The most common type of cataract is known as nuclear sclerosis. It is associated with aging and prolonged exposure to ultraviolet light. This type of cataract in the earliest form sometimes causes an increased ability to see objects up close. This paradoxical increase in vision is commonly known as "second sight." Other types of cataract display different characteristic symptoms. For instance, a posterior sub-capsular cataract often occurs earlier in life than a nuclear sclerotic cataract and may cause vision loss more rapidly. This type of cataract makes it more difficult to see up close. It can be associated with the use of certain medications and systemic medical diseases.

How does cataractous visual loss occur? Light rays travel through several structures of the eye before being translated into nervous impulses. They first encounter the cornea. The cornea is now commonly operated on to obviate the need for eyeglasses using laser vision correction methods like LASIK. Next light travels through the pupil. The pupil is the opening in the center of the iris, and the iris is colored part of the eye. The natural lens follows, and it is subject to opacification, which leads to cataractous visual loss. After passing through the lens, light travels through the large vitreous cavity. The vitreous is often associated with it's own opacities which are commonly known as vitreous floaters. Finally the light arrives at the retina where it is translated into nervous impulses which are sent via the optic nerve to the brain.

Thus cataractous change occurs just behind the iris. This is why the evaluation of cataract involves pupil dilation. Dilation of the pupil causes the iris to open widely and allows the ophthalmologist to evaluate the cataractous lens more carefully. Other important examination techniques in the evaluation of cataract include eyeglass measurement and careful examination of the optic nerve and retina. Each of these are included in a routine complete eye examination.

The initial treatment for cataractous visual changes is usually a change in eyeglasses. Typically when there is a change in vision associated with cataract, a new pair of eyeglasses will help to restore vision to an acceptable level. When vision cannot be restored to an acceptable level, cataract surgery should be considered. The decision for cataract surgery hinges on what acceptable vision is for a given patient. This is quite variable and must be considered on an individual basis. An airline pilot or a bus driver would have a greater need for sharp vision than a person who doesn't drive a car. Careful consideration of a person's visual needs relative to their lifestyle and activities of daily living by the surgeon and patient is necessary in the decision for surgery. Cataract surgery is almost never an urgent matter, and therefore there is almost always plenty of time for consideration of how a decrease in vision is affecting a patient's quality of life. Although the risk of cataract surgery is minimal, it is not completely risk free, so the decision for surgery must be made very carefully.

Once the decision for cataract surgery to be performed has been made, several things must occur. These include selection of an intraocular lens and a visit to one’s private medical doctor. The removal of a cataractous lens leads to a large decrease in the ability of the eye to focus light. A replacement artificial lens is placed in the eye at the time of surgery to restore that focusing power. The lens is chosen based on the shape of the cornea and the length of the eye. An attempt is made to choose a lens that will obviate or at least decrease the need for eyeglasses. This cannot always be done if conditions like astigmatism are present. A visit to the patient’s private medical doctor is needed to ensure that general health is sufficient to undergo the minimal medical stress associated with surgery. This visit should be timed within a month from the operation.

The evening prior to surgery antibiotic eye drops are sometimes used to help prevent the risk of infection during surgery. No food or water should be taken after midnight on the evening prior to surgery, and loose, comfortable clothing should be worn to the surgery center. The stay at the surgery center is usually about three hours, and the patient is sent home with the operated eye patched. This patch should be left on until the visit to the doctor’s office on the first postoperative day. Arrangements should be made to have a ride to and from the surgery center and the first postoperative appointment.

Usually three postoperative visits are needed, and these visits occur at one day, one week, and one month. Aftercare involves the use of two or three eye medications, keeping the eye dry, limitation of strenuous activity, and the use of a shield over the eye while sleeping. At the last postoperative visit, a measurement for eyeglasses is performed. Hopefully all would have gone well and a significant increase in vision will be noticed.

Modern cataract surgery is highly successful and although it is not without risk, it is extremely safe. With careful consideration for the timing of surgery and careful postoperative follow-up, a successful surgical outcome is almost always enjoyed by the patient.

January 2003

Current laser technology is optimal for the vast majority of patients who want to decrease their dependence on glasses and contact lenses, including myself. I had LASIK done over a year ago and see 20/25 in my right eye and 20/20 in my left eye without correction. Nonetheless, new laser vision correction procedures are adding to our options for patients who are not candidates for LASIK eye surgery. LASIK (which is an acronym for Laser-assisted-in-situ-keratomileusis) involves cutting a flap in the cornea prior to performing a laser ablation. It is this laser ablation of the cornea that reduces the need for corrective lenses. When the flap heals, it is not as strong as the original uncut cornea. Usually this isn’t a problem because the flap is very thin compared to the overall thickness of the cornea. However, patients with high myopia (that is, very nearsighted people) require a lot of laser correction, resulting in very thin corneas. Patients with thin corneas are more at risk for corneal weakening after LASIK and should not undergo this procedure.They may suffer corneal ectasia (an outward bulging of the cornea) after LASIK, resulting in a reduction of vision even with corrective lenses.

Until recently these patients have been advised to avoid laser corrective surgery. However, if the creation of a flap can be avoided, a great deal of corneal weakening can be prevented. Photorefractive Keratotomy (PRK) is an established procedure that avoids creating a flap. Only the very superficial layer of corneal cells (the epithelial layer) is removed prior to performing the laser corrective ablation, leaving a stronger, thicker cornea even in very near-sighted patients requiring a deep ablation. This procedure, although slightly more uncomfortable, is just as accurate as LASIK. In the recent past, it has not been offered to very nearsighted patients because they have been more at risk for post-operative corneal haze or scarring. This scarring can lead to reduced vision even with corrective lenses.

Fortunately, an exciting new development addresses this problem. Refractive surgeons have discovered that mitomycin C, a medication used to prevent scarring in other types of ocular surgery (glaucoma and pterygium surgery), can also prevent scarring after PRK. When used as described in an article published in one of our most respected journals (Ophthalmology, January 2000 issue, Volume 107, pp. 89-94), this medication has been very effective with very few complications. For patients with haze or scarring from a previous PRK surgery, this medication can also be used to prevent recurrence after removal of the haze or scar with the laser.

A few patients treated to prevent haze have suffered over-corrections after the laser procedure and have needed a second“touch-up” treatment after the original procedure. Consequently, many refractive surgeons are adjusting their formulas for laser correction when treating patients who need mitomycin C since the final result is not as predictable as that after traditional PRK without the use of this medication. Although this new technique appears to be safe, we have only 5 years of experience, and it is impossible to be completely sure that future corneal problems will not develop many years later.

A second option is also available for very nearsighted patients. LASEK (Laser-Assisted-In-Situ-Epithelial-Keratomileusis) is exactly like PRK except the epithelium is preserved instead of discarded. Instead of scraping off the epithelium and allowing it heal post-operatively, the epithelium is carefully pulled aside prior to performing the laser procedure. After the laser ablation is completed, the epithelial layer is carefully replaced. This replacement of the epithelium may reduce some of the postoperative discomfort after PRK.

Does this replacement of the epithelium prevent the scarring and haze formation we see after deep laser treatments performed in PRK? At this point in time, we do not know. Since the two procedures are so similar, many refractive surgeons are also recommending the use of mitomycin C for patients who are very nearsighted and have chosen to undergo LASEK.

Patients with high myopia who are not candidates for even these procedures soon may benefit from an implanted intra-ocular lens. This technique involves inserting a lens through an incision into the eye without performing a laser ablation on the cornea. Although not yet approved by the FDA, this procedure may soon be an additional option for these patients.

Certainly, as refractive surgical technology continues to evolve, the variety of surgical options will broaden. Similarly, our established procedures will evolve as we gain experience. In this rapidly advancing specialty, there always seems to be something new just over the horizon.

October 2002

When the results of the Ocular Hypertension Treatment Study were published in the June 2002 issue of the Archives of Ophthalmology, some in the press reported that there would be a revolutionary change in the way patients with Ocular Hypertension (elevated pressure inside the eye) are managed by ophthalmologists. Some of our patients have read these reports and have urged us to provide them with medication. Is this the right thing to do?

Glaucoma is a disease of the optic nerve, the nerve that carries visual signals from the eye to the brain. In glaucoma the optic nerve sustains gradual progressive damage of a very characteristic type. This damage in turn produces irreversible vision loss, which begins in the periphery and slowly progresses toward the center over many years. The nerve damage can be detected with a dilated eye examination and documented with photographs. The resulting vision loss can be detected with visual field testing long before it is noticeable to the patient.

Since most cases of glaucoma are caused or accelerated by elevated intraocular pressure, loss of vision can usually be prevented by lowering the pressure with medications. Individuals who have ocular hypertension without optic nerve damage are said to be Ocular Hypertensives or Glaucoma Suspects. There has long been a therapeutic controversy: should ocular hypertensives be treated with medication in an attempt to prevent or delay the onset of glaucoma?

Traditionally, a majority of ophthalmologists have followed ocular hypertensives (glaucoma suspects) closely without treatment, measuring their intraocular pressures several times a year and performing a visual field test and a dilated eye examination to visualize the optic nerves at least once a year. At the first sign of glaucoma, they begin therapy. A minority of ophthalmologists place ocular hypertensives on medication, even though they do not have glaucoma. They do this in the belief that by lowering the pressure, they can prevent glaucoma, or at least delay its onset. Which approach is best?

The Ocular Hypertension Treatment Study was designed to answer this question. It did so by recruiting a large group of people with elevated eye pressure but without glaucoma and dividing them into two groups. One group was carefully observed and the other group was treated with pressure lowering medications. Over the five years of the study, twice as many people in the observation group developed glaucoma as compared to the treatment group. At first glance, it would seem that the minority approach to the problem is the better one. So we should be treating everyone with elevated pressure. Or should we?

It is very important that scientific studies be carefully read and analyzed, lest we draw the wrong conclusions. Careful analysis of the Ocular Hypertension Treatment Study reveals that approximately 10% of the observation group developed glaucoma within the five years of the study, while only 5% of the treated group did so.

Let’s put this information in perspective. Given that glaucoma is a very slowly developing disease and that at the first sign of it, starting treatment prevents any significant loss of vision, is there really anything to be gained from“preventive” treatment? If a person with ocular hypertension receives treatment, (s)he has a 95% chance of NOT developing glaucoma within five years but if (s)he is observed, (s)he still has a 90% chance of NOT developing glaucoma. Another way to state this is that if ocular hypertensives are treated with medication, 95% of them will be wasting their time and their money.

Consider the cost. Based on the average price of a bottle of the most commonly used glaucoma medications, each patient will spend about $600.00 dollars every year (or $3,000.00 over the five year study period) to improve their chances of NOT developing glaucoma from 90% to 95%!

Consider possible side effects. While the medications are very safe, there have been reports of severe reactions in people with certain heart and lung conditions, in very rare cases even death!

Certain groups of people have long been known to be at increased risk for glaucoma and most ophthalmologists already recommend early treatment for these groups. They include people of African-American race, people with a strong family history of glaucoma, and people who have intra-ocular pressure readings over 30.

In our practice, we ask the patient to participate in the decision. Some patients choose medication but they understand that they may never get glaucoma and therefore may be wasting their time and money and exposing themselves to possible medication side effects. Most patients choose observation and they understand that they run a small risk of minimal but permanent visual loss before we confirm that treatment is necessary. They are willing to take this small risk to avoid the expense of treatment and its possible side effects.

The first thing that all medical students learn is: “primum non nocere,” which is Latin for above all, do no harm. This means that if a proposed treatment is not clearly better than no treatment, we should not use it. As we have seen, for those people without increased risk factors, treatment of ocular hypertension is neither cost-effective nor clearly beneficial. Those people with strong risk factors are already being treated. So the results of the Ocular Hypertension Treatment Study will probably not lead to any real change in the practice of ophthalmology after all!

July 2002

Holly M. Spanggord, M.D.

The physicians and staff of South Coast Eye Care Centers are very pleased to announce that Holly M. Spanggord, M.D. will join our practice on August 1, 2002. She will practice general ophthalmology with a subspecialty emphasis on corneal and refractive surgery, including corneal transplants, LASIK, PRK, LASEK, and other types of refractive surgery. She will be one of a very few fellowship trained corneal and refractive surgeons in south Orange County.

Dr. Spanggord did her undergraduate work right here in south county. She graduated from U.C.I cum laude and she received two Bachelor's degrees, one in biology and one in psychology. She received her medical education at the University of California, San Francisco, where she was awarded the M.D. degree in 1997. While in medical school, she received two awards for outstanding medical research. She went on to serve her internship in general medicine at Mount Zion Hospital in San Francisco.

Dr. Spanggord completed her residency in ophthalmology at the Cullen Eye Institute of the Baylor College of Medicine in Houston, Texas. She then went on to complete an optional fellowship in corneal and refractive surgery at the prestigious Rush-Presbyterian-St. Luke's Medical Center in Chicago, Illinois.

Dr. Spanggord has published three original research papers in peer reviewed medical journals and she has presented the results of some of her research at three major medical meetings. She has performed hundreds of cataract, corneal transplant, and refractive surgery procedures. She will live in Aliso Viejo.

All of us at South Coast Eye Care join in welcoming Dr. Spanggord to our practice. She will be a valuable asset in our ongoing mission of providing ethical patient care of the highest quality in a friendly and pleasant setting.

April 2002

What is glaucoma?

Glaucoma used to be thought of as a disease of uncontrolled pressure in the eye which over many years results in damage to the optic nerve and eventually in permanent loss of vision. The optic nerve conducts the image captured by the eye to the brain via electrical impulses, much like a cable brings the TV signal to a TV. The optic nerve contains one million tiny nerve fibers, each one connected to a different part of the retina in the back of the eye. The retina acts much like the film in a camera, capturing the image. In glaucoma the optic nerve is damaged and individual nerve fibers begin to drop out. Eventually the image seen by the brain is degraded and gaps occur in what is seen. This damage is permanent. There are actually at least 70 types of glaucoma but only the most common type, Primary Open Angle Glaucoma, will be discussed.

We now know that pressure is not the only story. Other factors such as blood flow to the eye, and genetically programmed “suicide” of cells also play a role. How else can we explain why some people with high eye pressure do not develop optic nerve damage while others with normal, or even low, pressures do. We now define glaucoma as a disease of the optic nerve which results in gradual permanent loss of optic nerve fibers, and hence vision, sometimes (but not always) associated with high eye pressure.

Why does the eye pressure go up?

The pressure in the eye must be higher than the air (atmospheric) pressure in order for the eye to maintain its ball shape. If the pressure were the same as that of the atmosphere, the eye would collapse! There is a constant circulation of fluid inside the eye. This is not the same as tears! In order to better understand this concept, it may be beneficial to think of the eye as a closed tank with a faucet letting water run in and a drain allowing water to run out. As long as the inflow of water equals the outflow, the pressure in the tank remains constant. But now suppose that the drain becomes partly clogged so that the inflow is greater than the outflow. Eventually the pressure in the tank increases. This is exactly what happens in the eye. Through age or disease the drainage system becomes partly obstructed and the pressure rises.

Can glaucoma be cured?

No! Unfortunately a cure has not been discovered. But the disease can be controlled, requiring a lifetime of treatment and medical follow-ups, just like high blood pressure.

How is glaucoma treated?

Although pressure is not always elevated in glaucoma, treatment is geared towards lowering pressure. No effective treatment exists to date to protect the optic nerve from further damage other than pressure lowering. It has been definitely shown that lowering pressure prevents further damage to the nerve. The goal of treatment is to lower pressure 20 to 30 percent, or more, from baseline untreated levels. In the vast majority of cases, this can be accomplished using eye drops. There are different classes of eye drop medications which may be used alone, or in combination, to achieve the desired pressure. They basically break down into two groups, those that decrease inflow of fluid into the eye, effectively turning down the faucet, and those that increase outflow of fluid from the eye, thus enlarging the drain. In addition to penetrating the eye, eye drop medications may also be absorbed into the blood stream and have an effect on the body. Be sure to ask your doctor about any side effects or drug interactions if you use such drops.

When eye drops fail to control the pressure adequately to prevent nerve damage, surgery in the form of laser or “drainage” procedures may become necessary. In the former, the laser beam is aimed at the drain in the eye to try to make it work better. In the latter, a small opening is made in the wall of the eye to allow the intra-ocular fluid to escape into a small reservoir fashioned on the outside of the eyeball. The excess fluid is then absorbed by the blood vessel lining the reservoir. The laser procedure is called Trabeculoplasty. The drainage procedure most commonly performed is called Trabeculectomy.

It is important to have the glaucoma monitored frequently by an Ophthalmologist. This monitoring includes checking the eye pressure, looking at the optic nerves, and checking the visual field. This latter is a test for optic nerve function and demonstrates any gaps in vision that have occurred. Usually a patient is not aware of gaps in vision until extensive damage to the nerve has occurred. Fortunately, in most cases, glaucoma progresses very slowly and progression may be slowed or halted with proper treatment.

What does the future hold?

Future innovations will include better pressure lowering drugs, treatment geared at improving blood flow to the optic nerve, and genetic treatment to prevent cell death. But early detection will always be the key to preventing damage. This underscores the need for periodic eye exams by an eye care professional trained and experienced in the early detection and treatment of glaucoma – your Ophthalmologist!

January 2002

Laser epithelial keratomileusis (LASEK) has added another option to our current armamentarium for laser vision correction. Hundreds of thousands of patients each year are gaining freedom from glasses and contact lenses through laser vision correction, and we are happy to offer the latest in refractive surgery technology to our patients including LASEK. Most refractive surgical procedures performed in the past have been either laser assisted in-situ keratomileusis (LASIK) or photorefractive keratectomy (PRK). The addition of LASEK will give some of our patients a new option that may be better for them.

Each of these three procedures can be used correct myopia and hyperopia with or without astigmatism. LASIK is performed by using a corneal microkeratome to create corneal flap in order to expose the corneal stroma for treatment with the excimer laser. LASIK allows for a rapid visual recovery with little or no discomfort, however in some situations LASIK is not advisable. These include inadequate corneal thickness, dry eye, and certain corneal abnormalities. Patients with these conditions may usually undergo either PRK or LASEK.

We have performed PRK on many patients that did not qualify or did not care to have LASIK. PRK involves slightly more discomfort than LASIK, and the visual recovery is not as rapid. It is however an excellent procedure, and studies have shown that in terms of efficacy and safety PRK and LASIK are totally equivalent. Sometimes a patient may be a more suitable candidate for either PRK or LASIK based on the condition of their eyes. This is usually not the case though, and generally we let our patients decide which procedure they would prefer. LASEK gives our patients another surgical option.

LASEK involves rolling the corneal epithelium off the corneal stromal bed in one sheet in order to expose the corneal stroma for laser treatment. The timing of visual recovery and the amount of discomfort are intermediate between PRK and LASIK, and initial results for LASEK have been excellent.

The procedure is extremely similar to PRK and LASIK as far as the patient’s experience. The patient is brought into the excimer laser operating suite after preparation of the eye with a surgical cleansing. The patient lies down, and a lid speculum is placed in the eye. A solution is placed on the eye in order to loosen the corneal epithelium, and the epithelium is rolled back in one sheet. The excimer laser is then used to treat the eye, and the epithelium is replaced. A soft contact lens is placed in the eye to enhance comfort and healing, and the patient is ready to go home. Like LASIK and PRK, LASEK only takes a few minutes.

We have had tremendous success with both PRK and LASIK in our practice, and we are excited to begin to offer LASEK as well. If your are interested in finding out if you are a candidate for one of these procedures, feel free to contact us about our monthly laser vision correction seminar or for a full laser vision correction work-up and evaluation.

October 26, 2001

The results of the long awaited Age-Related Eye Disease Study (AREDS) investigation regarding the use of anti-oxidant vitamin and mineral supplements to slow the progression of Age Related Macular Degeneration (ARMD) are finally available. They have just been published in this month’s Archives of Ophthalmology. Before I share the results with you, I would like to give you some important background information.

The inner lining of the back of the eye is called the retina. The retina receives the light rays, which have been focused by the cornea and lens. It then converts them to nerve impulses, which travel to the brain where they are converted into the visual images that we perceive. The retina is analogous to the film in a camera. However, in a camera, every bit of film is the same as every other bit. In the retina, there is a highly specialized area in the center, called the macula. This small area of the retina is responsible for our sharp central vision, including our ability to read, recognize faces, and to do fine detail work. It also provides the bulk of our color vision.

As some people get older, their macula in one or both eyes begins to degenerate, a condition known as Age Related Macular Degeneration (ARMD). There are two types of macular degeneration: atrophic (commonly known as “dry”) and exuda