Scott E. Pautler, M.D. Tampa

Treatment of diseases of the retina and vitreous

The Smudged Contact Lens

Posted on July 30, 2023 by Scott Pautler

Blurred vision due to smudge on the contact lens?

There are many causes of blurred vision. Sometimes, the eye doctor needs to update the power of the contact lens. At other times, there may be an eye disorder that requires diagnosis and treatment by an ophthalmologist. However, a smudged contact lens may be the problem. To find out, remove and inspect the contact lens for a smudge.

What are the causes of a smudge on the contact lens?

Many things may cause a smudge on the contact lens. A factory defect is rare and the contact lens specialist usually detects damaged lenses prior to dispensing. Makeup, creams, oils, or moisturizers on your fingers may cause the contact lens to be smudged. A moisturizer in your hand soap may cause blurred vision by smudging the lens.

What can be done to prevent smudges on the contact lens?

Proper contact lens maintenance and hygiene is important. Follow all instructions given by your contact lens provider to the letter. Make sure to wash your hands with hand detergent without moisturizers prior to inserting your contact lenses. This is very important to keep your lenses clear and free of germs that can cause serious infection.

How do you remove a smudge from a contact lens?

The management of a smudged contact lens depends, in part, on the type of contact lens you wear. If you use daily-wear contact lenses, it may be best to dispose of the smudged contact lens and replace it with a new lens. When wearing lenses made to wear for longer than a day, carefully clean them daily by following the manufacturer’s recommendations.

Rigid gas-permeable lenses are made for long-term use. If they become smudged, gently rinse them with conditioning solution or a cleaning solution. If this fails, an enzymatic cleaner may help. Follow all instructions on the contact lens product recommended by your doctor. Professional polishing is available by your contact lens provider.

Where do I go for urgent care?

If you have pain while wearing your contact, remove it immediately. If your eye remains blurred after you remove the contact lens, you may have a damaged cornea. Make a prompt appointment with your eye doctor. If you have pain or persistent foreign-body sensation (a feeling like sand in the eye), notify your eye doctor without delay. If you are unable to contact your eye doctor and there is significant pain and/or loss of vision, report to the hospital emergency department urgently.

By Scott E. Pautler, MD

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Visual Hallucinations and the Eye

Posted on May 21, 2023 by Scott Pautler

What are visual hallucinations?

A visual hallucination is the perception of a visual image that is not the result of seeing an object outside the eye. Normally, the eye perceives light from objects outside the eye and sends the image to the brain for interpretation. However, there are a number of circumstances that result in images being “seen” by a patient that do not originate from outside the eye. These images are referred to as hallucinations, especially if they appear as formed images of recognizable objects, like faces, trees, or other familiar things. Sometimes, hallucinations appear as dots, lines, or geometric shapes. The hallucinations may be in color or black and white.

What causes hallucinations?

A large list of problems may cause visual hallucinations. These include drug use and abuse, delirium, mental illness, and a variety of neurological conditions (including stroke, multiple sclerosis, and dementia). Sometimes, eye disease causes visual hallucinations; this is called the Charles Bonnet syndrome. It is a common condition in which the brain “makes up images” as a result of loss of vision from an eye condition (such as macular degeneration, diabetic retinopathy, or glaucoma). Charles Bonnet was an 18th century botanist and philosopher who described complex visual hallucinations in his grandfather after loss of vision.

How can a doctor find the underlying cause of visual hallucinations?

A doctor may determine the cause of visual hallucinations by careful examination and testing. If the hallucinations are interpreted by the patient as being “real,” the cause is more likely related to mental illness or may be due to drug intoxication or neurological disease. In these cases, the mental status exam is usually not normal. In the Charles Bonnet syndrome, the patient knows what he is seeing is not real, but sees the images nonetheless. An eye exam may make the diagnosis, but in some cases, further testing is needed. And these may include blood tests and imaging studies (CT scan and/or MRI brain scan). The final diagnosis of Charles Bonnet syndrome is made only after other more serious diagnoses are excluded.

What is the treatment of visual hallucinations?

The treatment depends on the underlying cause. In the case of the Charles Bonnet syndrome,
counseling may help. Much relief comes from knowing that the symptoms are benign and do not represent a serious medical condition. Some patients find the symptoms improve if they move their eyes up-and-down, or left-and-right, or look away from the hallucinations. Others find it helps to stare at the hallucination until it fades away. It may help to talk about the hallucination with a family member or friend. Because stress and fatigue may precipitate the hallucinations, some recommend getting plenty of sleep and rest. Exercise and meditation are helpful. Thankfully, the visual hallucinations from Charles Bonnet syndrome often subside with time and may disappear over months to years. Rarely, medication may be prescribed by a neurologist. New treatments are on the horizon.

Related blog: The Visual Snow Syndrome

By Scott E. Pautler, MD

For a telemedicine consultation with Dr Pautler, please send email request to spautler@rvaf.com. We accept Medicare and most insurances in Florida. Please include contact information (including phone number) in the email. We are unable to provide consultation for those living outside the state of Florida with the exception of limited one-time consultations with residents of the following states: Alabama, Arkansas, Connecticut, Georgia, Minnesota, and Washington.

Central Retinal Vein Occlusion

Posted on May 13, 2023 by Scott Pautler

globe anatomy — anatomy of the eye (click on image to enlarge)

What is a central retinal vein occlusion (CRVO)?

Retinal vein occlusion means blockage of a vein in the retina. A central retinal vein occlusion is a blockage of the main (central) vein on the retina. The retina in your eye is like the film inside a camera. The retina “takes the picture” of objects you look at and sends the message to the brain. The retina is a living tissue, which requires blood supplied by tiny vessels. Retinal veins are blood vessels that drain blood from the retina. The veins form as branches that drain sections of the retina. The branch veins all drain into the central retinal vein that exists the eye with the optic nerve. An abnormal blood clot in a retinal vein causes a blockage (occlusion) of the blood flowing out of the retina.

Who is at risk of a central retinal vein occlusion?

Retinal vein occlusions are more common in people who have risk factors for hardening of the arteries, which may compress the veins where they come in contact in the retina. Hardening of the arteries (arteriolar sclerosis) occurs in people who are overweight, use tobacco, or have diabetes, high blood pressure, or sleep apnea. Glaucoma is also a risk factor as intraocular pressure spikes affect blood flow in the retinal veins, and slow blood flow promotes blood clots. There are a number of blood disorders that may play a role in CRVO, especially in younger individuals. Estrogens may increase coagulation of the blood and lead to CRVO. Less commonly, inflammation may cause retinal vein occlusion.

What are the symptoms of a central retinal vein occlusion?

Blurring of vision may occur if excess fluid (edema) leaks from the veins into the center of the retina. Floaters can look like tiny dots or cobwebs moving about in your vision. They may be due to bleeding from the retina into the central gel (vitreous) of the eye. Pain is rare and may be due to high pressure in the eye (neovascular glaucoma).

What treatment is available?

There is no cure, but treatment may improve vision or keep the vision from worsening. Your doctor may allow time for the vein to heal, but this is rarely advisable if the vision is impaired. Medicine injections may help recover vision and may be given with little discomfort. The vision may not return to normal following treatment as there may be some permanent damage to the retina from the occlusion. Injections must be repeated in order to maintain vision. Over time, the retina does heal to some degree. However, after three years of treatment about half of eyes continue to require injections. In some cases when treatment cannot improve the vision, laser is used to prevent severe pain and complete blindness. Your doctor is going to order appropriate tests and recommend the best course of action to take at this time. The retinal vein occlusion will not be worsened by your daily activities or by using your eyes.

By Scott E. Pautler, MD

The Use of Steroids in Endophthalmitis

Posted on May 6, 2023 by Scott Pautler

Why use steroids in endophthalmitis?

Ophthalmologists often consider the use of steroids in endophthalmitis treatment. Steroids reduce inflammation in endophthalmitis. The decrease in inflammation helps improve comfort and potentially reduces inflammatory tissue damage, such as scarring. Although it is key to treat with appropriate antibiotics for infectious endophthalmitis, topical steroids (steroid eye drops) are included in the therapeutic regimen. The physician orders the steroid eye drops frequently at the onset and monitors inflammation and eye pressure to determine the best treatment schedule.

What is the role of intravitreal steroid injections?

The role of intravitreal steroids (dexamethasone) is controversial. In a recent review and meta-analysis of endophthalmitis, there was no added benefit with the use of intravitreal dexamethasone. The reason for lack of benefit may include the short half-life of intravitreal dexamethasone (<3 hours). Nonetheless, there may be benefit derived from the use of intravitreal dexamethasone in severe bacterial infections such as those caused by Bacillus species.

What about other ways to give steroids?

In select cases there may also be a role for periocular or systemic steroids for a more prolonged steroid effect. Periocular steroids require an injection next to the eye. My preferred technique is a subtenant’s injection as described by Nozik because it is fairly pain-free. Systemic steroids are given as a pill. There are potential side-effects to the use of steroids. With steroid injections come the risk of elevation of eye pressure, which may cause glaucoma. Many side effects may occur with steroid pills including depression, high blood sugar, weight gain, brittle bones, acne, stomach ulcers, and others. Usually side-effects are preventable or treatable. The final decision of how and when to use steroids lies with the treating physician based on the circumstances of the case.

By Scott E. Pautler, MD

The Far-Sighted Eye

Posted on September 18, 2022 by Scott Pautler

What is hypermetropia?

A hypermetropic eye is a far-sighted eye. Without glasses the vision may be good at distance or blurred, but the vision is usually blurred or strained at near without glasses. Hypermetropia is different from presbyopia (aging eyes). Hypermetropia affects many people and is treated with glasses, contact lenses, and, rarely, laser surgery. It is a common underlying reason for the need to wear optical correction (glasses).

What causes hypermetropia?

Hypermetropia is an inherited condition that usually develops in childhood or early adulthood. The eye develops with either a flat cornea or a short eyeball length, or both. As a result, the image entering the eye is focused behind the plane of the retina. In this case, the eye tries to focus the lens to make the image projection sharp. Sometimes, the natural lens in the eye can compensate for the focusing of images, but often eyeglasses or contact lenses are needed. The outer appearance of the eye is not usually changed. It is not obvious that an eye is hypermetropic by inspecting the outside of the eye.

Why is it important to know about hypermetropia?

Although most people with hypermetropia do not develop complications, some far-sighted people are at increased risk of losing vision from narrow-angle glaucoma, central serous choroidopathy (also known as central serous retinopathy), and choroidal effusion.

Angle-Closure Glaucoma is a condition in which the pressure inside the eye damages nerve tissue that helps you see. High pressure is the result of closure of the internal drain in the eye. The pump inside the eye does not sense the closure of the drain; it continues to pump fluid into the eye. The drain cannot keep up with the pump, so the pressure inside the eye rises. This pressure may or may not cause pain or discomfort. Over time, the pressure slowly takes away the side vision. If undetected and untreated, it may cause total, irreversible blindness. The best way to diagnose glaucoma is to have regular eye exams each year with pressure measurements and gonioscopy. Treatment is effective in preventing vision loss. Laser is often used to open the drain. Sometimes operative surgery is required with or without removal of the lens in the eye (to make more room for the drain to stay open). Often, eye drops are needed long-term to keep the pressure under control.

Central Serous Chorioreti n opathy is an uncommon cause of vision loss from hyperopia. The retina is a thin layer of delicate nerve tissue that lines the inside wall of the eye like the film in a camera. In the eye, light is focused onto the retina, which “takes the picture” and sends the image to the brain. In hypermetropic eyes, the layer under the retina called the choroid becomes crowded and thickened. The outer coat of the eye known as the sclera may be thickened as well. As a result of thickened choroid and sclera, the flow of fluid inside the eye that normally drains out through these structures, is restricted. This fluid may then collect under the retina and cause the central vision to become blurred or distorted even with proper glasses. Distortion is when straight lines look wavy or crooked. Blood vessels under the macula may bleed causing sudden blurring, blind spot, or distortion. Any of these symptoms should be reported to the eye doctor without delay, as early treatment with laser may prevent further loss of vision.

Choroidal Effusion is a separation of the choroid from the sclera, the wall of the eye. This is different from retinal detachment. When the choroid detaches, it is no longer in proper position inside the eye. As a result, symptoms of a dark curtain or shadow slowly starts off to the side and takes away the vision as the choroid detaches. Pain is not common. The diagnosis is made by a retinal specialist; it is critical to identify and differentiate choroidal detachment from retinal detachment and tumors. Treatment of choroidal effusion is typically started with medications. Sometimes, however, surgery is needed.

Will refractive surgery help prevent these complications of hypermetropia?

Although refractive surgery (laser correction) is effective at changing the shape of the cornea to help eliminate the need for corrective lenses (glasses and contacts lenses), it does not restore the natural shape of the eye. Therefore, it is still necessary to be aware of the warning signs of possible complications from hypermetropia.

What should a hypermetropic patient do?

Using your eyes to read or work at a computer will not weaken them. Remember to have your eyes examined once a year with special attention to the opening of the drainage apparatus (the corneoscleral angle). Not all eye doctors are proficient with determining the risk of angle-closure glaucoma; therefore, consider seeing a fellowship-trained glaucoma specialist if needed. In Tampa there are several choices including doctors Levitt, Gamell, Richards, King, and Fridman. Apart from an annual exam, report the following symptoms to your eye doctor without delay:

Sudden-onset pain in the eye (sometimes, associated with nausea)

Sudden-onset redness (especially, if associated with pain and blurred vision)

Loss of side-vision (possibly, a very late sign of glaucoma)

By Scott E. Pautler, MD

Visual Snow Syndrome

Posted on August 14, 2022 by Scott Pautler

What is visual snow?

Visual snow is the name for a visual symptom that looks like static on a television not tuned to a station. It has also been likened to pixelation on a computer screen. Many tiny flickering lights are usually seen in both eyes at the same time and encompasses the entire visual field. In some instances, it is worse in bright illumination like a bright sunny day.

What is the difference between primary and secondary visual snow syndrome?

Visual snow may be seen in patients without an underlying disease. In these cases it appears to be caused by hyperexcitability of the visual cortex of the brain. This is often called primary visual snow syndrome (VSS). Primary VSS is a diagnosis of exclusion. That is, other diagnoses must be excluded before the diagnosis of primary VSS is made. Primary VSS is related to migraine; indeed, many people who report visual snow also have migraine visual symptoms with or without headache. Other related symptoms include palinopsia (visual persistence of an image after the eyes are closed or look away), floaters and spots (entopsia), difficulty seeing in dim light (nyctalopia), difficulty seeing in bright light (hemeralopia), and flashes of light (photopsia). Other associated symptoms include ringing in the ears (tinnitus) and dizziness that varies with head position (postural vertigo).

Visual snow may be a symptom of an underlying disease (secondary visual snow syndrome). In this situation, it is critical to identify the underlying cause and offer treatment where possible. Secondary visual snow may originate from the retina or the brain. A well-described retinal cause of visual snow is due to digoxin toxicity. It usually occurs in elderly people who take digoxin for heart problems. It indicates the need to stop taking digoxin or lower the dose. Failure to reduce the dose may result in severe complications, including death. Other rare causes of visual snow include eye disease, immune disease, infectious disease, psychiatric disease, prescription drugs, past use of hallucinogens, head trauma, brain tumor, seizure disorder, and brain degenerative disease.

What causes the primary visual snow syndrome?

The cause of primary VSS is not known. It is felt to be due to an error in central processing in the back of the brain (occipital lobe). Special brain scans show hypermetabolism in the lingual gyrus of the occipital lobe in the back of the brain.

How is primary visual snow syndrome diagnosed?

The diagnosis is made on the basis of typical symptoms after testing has ruled out an underlying disease of the eye or brain. MRI brain scan is often used to rule out tumor, multiple sclerosis, degeneration, and stroke. EEG may be used to rule out seizure disorder. A spinal tap may be needed to rule out idiopathic intracranial hypertension. Pattern reversal VEP usually demonstrates loss of habituation of the occipital lobe in the brain (indicative of hyperexcitability). A neurologist usually arranges for testing as needed. An ophthalmologist may be helpful in ruling out eye disease.

What can be done about these symptoms?

It is difficult to treat primary VSS. Medications such as lamotrigine and topirimate may be helpful in some patients. Tinted glasses or clip-on lenses may also be helpful to minimize the symptoms of visual snow. Placing a yellow or orange tinted cellophane sheet on top of reading material helps some. Riboflavin and magnesium supplements may be of benefit for migraine and visual snow, as well. For many patients it is helpful to know that primary VSS is a benign condition that does not progress to blindness.

By Scott E. Pautler, MD

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Black Spots After Eye Injection

Posted on August 6, 2022 by Scott Pautler

What are these circular spots in my vision after an eye injection?

Sometimes after an eye injection, a patient may see one or more black circular spots that move in the vision with head movement. They are usually in the lower part of the visual field, though they move up toward the center of the visual field if you position your head face down.

What causes these symptoms?

These black spots are due to air bubbles in the medicine that is injected into the eye. They appear immediately after injection. They are harmless and take 1-2 days to dissolve and disappear. Less commonly, small black circular spots may float in the vision after injection due to small silicone bubbles that are used to lubricate the syringe. These silicone bubbles do not dissolve, but they may float away from the retina and become less noticeable over time.

What should be done about these symptoms?

If the spots are due to air bubbles, these symptoms fade without treatment. If the spots are due to silicone bubbles, they may come and go over time. It is best not to track them with your eyes as they may become more bothersome. Try to look past these floaters and ignore them if possible. If they persistently interfere with the vision, vitrectomy surgery may be considered to remove them. This is rarely necessary.

What other symptoms can mimic this problem?

These black spots are considered a type of “floater.” Floaters are any visual spot in the vision that “floats” or moves somewhat independent of eye movement. Sometimes floaters may come on suddenly and appear like dots and fibers. This is typical for bleeding inside the eye. If dots and fiber-like floaters come on more slowly (hours to days), they may be a sign of infection or inflammation. Rarely, cancer may present as many tiny floating spots in the vision.

Floaters are distinct from blind spots (scotoma) that are fixed in the visual field and move only when the eye moves. You cannot “catch up” or move away from a blind spot by moving the eye. Blind spots are usually due to problems with the retina or optic nerve. A progressive blind spot that begins in the peripheral vision and enlarges over hours to days may be due to a retinal detachment and requires a prompt examination. Retinal detachment is often described as a curtain or shadow covering the vision.

By Scott E. Pautler, MD

Byooviz Therapy

Posted on July 30, 2022 by Scott Pautler

What is Byooviz?

Byooviz is a drug used to treat wet-type macular degeneration, wet-type myopic macular degeneration, and macular edema due to retinal vein occlusion. It involves repeated injections of medication into the eye to stop abnormal, leaky blood vessels. Byooviz is an FDA-approved biosimilar drug similar to Lucentis. Consequently, it costs less than Lucentis (About $1100 per injection of Byooviz compared with $1800 per injection with Lucentis). Unlike Lucentis, Byooviz is not approved for diabetic retinopathy.

What is the difference between biosimilar drugs and generic drugs?

While generic drugs are chemically identical with trade-name drugs, biosimilars are not identical to their reference drugs which they attempt to duplicate. Because biosimilar drugs are different chemically, they may behave differently in terms of effectiveness and side effects. They may not be as effective as their reference drug and they may have more side effects. For this reason, biosimilar drugs need to be monitored closely prior to approval by the FDA, as well as after approval by health care providers. Some adverse effects are not recognized until a drug has been used in thousands (if not more) of patients.

How effective is Byooviz therapy?

Byooviz was shown to be very effective and similar to Lucentis when given every 4wks up to 48 weeks for wet-type macular degeneration. Currently, therapy often starts with monthly injections until maximal vision is restored. Afterwards, the injections may be given less frequently to maintain stable vision. It is not known how Byooviz will perform in this setting.

What are the risks of Byooviz therapy?

Severe complications are very rare, but risks of Byooviz injection (like Lucentis) include bleeding, infection, retinal detachment, glaucoma, cataract, and loss of vision/loss of the eye. There appears to be a small increased risk (1%) of stroke with these types of medications. The risk of stroke may be related to the older age of patients in which it is used. Pregnancy should be avoided while on Byooviz therapy.

What do I expect after a Byooviz injection?

Be careful not to rub the eye after the injection because the eye may remain anesthetized for several hours. You may be given eye drops and instructions on how to use them. Physical activity is not limited after the injection. Tylenol or Ibuprofen may be used if there is discomfort, but severe pain should be reported to your doctor without delay. It is normal to experience a red area on the white of the eye, which disappears in one to two weeks. If you have any questions or concerns, please call the office.

What does Dr Pautler think about Byooviz?

It is the opinion of the author that there are several concerns about Byooviz. First, the safety and effectiveness of Byooviz need to be determined on a large scale with many more patients than studied for FDA approval. This may take several years of use. Until then, I prefer Lucentis as it has a proven track record. Secondly, the cost of Byooviz appears too high. The cost of Byooviz is less than Lucentis, but not by much. A lower cost is more appropriate given the unknown risks and long-term effectiveness of Byooviz. If I have a patient whose insurance covers Lucentis, that is my choice over Byooviz at this time. If a patient has a Medicare Advantage insurance plan, I may be forced to use Byooviz.

By Scott E. Pautler, MD

What is the Best Drug for Eye Injections?

Posted on July 10, 2022 by Scott Pautler

Two common retinal causes of vision loss are wet age-related macular degeneration (wAMD) and diabetic macular edema (DME). In both of these conditions a signaling protein (called VEGF) is released that promotes blood vessel leakage with loss of vision. A major advance in treatment came about with the development of drugs that block the effect of VEGF. These drugs (called antiVEGF) reduce the risk of vision loss and offer some improvement in vision in patients with wAMD and DME. Unfortunately, these drugs need to be administered as an injection into the eye. Consequently, drug manufacturers work to design drugs offering the best vision with the longest interval between injections (fewer injections).

What drugs are available and how effective are they?

The first drug to reduce the rate of loss of vision in wAMD was Macugen (pegaptanib). It is no longer used because newer drugs are more effective in offering improvement in vision. While Lucentis (ranibizumab) was under development, its parent drug Avastin (bevacizumab) was found to be effective for wAMD. Both Avastin and Lucentis appear more effective than Macugen. Eylea (aflibercept) was developed to block the effect of VEGF and another factor (placental growth factor) involved in blood vessel leakage; consequently, there is moderate evidence that it is more effective than Avastin and Lucentis in DME and offers a longer treatment interval in wAMD. Newer drugs include Beovu (brolucizumab) and Vabysmo (faricimab). There is little evidence to know if they are more effective than Eylea. Finally, Eylea is now formulated in a higher concentration (Eylea HD).

What is the cost of these drugs?

All of the drugs used to treat wAMD and DME are expensive with the exception of Avastin. Avastin was manufactured and priced to treat colon cancer. After it was released, doctors at the Bascom Palmer Eye institute discovered it was effective in treating wAMD. Thus, the small dose needed to inject into the eye costs about $50. This is in contrast to the other drugs on the market, which cost around $2000 per injection.

What are the adverse effects of these drugs in the eye?

Problems may occur from the injection of medications into the eye. The injection itself has risks apart from the drug that is injected; we will not discuss those risks here, but they include pain, elevated eye pressure, hemorrhage, infection, retinal detachment, and loss of vision. The drugs themselves may cause inflammation in the eye. Usually, inflammation causes pain, redness, light sensitivity, floaters, and decreased vision. Typically, it can be treated with drops and it resolves without permanent damage. However, sometimes the inflammation can be severe with permanent loss of vision. Inflammation induced by drugs is very rare with Avastin and Lucentis. It occurs in about 1% of Eylea injections, 2% of Vabysmo injections, and 4-5% of Beovu injections. The inflammation with Beovu may be especially severe with permanent loss of vision. The risk of infection appears less in drugs that are pre-packaged in a syringe for injection (Lucentis and Eylea), and greater in drugs that must be prepared for injection (Avastin, Vabysmo, Eylea HD, and Beovu).

What are the adverse effects of these drugs outside the eye?

There is concern about effects of these drug outside the eye. All of these drugs leave the eye, enter the blood vessels and are removed from the body through the urine. On their way out of the body, there is concern that they may increase the risk of heart attack and/or stroke. There is considerable debate as to whether there is a measurable effect or not. Some have estimated that the systemic risk may be about 1%. However, patients with known risk factors (hardening of the arteries, tobacco use, high blood pressure, high cholesterol, overweight, and diabetes) may be more likely to suffer a heart attack or stroke with the use of antiVEGF drugs. In one study, patients with diabetic macular edema were at 17% (range: 2-33%) higher risk of death when undergoing frequent injections up to 2 years. Another study, demonstrated increased risk of stroke or heart attack in diabetic patients with a history of past stroke or heart attacks. Therefore, this group of patients may benefit from careful drug selection. Of all the drugs, Lucentis is cleared the most rapidly from the body and has the least systemic effects.

Want a summary of the cost, effectiveness, and safety?

Summary:

AntiVEGF drug	Cost	Effectiveness	Safety
Avastin	Cheap: ~$50	Good	Repackaging*
Lucentis	Expensive: ~$2,000	Good	safest systemically**
Eylea	Expensive: ~$2,000	Better	1% inflammation
Eylea HD	Expensive: ~$2000	?Better	1% inflammation or greater?
Vabysmo	Expensive: ~$2,000	?Better	2% inflammation
Beovu	Expensive: ~$2,000	?Better	4-5% inflammation

A list of drugs available in the US approved for injection into the eye

* Repackaging increases risk of infection, floaters, and discomfort for dull needles

** Especially relevant when repeated injections are required in diabetic patients

What is my professional preference?

I have employed all of these drugs for my patients. When cost is an issue, an insurance company may insist on the use of Avastin. I generally prefer Lucentis in my diabetic patients for its superior systemic safety. Eylea can be helpful to extend treatment intervals (longer time between injections) in wet macular degeneration. Eylea may also be safer in patients who also have glaucoma, or at risk of developing glaucoma. I have been favorably impressed with Vabysmo in extending treatment intervals even further in wAMD, but I am less impressed with any advantage in my patients with DME (diabetic macular edema). I am currently exploring the role of Eylea HD, especially to extend the treatment interval in patients with wet AMD. Due to the risk of inflammation with loss of vision from Beovu, it is not my preferred agent. Lucentis biosimilars (Cimerli and Byooviz) are not my preferred agents at this time…I am awaiting further evidence on their safety and effectiveness.

Are doctors paid by drug companies to use their drugs?

There are varying amounts of profit margins and rebates given to doctors by drug companies in an effort to promote the use of their drugs. Usually, the newer the drug, the greater the inducement. To determine if your doctor is receiving large payments by drug companies, visit the CMS website and enter your doctor’s name in the search box.

By Scott E Pautler, MD

Portable Low-Vision Magnifiers

Posted on May 22, 2022 by Scott Pautler

There are various eye conditions that may result in loss of vision with limited potential for recovery with treatment. In these situations, good lighting and magnifiers are essential for making best use of low vision. Magnifying glasses and large closed-circuit TV magnifiers are large and heavy. They are most useful for home use. However, away from home, these devices may be too cumbersome. An ideal solution to the problem, is the portable digital magnifier. The small magnifiers are lighter than an old-fashioned magnifying glass and are easily transportable. And, certainly, they may be used around the home, as well.

A number of my patients endorse the portable low-vision magnifiers listed below. They come in various sizes depending on your needs and the size of your carrying bag. They also vary in the amount of magnification provided. They are particularly helpful when shopping for brands and prices in the grocery store. Reading a menu at a restaurant is made much easier with these devices. The added independence gained with a proper magnifier makes my patients less dependent on others for help and adds to their quality of life.

Please refer to the links below for pricing on Amazon:

Small Portable Magnifier with 3.5″ screen with up to 25x zoom magnification

Large Portable Magnifier with 5″ screen with up to 32x magnification

Large Portable Magnifier with 5″ screen with up to 48x magnification and voice prompt function.

By Scott E. Pautler, MD

Note: This blog is supported by its readers via small commissions that may be earned through these links. The commissions do not increase the price you pay and do not affect the content of this article. Thank you for your support.

Susvimo: Lucentis Port Delivery

Posted on April 15, 2022 by Scott Pautler

What is Lucentis therapy?

Lucentis therapy is a treatment for wet-type macular degeneration. It usually involves repeated injections of medication into the eye to stop abnormal, leaky blood vessels. It is now also available through port delivery (called Susvimo). After a tiny reservoir is implanted in the eye at surgery, a painless injection to fill the port is performed every 6 months.

How effective is Lucentis therapy?

Lucentis was proven in extensive studies to be very effective. In wet-type macular degeneration, a large study showed that monthly injections of Lucentis over a two-year period offered a 90% chance of stable or improved vision. Similar benefits are seen in other retinal conditions as well. Traditionally, therapy often starts with monthly injections until maximal vision is restored. Afterwards, the injections may be given less frequently to maintain stable vision. The Lucentis port delivery appears to be as effective as Lucentis monthly injections, but with fewer injections.

What are the risks of Lucentis therapy?

Severe complications are very rare, but risks of Lucentis injection include bleeding, infection, retinal detachment, glaucoma, cataract, and loss of vision. There appears to be a small increased risk (1%) of stroke with Lucentis. The risk of stroke may be related to the older age of patients in which it is used. Pregnancy should be avoided while on Lucentis therapy.

The port delivery method (Susvimo) is associated with more adverse events (19%) compared with monthly Lucentis injections (6%). Among eyes with the implanted port, 5-10% had bleeding inside the eye causing floaters and blurred vision. The blood cleared over several weeks to months. In 5.4% of eyes with the implanted port, the conjunctiva (skin-like layer that covers the eye) does not remain intact overlying the implant and additional surgery is often needed. In 1-2% of eyes with an implanted port, infection may occur. This is a very serious event that requires surgery and may result in permanent loss of vision/loss of the eye. In 1-3% of eyes with an implanted port, a retinal detachment required additional surgery and sometimes resulted in loss of vision. Non-infectious inflammation occurs in about 20% of implanted eyes; it usually responds to eye drops. The benefits of fewer injections with the port delivery method must be weighed against the risks involved with the port. It is the opinion of the author that the risks of the Susvimo port delivery may outweigh the benefits at this time for most patients. Newer medications (Vabysmo) are available that appear to last longer than other treatments such as Lucentis injections. Therefore, Susvimo port delivery may be unnecessary.

What do I expect after a Lucentis injection?

By Scott E. Pautler, MD

Vabysmo better than Eylea?

Posted on March 20, 2022 by Scott Pautler

Yosemite/Rhine Studies: a critical analysis

The Yosemite and Rhine Studies were twin randomized, double-masked, multicenter non-inferiority trials comparing the efficacy of faricimab (Vabysmo) vs aflibercept (Eylea) in the treatment of diabetic macular edema.

The study abstract begins with the statement, “To reduce treatment burden and optimize patient outcomes in diabetic macular oedema, we present the 1-year results from two phase 3 trials of faricimab, a novel angiopoeitin-2 and vascular endothelial growth factor-A bispecific antibody.” However, analysis of the data reveals the study report did NOT demonstrate reduced treatment burden at one year. It did demonstrate potential non-inferiority of faricimab compared with aflibercept with an increased treatment burden in the faricimab arms of the studies.

Treatment burden was greater in both faricimab treatment arms of both studies compared with aflibercept. Table 1 reveals 25% greater injections in the faricimab q8 week group compared with aflibercept. The faricimab group received 10 injections at 52 weeks compared with aflibercept at 9 injections. The faricimab group did not experienced a reduced treatment burden compared with aflibercept. Moreover, the faricimab group sustained a more intense treatment burden to meet the “non-inferiority” assessment compared with aflibercept.

Table 1. Injection schedule for faricimab (Fq8) and aflibercept (Aq8) q8 week study arms.

wk#	1	4	8	12	16	20	24	28	32	36	40	44	48	52	total
Fq8	1	1	1	1	1	1	0	1	0	1	0	1	0	1	10
Aq8	1	1	1	1	1	0	1	0	1	0	1	0	1	0	9

There was only one subgroup of eyes that received one less injection of faricimab at one year compared with aflibercept. There were 63 eyes of 286 (22%) in Yosemite and 66 eyes of 308 (21%) in Rhine who underwent 7 faricimab injections within the group randomized to “personalized treatment interval” (PTI) compared with 8 injections in the aflibercept group. Unfortunately, the visual and anatomic outcomes of this subgroup of faricimab eyes were reported a part of the entire PTI group, which overall had more injections than the aflibercept group.

The primary outcome of the study was the number of letters of improvement on the standard ETDRS chart. However, because of the uneven staggered injection schedule between the q8 week treatments groups, the method to calculate the visual improvement outcome favored faricimab over aflibercept. The study design called for averaging the measurements of visual improvement over a three-month time frame (i.e. at week 48, 52, and 56). As a result, the three averaged measurements for faricimab (Fq8) was 4 weeks, 8 weeks, and 4 weeks post-injection (average 5.3 weeks), while the three measurements for aflibercept (Aq8) were 8, 4, and 8 weeks post injection (average 6.6 weeks). Thus, the unevenly staggered injection schedule resulted in a final visual endpoint measurement inappropriately in favor of faricimab.

Even in the subgroup of faricimab (Fpti) that touted one 16week treatment interval, the visual acuity measurements were taken at 16weeks, 4weeks, and 8 weeks post-injection. This represents an average of 9.3 weeks post-injection; this is nowhere near the measurement taken at 16 weeks. In addition, the acuity outcomes in the Fpti group were reported as a group without reporting the acuity gains made specifically by the subgroup of eyes extended to a 16-week interval. Therefore, the reported acuity gains do not apply to this subgroup with extended treatment.

A secondary outcome of the study was the central subfield macular thickness (CST). This measurement shows the anatomic improvement in macular edema. The slope of the thickness curve trended toward a more rapid decrease in both arms of faricimab compared with aflibercept during the monthly injection stage (initial loading stage). Analysis of the results after the loading stage (monthly injections), both faricimab and aflibercept showed a similar jagged curve demonstrating a drop-off of treatment effect during the no-treatment month. A similar jagged response is not seen in the Fpti group as the treatment intervals varied within that group. The rebound in edema seen in both faricimab and aflibercept suggests the durability of the treatment effect may be similar. These studies did not perform a direct comparison of faricimab and aflibercept on the same personalized treatment interval protocol.

Remarkably, these limitations of the study were not discussed in the published article and the FDA granted approval of faricimab for use in the United States based on these data drawn from an imperfect study design that favored faricimab. More research is needed in order to determine if faricimab is truly non-inferior to aflibercept and whether faricimab may offer a reduced treatment burden.

UPDATE Oct 2022: I have been using Vabysmo in the office. I am please with the results in patients with wet AMD in that I can extend the treatment interval further than with older drugs. However, patients with large serous pigment epithelial detachments (PED) appear to be at greater risk of vision loss from rips in the PED. I have not been impressed with superior effectiveness of Vabysmo in patients with diabetic retinopathy.

By Scott E. Pautler, MD

Yosemite and Rhine Studies: an editorial

Posted on March 20, 2022 by Scott Pautler

Faricimab was recently approved by the FDA for the treatment of diabetic macular edema (DME). It is the first drug which simultaneously blocks vascular endothelial growth factor A (VEGF-A) and angiopoietin-2 (Ang 2). The anti-VEGF-A action is shared with bevacizumab, ranibizumab, and aflibercept; and stabilizes microvascular permeability and inhibits neovascularization. The Ang 2 inhibition works via the angiopoietin and Tie signaling pathway to reduce microvascular permeability by a pathway independent of VEGF-A blockade. Preclinical studies suggested that faricimab might be more effective than simple anti-VEGF inhibition in treating diabetic macular edema. In particular, there were expectations for improvement over the status quo in duration of action. If similar efficacy with lesser treatment burden were possible, this would help overtaxed clinicians and patients and begin to close the real-world versus randomized trial performance gap.¹

The results of two identical, phase 3 randomized clinical trials, YOSEMITE and RHINE, were recently published, allowing clinicians the opportunity to assess how the efficacy of faricimab matches the promise of the preclinical studies.² There were 3 groups in the randomization: faricimab 6 mg q 8 weeks (F8), faricimab 6 mg with a personalized treatment interval (FPTI), and aflibercept 2 mg q 8 weeks (A8). The study authors reported the following in their paper:

With A8 as the comparator, both F8 and FPTI were noninferior (4 letter margin) based on a primary outcome of mean change in best-corrected visual acuity at 1 year, averaged over weeks 48, 52, and 56.
There were no differences in safety events among the 3 groups.
In the FPTI group, more than 70% of patients achieved every-12-week dosing or longer at 1 year.
Reductions in CST and proportions of eyes without center-involved DME (CI-DME) over 1 year consistently favored faricimab over aflibercept.
Faricimab demonstrated a potential for extended durability in treating CI-DME.

Based on the evidence in the paper, are the claims substantiated?

With respect to noninferiority of mean change in best corrected visual acuity, the answer is qualified by the authors’ method of measurement. Because the three groups got last injections at different times, there was no single visit for which assessment of final visual acuity was intuitive. Therefore, the authors averaged the visual acuities measured at 48, 52, and 56 weeks. For the F8 group, the 3 components of the average were 4 weeks post-injection (the measurements taken at 48 weeks), 8 weeks post-injection (the measurements taken at 52 weeks), and 4 weeks post-injection (the measurements taken at 56 weeks), implying that the average last visual acuity was at 5.33 weeks post-injection ([4+8+4]/3=5.33). For the A8 group, the 3 components of the average were 8 weeks post-injection (the measurements taken at 48 weeks), 4 weeks post-injection (the measurements taken at 52 weeks), and 8 weeks post-injection (the measurements taken at 56 weeks), implying that the average last visual acuity was at 6.66 weeks post-injection ([8+4+8]/3=6.66). That is, the A8 group was disadvantaged relative to the F8 group by virtue of the F8 group having more injections in the first year, and an injection nearer to the outcome measurement times. This issue might have been averted had the F8 group received the same 5 initial monthly injections as the A8 group.

It is difficult to provide an analogous comparative calculation for the FPTI group. The relevant information is depicted in figure 3B, but the scale of the figure is microscopic, and only estimates can be made. For example, the YOSEMITE panel of figure 3B, the red-boxed subgroup, appears to comprise 63 patients. For these patients, the 3 components of the average were 16 weeks post-injection (the measurements taken at 48 weeks), 4 weeks post-injection (the measurements taken at 52 weeks), and 8 weeks post-injection (the measurements taken at 56 weeks), implying that the average last visual acuity was at 9.3 weeks post-injection ([16+4+8]/3=9.3). Likewise, for the RHINE panel of figure 3B, the red-boxed subgroup, appears to comprise 67 patients with the average last visual acuity at 9.3 weeks. At the other extreme of the figure (the bottom) sits the group of eyes that could never be extended beyond 4 weeks. For YOSEMITE and RHINE this group appears to comprise 19 and 23 patients, respectively. The average last visual acuity for these eyes would be 4 weeks. In between these extremes of the figure, one would need to do an analogous calculation for every row in the figure, pooling all the results for an overall average. This is clearly more than a reader can be asked to do. The authors should have done it and reported the result in the paper, to allow the reader to see if the outcome time for the FPTI group is comparable to the A8 group. The suspicion is that they are not comparable.

Regarding the claim that the safety results of the three groups were equivalent, we agree with the authors’ interpretation. There is no evidence that faricimab is less safe to use over the 52 weeks of follow-up reported.

The authors claim that over 70% of the FPTI group were able to enter the q 12 week dosing interval. The specific term they chose was “achieved” to signal this distinction. However, entering 12 week dosing is different from demonstrating that faricimab can sustain such intervals. The primary outcome at 52 weeks did not give enough time to determine if those eyes entering 12 week or longer durations could sustain that performance, or whether they would regress to require shorter interval injections. In YOSEMITE, 169 eyes (59%) and in RHINE, 172 eyes (56%) completed one 12wk interval to be assessed for successful completion. The reader has no idea if this proportion will be sustained in the second year of the trial, and it would be an unfounded assumption to expect the entrance to q12 week intervals to be maintained. This outcome will be of great interest when the 2-year results are reported. Only 22%/21% (Yosemite/Rhine) actually completed a 16-week interval and none were treated long enough to determine sustainability of this interval.

Another problem with the authors’ claim on duration of effect has to do with a form of spin, specifically type 3 spin, in the classification of Demla and colleagues.³ A reader might think that this achievement by faricimab distinguishes it from aflibercept, but that inference would not be warranted because of the study design. There was no aflibercept personalized treatment interval arm of the randomization, which would be required to make a claim that increased duration between injections was an advantage of faricimab. While true that a drug company investing in faricimab has no obligation to provide an opportunity for the competitor’s comparator drug to perform as well, the authors cannot claim that the feature displayed by faricimab is a differentiator worthy of a clinician’s choice as a deciding factor in the question of which drug to use. It is also true that the authors don’t make this claim differentiating the drugs, but in presenting asymmetric evidence as they do, an erroneous inference is easy to make, which we seek to avert.

The authors’ claim of superior drying effectiveness for faricimab is supported by the presented data, but unremarked by the authors was evidence of similar durations of drying action of faricimab and aflibercept. To see this, examine figure 3C. The slope of the thickness curve trended toward a more rapid decrease in both arms of faricimab compared with aflibercept during the monthly injection stage (initial loading stage). In an analysis of the graphs after the loading stage (monthly injections), both faricimab and aflibercept showed a similar jagged curve demonstrating a drop-off of treatment effect during the no-treatment month. A jagged response is not seen in the FPTI group because the treatment intervals varied within that group. The zig-zag rebound of edema seen in both faricimab (F8) and aflibercept (A8) groups suggests the durability of the treatment effect may be similar between the two drugs. These studies did not perform a direct comparison of faricimab and aflibercept on the same personalized treatment interval protocol.

The authors’ contention that faricimab rendered a higher proportion of eyes free of CI-DME is warranted by the data they present.

Finally, the authors emphasize the potential of faricimab for lesser burden of treatment because of potential longer durability. This emphasis is unsupported by the evidence presented. The F8 group received 10 injections. The A8 group received 9 injections – hence no decreased burden favoring faricimab over aflibercept in this comparison. It is more complicated to analyze in the FPTI group because the needed information is not reported, but we can make some inferences. There were 63 eyes of 286 (22%) in Yosemite and 66 eyes of 308 (21%) in Rhine that achieved the opportunity to extend treatment; these eyes underwent a total of 8 faricimab injections at week 52. This number represents the least number of scheduled injections and only one less than the aflibercept group. The remainder of eyes were scheduled to have more than 8 injections, but the pooled average is difficult to parse from figure 3B. We can easily note that from the figure that the greatest number of injections at week 52 in this arm of the study was 14 injections in eyes that required monthly treatment (19 eyes (7%) in Yosemite, and 22 eyes (7%) in Rhine). This is far more than the 9 injections of A8, and does not demonstrate a reduced treatment burden among eyes in the faricimab group compared with aflibercept. When the remainder of eyes between the extremes of figure 3B are added in to the calculation of average treatment burden, which we encourage the authors to report, we suspect that it was greater for the FPTI arm of the study than for A8, not less.

In summary, YOSEMITE and RHINE provide data that faricimab as administered in the studies was equivalent to aflibercept in the primary visual outcome, and superior to aflibercept as given in the study in drying the macula. No data were presented supporting a claim that treatment burden is less with faricimab than aflibercept. The published data show that a proportion of eyes can be managed with a reduced injection burden with faricimab, but provide no evidence that this would differentiate faricimab from aflibercept were aflibercept plugged into the same personal treatment interval algorithm. There was no arm of the study that would allow such a comparison to be made. The published data substantiate that faricimab has a greater macular drying effect than aflibercept, but the see-saw central subfield thickness curve in the non-loading phase of the first year suggests that the duration of drying by faricimab is no greater than with aflibercept.

The FDA has approved faricimab for the treatment of CI-DME based on YOSEMITE and RHINE. Retinal specialists will be making choices of which drug to use. An economic perspective will enter into the decision. The clinical decision will not be based exclusively on efficacy. The offered average costs for aflibercept and faricimab to the editorialists are $1747 and $2168, respectively. Is the $441 differential cost a reasonable price to pay for the documented differences in drug performance? Our opinion is no. There is no published difference in visual outcomes, nor any published difference in durability, because it wasn’t checked. There is a difference in macular drying, analogous to the superior drying effect of aflibercept over bevacizumab in the better-vision group of protocol T (eyes with CI-DME)or in the aflibercept versus bevacizumab group in SCORE-2 (eyes with central retinal vein occlusion with macular edema).^4,5 We, and many others, did not think that differences warranted the use of aflibercept over the less expensive bevacizumab in cases similar to those in the better seeing group of protocol T or eyes like those studied in SCORE-2, nor do we think that drying difference seen in YOSEMITE and RHINE between faricimab and aflibercept is reason to choose the more expensive drug. We congratulate the authors of these studies for providing ophthalmologists with new options for treating diabetic macular edema, but nothing they have published suggests that this option marks a milestone in reducing treatment burden in DME. The 2-year results will be more informative for decision-making than the 1-year results, and we encourage the authors to remedy the flaws in their year -1 results data presentation so that the 2-year data are more useful.

By David J. Browning, MD, PhD and Scott E. Pautler, MD

References

1. Kiss S, Liu Y, Brown J, et al. Clinical utilization of anti-vascular endothelial growth-factor agents and patient monitoring in retinal vein occlusion and diabetic macular edema. Clin Ophthalmol 2014;8:1611-1621.

2. Wykoff CC, Abreu F, Adamis AP, et al. Efficacy, durability, and safety of intravitreal faricimab with extended dosing up to every 16 weeks in patients with diabetic macular oedema (YOSEMITE and RHINE): two randomised, double-masked, phase 3 trials. Lancet 2022;DOI:https://doi.org/10.1016/S0140-6736(22)00018-6.

3. Demla S, Shinn E, Ottwell R, Arthur W, Khattab M, Hartwell M, Wright DN, Vassar M. Evaluaton of “spin” in the abstracts of systematic reviews and meta-analyses focused on cataract therapies. Am J Ophthalmol 2021;228:47-57.

4. Diabetic Retinopathy Clinical Research Network, Welss JA, Glassman AR, Ayala AR, Jampol LM, Aiello LP, Antoszyk AN, Arnold-Bush AN, Baker CW, Bressler NM, Browning DJ, Elman MJ, Ferris FJ, Friedman SJ, Melia M, Pieramici D, Sun JK, Beck RW. Aflibercept, bevacizumab, or ranibizumab for diabetic macular edema. N Engl J Med 2015;372:1193-1203.

5. Scott IU, VanVeldhuisen PC, Ip MS, et al, SCORE2 Investigator group. Effect of bevacizumab vs aflibercept on visual acuity among patients with macular edema due to central retinal vein occlusion: the SCORE2 randomized clinical trial. JAMA 2017;317:2072-2087.

Diamox and Neptazane for the Eye

Posted on March 12, 2022 by Scott Pautler

What are carbonic anhydrase inhibitors (CAI)?

CAI medicines are sometimes prescribed to lower the pressure in the eye either to control pain or to decrease the chances of damage to the eye from high pressure (as in glaucoma). They may also be used to decrease abnormal fluid leakage from blood vessels in the retina (e.g. retinitis pigmentosa). These pills are very effective and may be used along with eye drops to lower the eye pressure. The two most common pills used are Diamox (acetazolamide) and Neptazane (methazolamide).

What side effects might be encountered?

While you are taking these medicines, you may notice a tingling sensation in the fingers, toes, or lips; an altered sense of taste; a loss of appetite; drowsiness; a “washed out” feeling; or an increase in urination. These are not allergic reactions, but should be reported to the doctor if they become bothersome.

It may be helpful to take potassium supplements (e.g. banana) while on CAI to prevent low potassium levels in the blood. Low serum potassium may cause muscle cramps and weakess, abdominal cramps, palpitations, faintness from low blood pressure, and depression.

The dosage of CAI may be reduced in patients with reduced kidney function (see table below). CAI may not be used in advanced cases of liver cirrhosis.

Only rarely do severe reactions occur. Be sure to report hives, skin rashes, gout, allergy to sulfa antibiotics, kidney stones, kidney failure, mental depression, liver failure, blood in stool or mouth, easy bruising, or anemia.

What other medicines might interact with CAI?

Other drugs rarely interact with CAI and an adjustment in dosage is sometimes needed. CAI may increase the effect of diuretics (HCTZ, lasix, bumex, etc.), high-dose aspirin, and quinidine. CAI may increase the effect of digoxin (lanoxin), phenytoin (Dilantin), carbamazepine, primidone, and lithium. Caution should be used when taking metformin for diabetes; CAI may increase the risk of lactic acidosis. Be sure to notify your doctor if you are taking any of these medicines.

How to adjust the dosage in kidney failure?

The table below shows how to adjust dosage of acetazolamide (Diamox) in the setting of kidney disease.

Glomerular Filtration Rate (GFR) in mL/min	Dosage
20-50	250 mg up to 4 times a day
10-20	250 mg up to 2 times a day
<10 or on dialysis	250 mg daily or 3 times a week

reference: https://kidneydiseaseclinic.net/renaldrugs/Acetazolamide.php

By Scott E. Pautler, MD

Lattice Degeneration

Posted on March 4, 2022 by Scott Pautler

What is lattice degeneration?

Lattice degeneration is a condition in which the retina develops areas of abnormal thinning. The thinning occurs as the retina stretches during growth of the eye. The retina is a “tissue-paper” thin layer of nerve tissue, which lines the inside of the eye like the film in a camera. In the eye, light is focused onto the retina, which “takes the picture” and sends the image to the brain. Lattice degeneration is most common in near-sighted people and affects about 7% of the general population.

What causes lattice degeneration?

Lattice degeneration appears to be an inherited condition that usually develops in childhood or early adulthood. The eye, which is round like a ball at birth, becomes oval like an egg. The elongation of the eye causes the retina to stretch. As a result, thin areas develop in the retina similar to “stretch marks” that occur in the skin with growth or weight gain.

Why is it important to know about lattice degeneration?

Lattice degeneration in itself causes no symptoms or loss of vision. It is important because lattice degeneration predisposes eyes to retinal detachment, which can cause permanent blindness without treatment. With age, trauma, or inflammation, the vitreous gel that fills the eye begins to condense and pull away from the retina. If the retina has become weakened by lattice degeneration, it is more likely to tear when pulled upon. A tear in the retina allows fluid from the vitreous gel to seep under the retina as the retina detaches. Fortunately, only one in 200 eyes with lattice degeneration ever develop retinal detachment. Usually no treatment of lattice degeneration is needed, but symptoms of new floating spots or fibers should be reported to the doctor promptly. An examination may disclose breaks in the retina, which may be treated in the office with laser. The appearance of a dark curtain or shadow from the side-vision like an eclipse of the moon is an even more serious symptom that may indicate retinal detachment and require major eye surgery to repair.

By Scott E. Pautler, MD

Alport Syndrome and the Eyes

Posted on February 4, 2022 by Scott Pautler

Alport syndrome is an inherited condition that prominently affects the kidneys. It may also cause hearing loss and affect the eyes. It is due to an alteration in genes that codes for a protein called collagen. Alport syndrome affects about 1 in 5,000 to 10,000 people in the US. Depending on which gene is affected, there are three types of Alport syndrome:

1.) X-Linked Alport syndrome is the most common type (80% of cases) and it affects males more severely than females.

2.) Autosomal recessive Alport syndrome must be inherited by an affected gene in both parents. It is rare and affects males and females equally.

3.) Autosomal dominant Alport syndrome is inherited from one parent with an abnormal gene. It affects males and females equally and may be less severe.

How does Alport syndrome damage the kidney?

Alport syndrome causes abnormal collagen to form. There are many different types of collagen, which is deposited outside the cells to give structural and functional support to cells in the body. The collagen (type IV) affected by Alport syndrome is important for kidney function. It affects the glomerulus, which is the blood filtering unit of the kidney. The decline in kidney function may eventually require kidney transplantation.

What kidney symptoms does it cause?

Alport syndrome causes blood in the urine, the most common early sign of disease. Urinalysis reveals protein in the urine, as well. Related to damage in the kidney, Alport syndrome may also cause swelling (edema) of the extremities (especially, the legs). High blood pressure is also common. Other symptoms include weakness, fatigue, loss of appetite, poor digestion, excessive thirst, and frequent urination.

How are the eyes affected?

Alport syndrome affects the cornea, lens, and retina of the eye. The changes in the eye are more common with X-linked and autosomal recessive disease than in autosomal dominant cases.

The cornea is the clear front window of the eye. Alport syndrome may cause recurrent corneal erosions (similar to a scratched cornea, but without trauma). Symptoms include intermittent pain, redness, tearing, blurred vision. PPCD is a corneal dystrophy that may occur and cause similar symptoms.

The lens is positioned behind the colored iris and focuses light onto the retina in the back of the eye. Alport syndrome may cause an unusual bulging of the anterior surface of the lens (anterior lenticonus), which may require the use of glasses and may cause cataract formation.

What is the retina?

The retina is a thin layer of delicate nerve tissue, which lines the inside wall of the eye like the film in a camera. In the eye, light is focused onto the retina, which “takes the picture” and sends the image to the brain. The retina has two main areas. The macula is the central area that gives you sharp, central vision and color vision. The peripheral retina is the part of the retina that gives you side vision and night vision.

How is the retina affected in Alport syndrome?

Alport syndrome causes abnormalities of the inner the retina, especially evident in the macula. Inner retinal deposits cause no symptoms, but may be mistaken for dry macular degeneration on a routine eye exam. These deposits rarely cause symptoms; though a hole in the center of the retina (macular hole) has been reported.

There appears to be an increased risk of lattice degeneration in Alport syndrome. This may increase the risk of retinal detachment later in life.

How are eye problems in Alport syndrome diagnosed?

An ophthalmologist may diagnose eye changes on a careful routine examination. Sometimes, special scans and photographs are needed. The patient may perform vision checks at home with the help of an Amsler grid. Distortion of the grid indicates macular problems and warrants a prompt eye exam.

How are eye problems associated with Alport syndrome treated?

No treatment is needed if the vision is not threatened. Corneal problems may be treated with eye drops and contact lenses. Only rarely is surgery needed. Lens changes may be compensated for with the use of prescription glasses. In some cases, cataract surgery is needed. Only in severe cases of retinal disease is treatment needed by eye injections or surgery.

By Scott E. Pautler, MD

Vabysmo (faricimab) Therapy

Posted on January 29, 2022 by Scott Pautler

What is Vabysmo therapy?

Vabysmo therapy (pronounced, “vah-BYE-smo”) is a treatment for wet-type macular degeneration and diabetic macular edema. It involves repeated inje ctions of medication into the eye to stop abnormally leaky blood vessels. Vabysmo is the trade name of the medication and faricimab is the research/generic name. On January 28, 2022, the FDA approved Vabysmo for use in the United States based on standard phase 3 study results (Yosemite/Rhine Studies for diabetic macular edema and Tenaya/Lucerne Studies for wet macular degeneration).

How effective is Vabysmo therapy?

Vabysmo may last longer than other drugs currently available to treat these conditions. However, it has been my experience that Vabysmo offers little additional benefit in diabetic macular edema. I currently prefer Lucentis in patients treated for diabetic macular edema.

In wet-type macular degeneration (wAMD), Vabysmo does appear to last longer than other currently approved medications in some patients. However, there appears to be an increased risk of loss of vision from RPE tear in patients with serous retinal pigment epithelial detachment in the setting of age-related macular degeneration.

What are the risks of Vabysmo therapy?

Severe complications are very rare, but risks of Vabysmo injection include bleeding, infection, retinal detachment, glaucoma, cataract, and loss of vision/loss of the eye. The risk of retinal detachment is about 1 in 5,000 injections, but the visual results are poor despite surgical repair. In initial studies there appeared to be a low risk (1.8%) of stroke with this type of therapy. The risk of stroke may be related to the older age of patients in which it is used. Further investigation will provide more information. Non-infectious inflammation is less common with Vabysmo than brolucizumab (Beovu), another drug that offered drug treatment at reduced intervals. Although rare, inflammation did occur in Vabysmo (1-2% of cases) more than twice as often as it did with Eylea (1% or less). Pregnancy should be avoided while on Vabysmo therapy.

What do I expect after a Vabysmo injection?

UPDATE October 2022: I have been using Vabysmo in the office. I am pleased with the results in patients with wet AMD in that I can extend the treatment interval further than with older drugs. These findings are in concert with a recent two-year report of the Tanaya Study at the American Academy of Ophthalmology. However, patients with large serous pigment epithelial detachments (PED) appear to be at greater risk of vision loss from rips in the PED. In contrast to eyes with macular degeneration, I have not been impressed with superior effectiveness of Vabysmo in patients with diabetic retinopathy.

By Scott E. Pautler, MD

Vuity Eye Drops for Near Vision

Posted on December 20, 2021 by Scott Pautler

Eye Anatomy. Image courtesy of Caitlin Albritton.

What is Vuity?

Vuity is a new eye drop to improve near vision in mature adults and is available with a prescription. It became available with FDA approval in 2021. The generic name for Vuity is pilocarpine, a drug used for years to treat some types of glaucoma.

How does Vuity work?

Vuity works by causing the pupil to constrict. The pupil is the small black opening in the center of the iris (the colored part of the eye, usually blue or brown). When the pupil constricts it provides a greater depth of field just like a camera with a small aperture. Vuity also constricts the ciliary muscle inside the eye. This is the muscle that normally focuses the eye from distance to near.

What did the studies of Vuity show?

Gemini I and II were studies to prove the benefit of Vuity. Between the two studies a total of 375 patients were treated. One hour after instilling Vuity, about 26% more patients on Vuity had an improvement in near vision (three lines on the eye chart) compared with patients given a placebo. This suggests that a majority of patients may experience less of an effect. Vuity likely provides a modest short-term effect with minimal risk to most people making it of marginal value (cost/benefit ratio).

How do you use Vuity?

Apply a drop of Vuity to each eye in the morning. The drop takes affect within an hour and slowly loses its effect over 6-10 hours. If Vuity is used more than once a day, it is more likely to cause side effects.

What are the adverse effects of Vuity?

Vuity should not be used by anyone with an allergy to pilocarpine. It should also be avoided in people prone to iritis. Some patients notice poor vision at night while using Vuity; this is especially true if it is used after noon or in eyes with cataract. Therefore, caution may be needed while driving at night. Sometimes, patients experience accommodative spasm in which they have trouble focusing from near to distance. A brow ache may occur when the drop is started, but usually subsides over time with continued use of Vuity. Little is known about the safety of Vuity in pregnancy and during breast feeding. If you use soft contact lenses, they should be removed before instilling Vuity. They may be placed back in the eye after 10 minutes. Use Vuity at least 5 minutes apart from other eye drops you use for other conditions. Very rare adverse effects from Vuity may include acute angle-closure glaucoma and retinal detachment. Therefore, the following symptoms should be reported promptly: new flashes and/or floaters, any loss of vision (including loss of side vision), pain, or significant redness.

By Scott E Pautler, MD

Retinitis Pigmentosa

Posted on October 7, 2021 by Scott Pautler

What is retinitis pigmentosa?

Retinitis pigmentosa (RP) is a group of inherited problems of the retina. The retina is a thin layer of delicate nerve tissue that lines the inside wall of the eye like the film in a camera. In the eye, light is focused onto the retina, which “takes the picture” and sends the image to the brain. Retinitis pigmentosa especially affects the peripheral part of the retina where there are many rod-shaped cells that normally provide side vision and night vision. In advanced cases it may also affect the sharp, central, reading vision and color vision.

What causes retinitis pigmentosa?

Retinitis pigmentosa is inherited through a variety of different genes. Because it is hereditary, other members of the family may have retinitis pigmentosa. However, sometimes the symptoms are mild and special testing may be required. At other times the abnormal gene that causes retinitis pigmentosa may skip several generations. In these families no other members can be found to have the problem.

What are the symptoms of retinitis pigmentosa?

Retinitis pigmentosa may cause no symptoms in the early stages. And symptoms may begin early or late in life. Initially, night vision is impaired. This makes it difficult to walk in unfamiliar surroundings in dim illumination. When the peripheral vision (side vision) is affected, an individual with retinitis pigmentosa may accidentally bump into things that are not directly in view. The severity of these symptoms slowly progresses over years and may impair safe driving vision or result in legal blindness. The rate of progression tends to be consistent in each family affected. Therefore, older family members may be able to provide useful information to younger family members. Late in the course of retinitis pigmentosa, the central vision and color vision may be affected. Make a point to have trusted family and friends help to monitor your ability to drive safely and ask your doctor annually if you have sufficient vision to drive safely and legally.

How is retinitis pigmentosa diagnosed?

The symptoms listed above may be the first clue to the diagnosis. A routine dilated eye examination can detect the retinal changes of retinitis pigmentosa. In some cases, a fluorescein angiogram is helpful. In this procedure the ophthalmologist injects a dye into the vein of the arm. Special photographs are taken of the eye, which show the degeneration of the retina. An electroretinogram (ERG) is also used to demonstrate faint electrical abnormalities in retinal function. In this test, electrodes are taped to the head and to contact lenses. A computer magnifies the electrical impulses generated by the retina in response to carefully programmed flashing lights. Finally, genetic testing may be considered in order to identify a specific gene variant that may be responsible for causing the problem. This may be important in confirming the diagnosis, genetic counseling, and treatment. Blueprint genetics offers free testing for US residents.

How is retinitis pigmentosa treated?

There is currently no proven treatment for most forms of retinitis pigmentosa. One type of retinitis pigmentosa is caused by a gene called RPE65. Patients with this gene variant may undergo gene therapy to treat this type of retinitis pigmentosa. Future research offers the hope of treatment of additional genes that cause retinitis pigmentosa. A mouth swab may be sent for free gene testing.

What about vitamins and nutritional supplements?

For many years research indicated that high doses of vitamin A may be helpful to slow the progression of RP. However, in 2023 a carefully designed analysis revealed there is no benefit, in general. They did report a possible benefit in a rare type of RP seen in families with mutations in the RHO gene. High doses of vitamin A may cause liver damage and should be administered under the care of a physician.

Vitamin E appears to be harmful in high doses for people with RP. It appears to worsen the vision. Therefore, the AREDS vitamins that are recommended for people with age-related macular degeneration should be avoided in people with retinitis pigmentosa. However, routine use of multi-vitamins are safe in RP, as they usually contain less than 30 IU vitamin E per day.

There are other supplements that are often recommended. Lutein is often recommended in RP at a dose of 10-20 mg per day. Fish oil (DHA 200mg per day) may be a helpful antioxidant in RP. Much research needs to be done to prove they are helpful, but there is no compelling evidence to indicate that they are harmful.

Should patients with RP avoid sunlight?

There appears to be consensus among experts in the field, that sunlight tends to worsen the progression of retinitis pigmentosa. Therefore, most recommend avoiding excess exposure to sunlight. Wear a broad-brimmed hat and sunglasses when out-of-doors.

What support services are available?

A wide range of support services, rehabilitation programs, and devices are available to help people with retinitis pigmentosa continue with many of their favorite activities. The use of a white cane can be a valuable aid in navigating in unfamiliar surroundings. It also serves to notify other people to be more courteous. The Lighthouse for the Blind and the Watson Center have classes and specialists in providing prescription lenses to magnify printed material. The Argus II Retinal Implant was approved by the FDA in 2013 for patients with very severe loss of vision from retinitis pigmentosa. The Division of Blind Services provides rehabilitation services and financial aid for eye care in selected cases. Your doctor can give free access to the “talking book” library to make “books on tape” available. A form is available from your doctor that establishes legal blindness to be used for property tax and income tax deductions. As always, if you have any questions please do not hesitate to contact your doctor for more information.

By Scott E. Pautler, MD

Diabetic Vitreous Hemorrhage

Posted on July 22, 2021 by Scott Pautler

What is diabetic vitreous hemorrhage?

Diabetic vitreous hemorrhage means blood has leaked into the vitreous gel of the eye as a result of diabetic damage. The vitreous is a clear gel that fills the center of the eye and helps to hold the retina in place against the eye-wall like wallpaper in a room. The retina is a thin layer of delicate nerve tissue, which acts like film in a camera. In the eye, light is focused onto the retina, which “takes the picture” and sends the image to the brain. The retina has many fine blood vessels that may become damaged from diabetes leading to bleeding into the vitreous. Blood in the vitreous (vitreous hemorrhage) interferes with vision.

What symptoms does diabetic vitreous hemorrhage cause?

Diabetic vitreous hemorrhage usually causes many new floaters in the vision. Floaters may appear as round specks, hair-like or bug-like debris, or clouds moving in your vision as though they were in front of your eye. They are more noticeable when looking at a blank surface and may interfere with the good vision in the fellow eye. If vitreous hemorrhage is severe, the vision may be severely limited. Patients may only see shadows or light, but no details.

Flashes are brief streaks of light that are usually seen off to the side, especially at night when you turn your head or eyes. Flashes are caused by vitreous gel pulling on the retina with eye movement. They may be seen in the setting of diabetic vitreous hemorrhage, but are not worrisome in themselves.

Although many people have occasional floaters or flashes of light, the sudden onset of many new floaters with or without flashes is an important sign of abnormal pulling on the retina by the vitreous. In some people with these symptoms, the retina may tear and detach resulting in loss of vision. Therefore, these new symptoms warrant prompt evaluation.

What causes diabetic vitreous hemorrhage?

Diabetes can cause vitreous hemorrhage by weakening the blood vessels in the retina and by causing the vitreous gel to shrink and pull on the retinal vessels. Aging also causes changes in the vitreous gel and can cause it to pull on the retina. In any given patient with diabetes, both weakened retinal blood vessels, as well as tugging on the blood vessels from the vitreous play a role in causing vitreous hemorrhage. However, in some eyes weakened blood vessels may be the main reason and in other eyes the main reason for bleeding may be tugging from the vitreous. This is an important issue as diabetic vitreous hemorrhage may be treated differently depending on its underlying cause.

How is diabetic vitreous hemorrhage treated?

The most important step is to have a thorough eye examination with ultrasonography. The ultrasound machine uses sound waves to safely and effectively “look through” the blood in the vitreous to see if the retina is attached. If a retinal detachment is found, surgery is required in an attempt to repair it. If no retinal detachment is found on ultrasound exam, your doctor may allow the vitreous hemorrhage to clear on its own with time. The ultrasound exam may be repeated periodically to assure the retina remains attached. If the hemorrhage does not clear on its own, vitrectomy surgery as a one-day surgery in the hospital operating room may be considered. The amount of visual return depends on several factors including the health of the underlying retina.

In an effort to prevent additional bleeding, the underlying diabetic retinopathy may be treated with medication injections (e.g. Avastin, Lucentis, or Eylea) into the eye. These injections can usually be given without significant pain by using anesthetics. The injections reduce the risk of future bleeding, but do not hasten the clearing of the bleeding that has already occurred. These medication injections may be especially important if no previous laser (or insufficient laser) has been given for diabetic retinal damage (diabetic retinopathy) prior to the vitreous hemorrhage. Medication injections do not help with tugging on the retinal blood vessels by the vitreous. Indeed, in rare cases the injections may increase the tugging. Therefore, if tugging from the vitreous is determined to be the main factor in causing the diabetic vitreous hemorrhage, injections may not be used. Instead, vitrectomy surgery is more effective at relieving the tugging.

Once the vitreous hemorrhage has cleared over time with observation or with vitrectomy surgery, laser is often used to stabilize the retinal blood vessels that have been weakened from diabetes. This helps reduce the chances of reoccurrence of vitreous hemorrhage in the future.

What should I be on the lookout for?

After examination or treatment for a vitreous hemorrhage, you should notify your doctor if you have a burst of new floaters, a loss of side vision, or pain. Sometimes, retinal tears or a retinal detachment occur at a later date after the examination.

By Scott E. Pautler, MD

Neovascular Glaucoma

Posted on June 11, 2021 by Scott Pautler

What is neovascular glaucoma (NVG)?

Neovascular glaucoma (NVG) is a severe type of glaucoma. Glaucoma is a condition in which the pressure inside the eye damages the cells of the optic nerve. The normal range of pressure in the eye is between 8-21 units of measurement. There is a tissue inside the eye called the ciliary body that pumps a clear fluid (aqueous) into the eye keeping the eye from collapsing. Another tissue called the trabecular meshwork drains the aqueous from the eye preventing the pressure from building up too high. The pump and the drain are not connected and do not communicate with each other. However, there is a normal balance between the pump and drain so that the eye pressure remains normal and healthy for the eye. In neovascular glaucoma (NVG) abnormal blood vessels grow inside the eye where they block the drain resulting in high pressure. High pressure inside the eye damages the cells of the optic nerve. The optic nerve transmits information from the eye to the brain to provide vision. Therefore, NVG can cause pain, loss of vision, and blindness if left untreated.

What causes neovascular glaucoma (NVG)?

The abnormal blood vessels in NVG grow inside the eye as a result of poor retinal blood supply. There are many conditions that cause abnormal blood supply to the retina. They include diabetic retinopathy, retinal vein occlusion, retinal artery occlusion, ocular ischemic syndrome, retinal detachment, and inflammation. In these conditions the blood supply to the retina is impaired, so the retina sends out chemical messages that it needs more blood supply. As a result, new blood vessels begin to grow inside the eye. Unfortunately, these new blood vessels may grow into the drain (trabecular meshwork) where they cause harm.

What are the symptoms of neovascular glaucoma (NVG)?

In the early stages of NVG, there may be no symptoms. However, as the pressure inside the eye rises, symptoms include pain, redness, and loss of vision. Sometimes, the pain is so severe that it causes nausea and vomiting. If left untreated, NVG frequently results in a blind eye.

How is neovascular glaucoma (NVG) diagnosed?

The most common test for glaucoma in an eye examination is tonometry. Tonometry measures the pressure inside the eye. Most people are first suspected to have glaucoma because high pressure is found on an eye exam. In NVG the ophthalmologist then detects abnormal blood vessels growing in the drain (called NVA) by an office exam called gonioscopy. The presence of high pressure in an eye with NVA makes the diagnosis of neovascular glaucoma.

What treatment is available?

The key to treating NVG is addressing the underlying cause of poor blood supply to the retina. Examination and testing usually provides the retinal diagnosis and treatment is directed toward treating that condition. Frequently, medication injections (Avastin, Lucentis, and Eylea) initially help control the growth of abnormal blood vessels until laser or cryopexy can provide a more permanent effect.

If the drain (trabecular meshwork) has not been permanently damaged by scar tissue induced by the abnormal blood vessels, the pressure inside the eye may return to normal. However, if permanent damage has occurred, eye drops and/or surgery may be needed to control the pressure. The first line of treatment in most cases includes prescription eye drops. There are a number of very effective eye drops that work by either opening the drain or by slowing down the pump to lower the pressure. These drops are powerful medicines that should be used exactly as prescribed to prevent blindness from glaucoma and minimize side effects from the eye drops. Side effects are not common, but may include burning, itching, redness, dry mouth, and worsening of bronchitis or asthma. It is very important to take the eye drops exactly as prescribed to prevent blindness. If eye drops fail to control the pressure, surgery may help. Surgery, performed in the operating room (trabeculectomy or glaucoma drainage device), creates an artificial drain to lower the pressure. After trabeculectomy patients are warned to notify the doctor urgently if the eye becomes red or appears to be infected, because infection may enter the eye after glaucoma surgery and result in severe damage or blindness. In general, patients with glaucoma may require regular examinations every three to four months to preserve vision.

The goal of treatment is to protect the vision and relieve pain. If there is no usable vision, the pressure only needs to be controlled enough to prevent pain. In severe cases surgery is performed to remove the eye (enucleation or evisceration) to relieve pain in a blind, painful eye. An artificial eye is made to appear cosmetically acceptable.

by Scott E Pautler, MD

Sickle Cell and the Eyes

Posted on June 6, 2021 by Scott Pautler

What is Sickle Cell Disease?

Sickle cell disease is the most common genetic disease, affecting about 400,000 newborns each year. It is caused by a mutation in the gene that codes for the hemoglobin protein that carries oxygen in the blood stream. Sickle hemoglobin tends to clump into a sickle shape when it gives up its oxygen molecule to the tissues it supplies. When this occurs, the red blood cells lose their flexibility and tend to block the small blood vessels in the body. The retina in your eye is like the film inside a camera. The retina “takes the picture” of objects you look at and sends the message to the brain. The retina is a living tissue, which requires blood supplied by tiny vessels. These blood vessels may be damaged in people with sickle cell disease.

Who is at risk of eye problems in sickle cell disease?

Although more extensive blockage of retinal blood vessels occurs in sickle cell disease, more severe complications (bleeding and retinal detachment) occur in people with a combination of sickle hemoglobin and hemoglobin C (called Hemoglobin SC disease). Some studies suggest men are more likely than women to have loss of vision.

What are the visual symptoms of sickle cell disease?

Blurring of vision may occur if excess damage occurs to the retinal blood vessels. Floaters can look like tiny dots or cobwebs moving about in your vision. They may be due to bleeding from the retina into the central gel of the eye. Retinal detachment may cause a dark shadow to appear off to the side (in the peripheral visual field) and may progress to total loss of vision. Pain is rare and may be due to high pressure in the eye (neovascular glaucoma).

What treatment is available?

There is no cure, but treatment may improve vision or keep the vision from worsening. If bleeding occurs inside the eye due to blocked blood vessels, floaters are seen by the patient. Medicine injections may help recover vision and may be applied without pain in most cases. Laser may stabilize or improve the vision. In some situations, surgery is required. The vision may not return to normal following treatment as there may be some permanent damage to the retina. The earlier retinal problems are found, the better the outcome of treatment. Therefore, annual exams are important and it is critical to report new floaters without delay.

By Scott E Pautler, MD

Vision Loss in ARMD

Posted on May 31, 2021 by Scott Pautler

Why am I losing vision despite treatment for age-related macular degeneration?

Age-related macular degeneration (ARMD) is the most common cause of visual loss in older Americans. Vision may be lost from dry-type or wet-type ARMD:

Dry-type macular degeneration is the most common type and involves the disintegration of the light-sensitive tissues in the macula. Loss of vision is usually gradual in dry macular degeneration. Small blind spots interfere with reading numbers in a row and all the letters of a word. Over time, these blind spots usually enlarge and take away most of the central vision.

Wet-type macular degeneration accounts for about 10% of all cases of ARMD. It occurs in patients with dry-type ARMD when abnormal blood vessels grow under the macula and cause fluid leakage, bleeding, and scarring of the macula. Vision loss may be rapid and severe. Straight lines may appear distorted and the central vision appears blurred early in wet-type ARMD. Over time, a large blind spot may develop in the center of the vision. If one eye develops wet ARMD, there is about a 50% chance the other eye will be affected within the next five years.

There is currently no proven drug treatment to stop dry-type ARMD. Eye vitamins are prescribed for dry-type ARMD. However, the main purpose of the vitamins is to stave off the start of wet-type ARMD. Although AREDS eye vitamins appear to slow the start of blind spots in the vision from dye-type AMD, they do not slow the progression of blind spots once they start. A Meditteranean diet appears to reduce the onset and progression of blind spots from dry-type macular degeneration. Therefore, it is important to limit red meat intake to once per week, eat two servings of whole fruit per day, include fish in the diet, and rely on olive oil rather than other oils with saturated fatty acids. There are a number of on-going research studies to find a treatment to slow or prevent loss of vision from dry-type ARMD. There is even hope for treatment to reverse the loss of vision from dry-type ARMD. Your doctor can put you in touch with study centers if you are interested in learning more about or participating in these research studies. Age-related macular degeneration appears to be an inherited condition. However, it may be aggravated by factors that cause hardening of the arteries like high blood pressure, high cholesterol, overweight, physical inactivity, and tobacco use. Efforts to control these factors may be helpful in slowing loss of vision in dry-type ARMD.

There are fairly good treatment options for wet-type ARMD. Injection therapy (Avastin, Lucentis, Eylea, and Beovu) is the first-line treatment for wet-type ARMD. Lasers are second-line treatment options. Lasers include photocoagulation (which is rarely used currently) and Visudyne photodynamic therapy. Treatment of wet-type ARMD is effective at slowing the loss of vision. Unfortunately, current treatments do not completely prevent the loss of vision from ARMD. There are several reasons why patients may continue to lose vision during treatment of ARMD:

1. Insufficient treatment

Some eyes require injection therapy every four weeks to optimal effect. If treatment is given less often, the wet-type ARMD may progress with loss of vision that may be irreversible. This is an important reason to continue monthly injections in some eyes (as determined by the retinal specialist).

2. Bleeding despite treatment

Bleeding under the retina from ARMD usually results in some degree of permanent scar tissue and loss of vision. Bleeding may occur if treatment is not given frequently enough and appears more likely in patients who take blood thinners. Blood thinners (including aspirin) are usually prescribed to prevent heart attack or stroke. If they are prescribed, the benefits likely outweigh the risks. However, if blood thinners are not prescribed for a patient with ARMD, they may be best avoided to reduce the risk of bleeding from ARMD.

3. Progression of dry-type ARMD while wet-type ARMD is being treated

Many patients are not aware that ARMD always starts with the dry-type. Wet-type ARMD develops later. Therefore, patients with wet-type ARMD may lose vision over time even though their wet-type ARMD is well controlled. That in, they may lose vision from a worsening of dry-type ARMD over time. Complicating this issue is the concern that the very treatment of wet-type ARMD may, in some cases, worsen the dry-type ARMD.

4. New eye problems develop during treatment of ARMD

The ophthalmologist will look for other problems that may cause a loss of vision unrelated to ARMD. Common causes of vision loss include cataract, which is treatable with surgery. Other problems include glaucoma, retinal vein occlusion, and diabetic retinopathy.

What is to be done about the continued loss of vision?

There are a number of actions that may be taken in response to continued loss of vision during treatment of ARMD. The retinal specialist will look for other causes of loss of vision and start appropriate treatment. The frequency of treatment may be changed in response to changes in the retina. Low vision aids (optical and electronic magnifiers) may be helpful. Specially-trained social workers may help make changes in the household to make it easier to remain self-sufficient. It is helpful to remember that the peripheral vision is rarely taken by ARMD. Therefore, although a patient may be determined to be legally blind, total blindness is rare. Most patients with advanced ARMD are able to ambulate and retain independence.

By Scott E Pautler, MD

Retinal Angiomatous Proliferation

Posted on May 23, 2021 by Scott Pautler

What is retinal angiomatous proliferation (RAP)?

Retinal angiomatous proliferation means there is a growth (proliferation) of abnormal blood vessels (angiomatous) in and under the retina (specifically, under the central part of the retina called the macula). Retinal angiomatous proliferation (RAP) is a sub-type of wet age-related macular degeneration (ARMD). Wet ARMD affects the central vision in older patients due to abnormal blood vessels growing under the macula. The macula is the area of the retina in the back of the eye that is responsible for seeing details in the central vision. The retina is a thin layer of delicate nerve tissue that lines the inside wall of the eye like the film in a camera. In the eye, light is focused through the lens onto the retina, which “takes the picture” and sends the image to the brain.

What causes retinal angiomatous proliferation (RAP)?

Retinal angiomatous proliferation (RAP) appears to be caused by the release of blood vessel growth factors in the retina in response to age-related changes. The age-related changes include the accumulation of cellular waste products under the retina (call subretinal drusenoid deposits). The build-up of waste products (SDD) under the retina interferes with retinal function. For one thing, the build-up of SDD separates the retinal cells from the normal blood vessels that nourish them. Without proper nourishment the retinal cells do not work well. Furthermore, when the retinal cells perceive that they are not getting enough oxygen and nutrients, they release growth factors (including one growth factor called VEGF). These growth factors stimulate the growth of new blood vessels to assist in delivering oxygen and nutrients. In other parts of the body, new blood vessels may grow to help or replace old blood vessels and it is a helpful response to poor blood supply. However, in RAP the new blood vessels cause loss of vision due to fluid leakage, bleeding, and scarring of the macula.

What are the symptoms of retinal angiomatous proliferation (RAP)?

Retinal angiomatous proliferation (RAP) may cause no symptoms in its early stages. Over time, symptoms may include blurred central vision, distortion of straight lines and/or a central, gray spot in the vision. In its advanced stages without treatment, RAP may cause a large permanent blind spot in the center of vision. At this stage no treatment is possible and low vision aids are used to compensate for loss of vision. If one eye develops wet AMD, there is about a 50% chance the other eye will be affected within the next five years.

How is retinal angiomatous proliferation (RAP) diagnosed?

Retinal angiomatous proliferation (RAP) is diagnosed in patients with known dry-type age-related macular degeneration. Before the proliferation or growth of blood vessels under the retina develop in RAP, subtle yellow deposits may be identified under the retina. These deposits are called subretinal drusenoid deposits (SDD). SDD develop many years before RAP occurs. A dilated eye examination can detect SDD and alert the retinal specialist to be on the lookout for RAP. Retinal angiomatous proliferation is suspected when a patient with SDD develops blurred vision and swelling (edema) is present in the retina on a retinal scan called OCT (optical coherence tomography). The diagnosis may be confirmed on a more extensive test called fluorescein angiography. This is a procedure where the ophthalmologist injects an organic dye into the vein of a patient’s arm. Then, photographs of the retina show the presence and location of the leaking blood vessels marked by the organic dye.

Why is this diagnosis important?

It is important to recognize RAP because it guides treatment recommendations. This type of wet ARMD is especially sensitive to antiVEGF therapy (injections with Avastin, Lucentis, and Eylea). RAP is so sensitive to antiVEGF therapy that the medication injections are sometimes not required as often as they are in other types of wet age-related macular degeneration such as PCV. Older treatments such as photocoagulation and photodynamic therapy historically do not work well in RAP and can be avoided. Treatment rarely returns vision to normal, but may limit the amount of vision loss from blood vessel growth and leakage. Frequent office visits and photographs are needed. It may be useful to stop smoking, avoid becoming overweight, exercise daily, and control blood pressure and cholesterol. Aspirin should only be used if required to treat disease as recommended by a doctor. Relatives should be checked for macular degeneration, as well.

By Scott E Pautler, MD

Giant Cell Arteritis and the Eyes

Posted on May 14, 2021 by Scott Pautler

What is giant cell arteritis (GCA)?

Giant cell arteritis (also called cranial arteritis or temporal arteritis) is an inflammatory condition affecting medium to larger arteries in people over the age of 50 years. GCA may cause headache, neck stiffness, tenderness of the temple, and/or cramping of the tongue or jaw while eating or talking. It may also cause fever, fatigue, weight loss, depression, night sweats and general feeling of illness or feeling unwell.

What causes giant cell arteritis (GCA)?

The cause of GCA is not very well understood. The inflammation from GCA is not due to infection. In GCA, it appears the body’s immune system attacks itself, in some ways similar to rheumatoid arthritis.

How is giant cell arteritis (GCA) diagnosed?

The diagnosis is first suspected by typical symptoms in an older patient. Blood tests may include complete blood count (CBC), sedimentation rate (ESR), and C-reactive protein (CRP). Biopsy of the temporal artery is necessary in most cases to confirm to diagnosis. Firmly establishing the diagnosis is critical, because treatment needs to be started quickly and continued for a long time in GCA.

How does giant cell arteritis (GCA) affect the eyes?

Giant cell arteritis (GCA) causes loss of vision due to retinal artery occlusion or ischemic optic neuropathy. Early diagnosis is critical to begin treatment and limit the damage from blood vessel inflammation, which includes complications of brain stroke.

How is giant cell arteritis (GCA) treated?

Prompt steroid treatment is important to stop inflammation from causing further damage with loss of vision and brain stroke. Prednisone is continued at a low dose for a year or more to prevent the inflammation from returning. In an effort to avoid or manage side-effects of steroids, methotrexate is sometimes used. Tocilizumab was approved in 2017 for use in GCA. It avoids the use of steroids, but is very expensive.

By Scott E Pautler, MD

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