- Cholesterol deposits in the eyes: Symptoms and treatment
- New Research: Tiny Calcium Deposits in the Eye May Trigger the Development of Macular Degeneration
- From Proceedings of the National Academy of Sciences
- About Age-Related Macular Degeneration
- About the Research
- More about the Study from Proceedings of the National Academy of Sciences
- Additional Information
- What Are Calcium Deposits?
- Major cause of blindness linked to calcium deposits in the eye
- What Causes Eye Mineral Buildup?
- Symptoms of Eye Mineral Buildup
- Diagnosing Eye Mineral Buildup
- Help for Eye Mineral Buildup
- Removal of calcific band keratopathy without ethylenediaminetetraacetic acid (EDTA) in eyes with limited visual potential
Cholesterol deposits in the eyes: Symptoms and treatment
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Cholesterol deposits around the eyes can be surgically removed. The growths usually cause no pain or discomfort, so a person will likely request removal for cosmetic reasons.
The method of removal will depend on the size, location, and characteristics of the deposit. Surgical options include:
- surgical excision
- carbon dioxide and argon laser ablation
- chemical cauterization
Following a procedure, there may be swelling and bruising around the eyelids for a few weeks. Risks of surgery include scarring and a change in the skin’s color.
Cholesterol deposits are very likely to reoccur following removal, especially in people with high cholesterol.
Normalizing lipid levels will have almost no effect on existing deposits. However, treating dyslipidemia is essential, because it can reduce the risk of heart problems. Treatment may also prevent more deposits from developing.
A doctor usually treats dyslipidemia by recommending lifestyle and dietary modifications. A doctor or dietitian can help to develop a plan that works for each individual.
Possible recommendations include:
Being overweight or obese can raise LDL cholesterol and triglyceride levels. Healthful methods of losing weight can help overweight people with dyslipidemia.
Eating a healthful diet
An individual with dyslipidemia should eat a balanced diet low in saturated fats, trans fats, and cholesterol. A doctor or dietician will likely recommend eating more fruits, vegetables, and whole grains. These foods are low in fat and contain no cholesterol.
Foods to avoid include:
- whole milk
- butter, cheese, and cream
- fatty meats and lard
- cakes and cookies
- foods containing coconut or palm oil
A person should consume healthful fats instead. These can be found in oily fish, nuts, seeds, and vegetable oils and spreads.
Foods rich in soluble fiber can also help to lower cholesterol. These include:
- beans, lentils, and other pulses
- oats and barley
- wholegrain rice
- citrus fruits
Regular physical activity is also essential in treating dyslipidemia. It can help to raise levels of HDL cholesterol, and lower levels of LDL cholesterol and triglycerides.
Activities such as brisk walking, cycling, swimming, and running can also improve cardio health and help someone to maintain healthy body weight.
Reducing alcohol consumption
Drinking too much alcohol can increase cholesterol and triglyceride levels. The United States Dietary Guidelines for Americans recommends that women consume no more than one alcoholic drink per day and men no more than two.
A single alcoholic drink is defined as:
- 12 fluid ounces (fl. oz) of regular beer, containing 5 percent alcohol
- 5 fl. oz of wine with 12 percent alcohol
- 1.5 fl. oz of 80-proof distilled spirits with 40 percent alcohol
Smoking tobacco products can raise LDL cholesterol and inhibit the positive effects of HDL cholesterol. A person with dyslipidemia who smokes should talk to a doctor about ways to quit.
Taking lipid-lowering medications
A doctor may also prescribe a lipid-lowering medication, such as a statin, ezetimibe, or niacin.
New Research: Tiny Calcium Deposits in the Eye May Trigger the Development of Macular Degeneration
Researchers from the United States, the United Kingdom, and Germany have discovered that tiny spheres of calcium phosphate, a component of teeth and bones in the human body, may also provide a significant early triggering mechanism for the development of age-related macular degeneration (AMD).
The research team is investigating the possibility of using the presence of these calcium spheres as an early warning signal for AMD risk that can help with earlier intervention and diagnosis. According to the study authors, this finding “could potentially advance AMD diagnoses by at least a decade,” although “the road ahead is still long.”
From Proceedings of the National Academy of Sciences
The research, entitled Identification of hydroxyapatite spherules provides new insight into subretinal pigment epithelial deposit formation in the aging eye (all explained below) has been published in the January 20, 2015 Early Edition of Proceedings of the National Academy of Sciences. Proceedings, first published in 1915, is the official journal of the National Academy of Sciences of the United States. It publishes research reports, commentaries, and reviews that span the biological, physical, and social sciences.
The authors are Richard B. Thompson, Valentina Reffatto, Jacob G. Bundy, Elod Kortvely, Jane M. Flinn, Antonio Lanzirotti, Emrys A. Jones, David S. McPhail, Sarah Fearn, Karsten Boldt, Marius Ueffing, Savanjeet Guy Singh Ratu, Laurenz Pauleikhoff, Alan C. Bird, and Imre Lengyel, who represent the following institutions: the University of Maryland School of Medicine; University College London; Imperial College London; University of Tübingen, Germany; George Mason University, Fairfax, VA; and The University of Chicago, IL.
About Age-Related Macular Degeneration
Age-related macular degeneration (AMD) is a gradual, progressive, painless deterioration of the macula, the small sensitive area in the center of the retina that provides clear central vision. It is the leading cause of vision loss for people aged 60 and older in the United States. According to the American Academy of Ophthalmology, 10-15 million individuals have AMD. Approximately 85-90% of affected persons have the “dry” type of AMD; 10-15% have the “wet” type.
Dry Macular Degeneration
The dry (also called atrophic) type of AMD affects approximately 85-90% of individuals with AMD. Its cause is unknown, it tends to progress more slowly than the wet type, and there is not – as of yet – an approved treatment or cure. “Atrophy” refers to the degeneration of cells in a portion of the body; in this case, the cell degeneration occurs in the retina.
In dry age-related macular degeneration, small white or yellowish deposits, called drusen, form on the retina, in the macula, causing it to deteriorate or degenerate over time.
A retina with drusen
Drusen are the hallmark of dry AMD. These small yellow deposits beneath the retina are a buildup of waste materials, composed of cholesterol, protein, and fats. Typically, when drusen first form, they do not cause vision loss; they are, however, a risk factor for progressing to vision loss.
Wet (Neovascular) Macular Degeneration
In wet, or exudative, macular degeneration (AMD), the choroid (a part of the eye containing blood vessels that nourish the retina) begins to sprout abnormal new blood vessels that develop into a cluster under the macula, called choroidal neovascularization (neo = new; vascular = blood vessels).
The macula is the part of the retina that provides the clearest central vision. Because these new blood vessels are abnormal, they tend to break, bleed, and leak fluid under the macula, causing it to lift up and pull away from its base. This damages the fragile photoreceptor cells, which sense and receive light, resulting in a rapid and severe loss of central vision.
About the Research
Excerpted from Calcium deposits may trigger degenerative blindness, via redOrbit:
Age-related macular degeneration (AMD) may be caused by deposits of microscopic calcium phosphate spheres in the eye. In the study, note that this is the first time these mineralized calcium phosphate spheres have been implicated in AMD. The possible involvement of these tiny calcium spheres, also known as hydroxyapatite (HAP), could ultimately lead to early detection of the disease.
As the researchers explain, HAP is common in the body. It makes up the hard part of teeth and bones, but it had never been detected in the retinal samples of elderly patients. This discovery could help scientists learn how AMD develops, as well as how to better diagnose and treat the condition.
AMD is characterized by a build-up of drusen (deposits of fat and protein) in the retina, which prevents essential nutrients from reaching light-sensitive cells called photoreceptors. Photoreceptors are regularly recycled by cellular processes, which create waste products. Drusen can trap this material, however, causing it to build up in the retina.
Previously, scientists did not fully understand how drusen formed and grew to clinically relevant size, but the new study shows that HAP particles could be responsible. The study authors believe that the calcium spheres could attract proteins and fats to the surface, causing them to accumulate over the course of several years or even decades to form drusen.
The researchers made their discovery through post-mortem examination of 30 eyes from donors between 43 and 96 years old. Using fluorescent dyes, they were able to identify the miniature calcium spheres. They also examined tissue samples from AMD patients using X-ray diffraction and fluorescent staining chemicals, which helped reveal the role of HAP in the process.
“We found these miniscule hollow spheres inside all of the eyes and all the deposits that we examined, from donors with and without AMD,” explains lead investigator Dr. Imre Lengyel. “Eyes with more of these spheres contained more drusen.”
Dr. Lengyel noted that the spheres appear long before the drusen itself becomes visible during a clinical examination, and that the new techniques can be used to identify drusen buildup long before it becomes visible using current techniques. The findings could potentially advance AMD diagnoses by at least a decade, she added.
More about the Study from Proceedings of the National Academy of Sciences
From the article abstract:
Significance: Proteins and lipids accumulating in deposits external to the retinal pigment epithelium (RPE) represent a barrier to metabolic exchange between the retina and the choroidal capillaries. With time, these deposits can lead to age-related macular degeneration (AMD), the most common cause of blindness in the elderly in the developed world.
It remains unclear how sub-RPE deposits are initiated and grow to clinically relevant features. Using a combination of high-resolution analytical techniques, we found that tiny hydroxyapatite (bone mineral) spherules with cholesterol-containing cores are present in all examined sub-RPE deposits, providing a scaffold to which proteins adhere.
If the spherules are important in initiating sub-RPE deposit formation, this finding may provide attractive new approaches for early identification and treatment of AMD.
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What Are Calcium Deposits?
Q1. My optometrist told me I have a calcium deposit in my right eye. What is this, and what can I do about it?
Calcium deposits may result from several conditions of the eye. Depending on their location, they can affect the function of the eye, or they can simply be an asymptomatic finding during a routine eye exam. Two common locations of calcium deposits in the eye are the cornea and the vitreous body. Calcium deposits in the cornea, which is the most superficial and transparent layer of the eye, can be mild, stationary, and peripheral (off to the side), in which case they don’t affect the vision (for example, Vogt’s limbal girdle). In some cases, however, they become progressively larger and compromise the central corneal transparency, thus affecting vision (for example, band keratopathy). In the latter case, the eye doctor might use a special solution to reduce the white opacities and improve vision.
In a condition called asteroides hyalosis, calcium deposits are found in the vitreous body, the gel that fills the eye. These little deposits floating in the vitreous gel look striking to the examining physician because they usually reflect brightly against the light of the instrument used to see the internal part of the eye. These white dots rarely cause visual problems — they are not normally seen in the course of daily activities. Sometimes patients may refer to “floaters” in the involved eye, meaning that they can actually see some of the deposits moving in the visual field, especially in clear environments, such as a blue sky on a sunny day. Still, in most cases, these deposits don’t cause any symptoms.
Q2. I wear gas-permeable contact lenses, and I have mucus buildup under my eyelids. How do I remove the mucus? I have already tried eyedrops and allergy drops.
Mucus associated with the use of rigid gas-permeable contact lenses may have many causes. One is the accumulation over time of deposits on the lenses themselves. If the contacts are old (over a year of continued use), it may be a good idea to replace them with fresh ones. Often, particular patients are especially prone to deposits on their contacts and should be evaluated every three to six months to determine whether a more frequent change of contacts is required. Another problem might involve the cleaning solution, which can trigger reactions in sensitive eyes. If this is the case, changing the cleaning solution may be helpful. Some patients develop allergies to one or more ingredients in cleaning solutions (for example, thimerosal), and this may induce a permanent condition of mucus buildup and red eyes. An easy way to overcome this problem is to use thimerosal-free cleaners. In your case, the best approach would be to find out what is causing the increased mucus production instead of “blocking” the normal reaction with medications (allergy drops and eyedrops). So try changing your solution or getting new lenses. If neither approach works, see your ophthalmologist to get help in finding a solution.
Learn more in the Everyday Health Vision Center.
AMD affects 1 in 5 people over 75, causing their vision to slowly deteriorate, but the cause of the most common form of the disease remains a mystery.* The ability to spot the disease early and reliably halt its progression would improve the lives of millions, but this is simply not possible with current knowledge and techniques.
The latest research, published in Proceedings of the National Academy of Sciences, has implicated tiny spheres of mineralised calcium phosphate, ‘hydroxylapatite’, in AMD progression. This not only offers a possible explanation for how AMD develops, but also opens up new ways to diagnose and treat the disease.
AMD is characterised by a build-up of mainly protein and fat containing deposits called ‘drusen’ in the retina, which can prevent essential nutrients from reaching the eye’s light-sensitive cells, ‘photoreceptors’. Photoreceptors are regularly recycled by cellular processes, creating waste products, but drusen can trap this ‘junk’ inside the retina, worsening the build-up. Until now, nobody understood how drusen formed and grew to clinically relevant size.
The new study shows that tiny calcium-based hydroxyapatite, commonly found in bones and teeth, could explain the origin of drusen. The researchers believe that these spheres attract proteins and fats to their surface, which build up over years to form drusen. Through post-mortem examination of 30 eyes from donors between 43 and 96 years old, the researchers used fluorescent dyes to identify the tiny spheres, just a few microns — thousandths of a millimetre — across.
“We found these miniscule hollow spheres inside all of the eyes and all the deposits that we examined, from donors with and without AMD,” explains Dr Imre Lengyel, Senior Research Fellow at the UCL Institute of Ophthalmology and Honorary Research Fellow at Moorfields Eye Hospital, who led the study. “Eyes with more of these spheres contained more drusen. The spheres appear long before drusen become visible on clinical examination.
“The fluorescent labelling technique that we used can identify the early signs of drusen build-up long before they become visible with current methods. The dyes that we used should be compatible with existing diagnostic machines. If we could develop a safe way of getting these dyes into the eye, we could advance AMD diagnoses by a decade or more and could follow early progression more precisely.”
Some of the mineral spheres identified in the eye samples were coated with amyloid beta, which is linked to Alzheimer’s disease. If a technique were developed to identify these spheres for AMD diagnosis, it may also aid early diagnosis of Alzheimer’s. Whether these spheres are a cause or symptom of AMD is still unclear, but their diagnostic value is significant either way. As drusen are hallmarks of AMD, then strategies to prevent build-up could potentially stop AMD from developing altogether.
“The calcium-based spheres are made up of the same compound that gives teeth and bone their strength, so removal may not be an option,” says Dr Lengyel. “However, if we could get to the spheres before the fat and protein build-up, we could prevent further growth. This can already be done in the lab, but much more work is needed before this could be translated into patients.”
“Our discovery opens up an exciting new avenue of scientific research into potential new diagnostics and treatments, but this is only the beginning of a long road.” says Dr Richard Thompson, the main international collaborator from the University of Maryland School of Medicine, USA.
The work was supported by the Bill Brown Charitable Trust, Moorfields Eye Hospital, Mercer Fund from Fight for Sight, and the Bright Focus Foundation. The UCL-led international collaboration involved researchers from the University of Maryland School of Medicine, Imperial College London, the University of Tübingen, George Mason University, Fairfax, and the University of Chicago.
*A minority (10%) of cases are ‘wet’ AMD, which is caused by leaking blood vessels and can sometimes be treated with eye injections. The majority (90%) of cases are ‘dry’ AMD, whose cause remains a mystery and for which there are no reliable treatments.
What Causes Eye Mineral Buildup?
There are several eye conditions that can lead to calcium deposits. The location of the deposits determines if they affect eye function. The most common locations for mineral deposits are the vitreous body and cornea. Deposits in the cornea can be mild, but in some cases they may become progressively larger and compromise vision.
Band keratopathy is a condition that is the result of renal failure or gout. Those with this condition will have calcium deposits in the cornea due to excess calcium levels in the body. Asteroides hyalosis is a condition where deposits are found in the gel that fills the eye. These can cause “floaters” where deposits can be seen moving in the visual field. In most cases, the calcium deposits from these conditions don’t cause major problems or permanent damage.
Symptoms of Eye Mineral Buildup
Mineral buildup behind or in the eyes can cause a variety of symptoms from benign to more serious. Common symptoms include redness, dryness and a feeling of something being in the eye. In some instances, the eye may water more as it works to clear the debris. Many people with calcium deposits report seeing floaters or in rare cases, cloudy, blurry or obstructed vision.
Diagnosing Eye Mineral Buildup
Mineral deposits in the eyes are often detected during routine eye examinations. The deposits gleam and reflect light as it crosses the surface of the eye. Further testing may be done to determine if the deposits are causing vision problems. Once the source of the deposits is determined, an optometrist or ophthalmologist will develop a treatment plan based on the unique needs of the individual.
Help for Eye Mineral Buildup
Treatment will depend upon the underlying conditions causing the mineral buildup. In some people, nutrient deficiencies can cause calcium deposits to develop in the soft tissues of the body, including the eyes. Increasing the amount of magnesium and vitamin K in the diet is a natural way to prevent buildup. In some cases, if deposits are starting to interfere with vision, the ophthalmologist may put a solution in the eye that reduces them and improves vision.
Eye drops or medications may be prescribed to deal with general irritation and inflammation that can be caused by calcium deposits. If the deposits are inside the lid or other areas where they can cause pain, anti-inflammatory medications and pain relievers may be used or in some cases surgical removal may be suggested.
Many people prefer not to use prescription drops due to potential side effects and choose to seek a safer, natural alternative instead. Homeopathic remedies are 100% safe and side effect free. Red Eye Reducer helps to reduce redness, soothe inflammation, relieve the bloodshot appearance and provide fast-acting relief from itching and burning sensations in the eyes.
Removal of calcific band keratopathy without ethylenediaminetetraacetic acid (EDTA) in eyes with limited visual potential
In calcific band keratopathy (CBK), calcium accumulates in the superficial layers of the cornea in the interpalpebral fissure zone, most often due to chronic ocular inflammation or systemic hypercalcemia.1,2 The calcium deposits cause pain, foreign body sensation, and decreased visual acuity. The most common methods for removing the calcium deposits are mechanical debridement with a blade, chemical chelation with ethylenediaminetetraacetic acid (EDTA), and phototherapeutic keratectomy.
Manual debridement of CBK by scraping with a blade is effective but can lead to an irregular corneal surface.3,4 Chelation with EDTA works by sequestering calcium and softening the deposits. Subsequent mechanical debridement is often required, but this method results in a smoother corneal surface. Chelation with EDTA is currently the most popular treatment for CBK, but EDTA recently ceased to be commercially available in the US. Another option for CBK treatment is phototherapeutic keratectomy, in which the superficial cornea is ablated with an excimer laser, but this method is costly and can cause refractive shifts. Even so, this method may be preferred for eyes with good visual potential. In this paper, we present a method for debridement of CBK with a diamond-dusted burr without EDTA. We provide the results of seven consecutive eyes with limited visual potential treated by this simple, quick, and inexpensive technique.
A retrospective chart review was conducted in accordance with the tenets of the Declaration of Helsinki. A waiver of informed consent and the study were approved by the Institutional Review Board of Medical College of Wisconsin. Using a computerized database, we searched for de-identified records of patients with a diagnosis of CBK who were evaluated at the Froedtert Eye Institute, Milwaukee, WI, between December 2012 and July 2015. We identified seven consecutive eyes that underwent CBK treatment with a diamond-dusted burr without EDTA. The procedure was performed by a single surgeon (SBK) using the standard technique as described below. Visual acuities were noted at the clinic visit preceding surgery (preoperative visual acuity) and at the last clinic visit (final visual acuity). Patients were noted to have symptomatic relief if they described improved eye comfort at any postoperative clinic visit. Recurrence was defined as increased calcium deposits on slit lamp examination by the surgeon.
Description of surgical technique
The procedure may be performed at a slit lamp or in a minor surgical suite using a portable microscope under topical anesthesia with 0.5% proparacaine. The eye is prepped with 10% povidone iodine and draped with a small pre-cut aperture plastic drape (style 1020; 3M, Maplewood, MN, USA). After placing a Nevyas Drape Retractor (Wilson Ophthalmics, Mustang, OK, USA), a thin wire Barraquer speculum is used to separate the lids. In eyes with markedly elevated calcific plaques, a #69 Beaver blade (Beaver Visitec, Waltham, MA, USA) may be used first to debulk the calcific deposits. This blade may also be used to debride the corneal epithelium overlying the calcific band, although this is not necessary. Using the battery-powered reusable 5.0 mm diamond-dusted burr (Ophtho-Burr®; Beaver Visitec), the surgeon applies gentle and even pressure to the cornea in either a rotary or a back-and-forth manner until the calcium is removed (Figure 1 and Video S1). It is important that excessive pressure is not applied to a single location to avoid creating a thin area and to “feather” the edges of the treatment zone to provide a gradual transition to healthy cornea. The cornea is lubricated with balanced salt solution at about one drop per second during the debridement. The debridement using the burr takes about 5 minutes. The remaining corneal epithelial defect is managed with a bandage soft contact lens, and Maxitrol ointment (neosporin, polymyxin B, and dexamethasone; Alcon, Fort Worth, TX, USA) is applied four times daily for 1 week. The bandage soft contact lens is typically removed after 1 week, and patients are treated with topical prednisolone acetate 1% drops tapered over a month.
Figure 1 Appearance before (A) and after (B) treatment of calcific band keratopathy with a diamond-dusted burr without ethylenediaminetetraacetic acid.
Seven eyes from six patients were included for analysis (Table 1). Preoperatively, all patients suffered from discomfort in the eye that underwent the procedure. All eyes had poor preoperative visual acuity due to non-corneal ocular disease. The average age was 22 years. The most common causes of CBK in this series were retinopathy of prematurity (three eyes) followed by chronic uveitis (two eyes). Postoperatively, all the patients reported partial or complete symptomatic relief.
The length of follow-up ranged from 15 days to 31 months (mean 12 months). At the last available follow-up visit, visual acuity improved in one eye, remained the same in three eyes, and worsened in three eyes. The primary cause of decreased visual acuity in all three cases was progression of non-corneal ocular disease. No complications occurred during surgery, and no complications were noted during long-term follow-up. Two eyes experienced recurrence of CBK. The recurrence episodes occurred at 4 and 28 months after treatment.
CBK results from the deposition of calcium salts in the Bowman’s layer and superficial corneal stroma.1 Opacification of the central cornea causes loss of vision and glare, while elevated calcific plaques may contribute to pain, foreign body sensation, photophobia, and tearing.2
The current options for treatment of CBK include scraping with a blade, chelation with EDTA, and phototherapeutic keratectomy. However, each of these methods has limitations. One major new limitation is that EDTA is no longer commercially available in the US, so surgeons must acquire EDTA from a compounding pharmacy.
This paper describes the use of a hand-held battery-powered diamond-dusted burr to treat CBK without using EDTA. Bokosky et al described treating CBK using a Fisch power-driven drill with a 5 mm diamond-dusted tip together with EDTA chelation.5 McGrath and Lee described debridement with a blade, needle, microsponge, and/or diamond-dusted burr without using EDTA for a variety of conditions, including band keratopathy.6 We confirm McGrath and Lee’s findings that EDTA is not needed to treat band keratopathy, and specifically highlight the use of the diamond-dusted burr. The diamond-dusted burr is inexpensive, highly portable, and unlikely to cause significant stromal thinning or perforation. We describe seven cases of successful relief of pain and foreign body sensation due to extensive CBK in eyes with poor visual potential. In these eyes, there is no expectation of improved vision, minimal concern about stromal thinning, and no reliable means of assessing preoperative topography or pachymetry due to the dense, elevated calcium deposits. For eyes with good visual potential, phototherapeutic keratectomy may be the best alternative to EDTA for optimal refractive outcomes.
In patients with elevated calcific plaques, the burr leaves a polished surface, with reduced pain and foreign body sensation. Postoperatively, patients receive a bandage soft contact lens and a combination antibiotic–steroid ointment to reduce foreign body sensation, prevent infection, and promote reepithelialization. Reepithelialization usually occurs within 1–2 weeks, depending upon the size of the residual epithelial defect. Although postoperative infection is a risk of this procedure, there were no cases of infectious keratitis in this series. Two patients experienced recurrence of CBK, which is a known outcome in all the methods of removal. This figure is in line with a recent series that described recurrence in 28% of patients after chelation with EDTA.7 The recurrence interval in our small series treated without EDTA (4 and 28 months) was also grossly similar to the recurrence interval in the large series of patients treated with EDTA (19 months).7 Our practice is to counsel all patients preoperatively that CBK is likely to recur and may require periodic retreatment.
A hand-held battery-powered diamond-dusted burr may be used to remove the calcium deposits without the use of blade or EDTA in patients with CBK. Since EDTA is no longer commercially available, this technique may be useful for eyes with poor visual potential. Future studies are needed with a larger sample size to determine whether this technique effectively relieves discomfort and to assess rates of complications and recurrences.
Source of funding: this work was supported by a gift from Doctor Myrna Larson and Doctor Nelson A Moffat and Research to Prevent Blindness.
The authors report no conflicts of interest in this work.
Video S1 Video demonstrating the technique for treatment of calcific band keratopathy with a diamond-dusted burr without ethylenediaminetetraacetic acid.