Macular Degeneration

Age related macular degeneration (AMD) is the leading cause for central vision loss and for legal blindness in patients over the age of 60 in developed countries. Due to the fact that this group of people represented in the population percentile continues to rise, the social and economic impacts become more evident.

With age, this disease determines anatomical changes to the macula, which is the central part of the retina that allows us to see clearly objects and people that surround us. There are two types of AMD: atrophic (not neovascular) and exudative (neovascular). Both, even though contain different pathogenetic mechanisms, can produce a dramatic reduction in visual perception, with central vision loss.

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Atrophic Macular Degeneration

The atrophic form, characterized by the presence of yellowish deposits (drusen) inside the macula, could be a first symptom. This form represents 85% of all forms of AMD. As the disease progresses, the development of retinal pigment epithelium atrophy and a loss of photoreceptors (cones and rods) cause a progressive and serious central loss of vision along with the capability to read. Unfortunately, at the present time, there does not exist a definite treatment for this type of AMD, despite findings that have shown effectiveness in delaying the progression from the use of high doses of antioxidants and supplementations of lutein and zeaxanthin.

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Exudative Macular Degeneration

The second type of AMD, the exudative form, can develop from an evolution of atrophic macular degeneration or may suddenly take place without forewarning. This represents 15% of all types of AMD and consists of the development of a number of neovessels originating from the choriocapillaris (vascular layer located under the retina) that rupture across an elastic membrane (Bruch), lifting the neurosensory retina and provoking image distortion, immediately perceived by the patient, which only increase with the progression of the disease. When the exudative type evolves into a haemorrhagic, the patient may lose completely, and within only a few seconds, central vision. With time, if not adequately treated, exudative macular degeneration may cause scarring that alters permanently the entire retinal structure, making it impossible to regain good quality vision. In contrary to the atrophic form, exudative, if diagnosed in time and treated adequately, today can offer substantial expectations for preserving vision.

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How to diagnose Macular Degeneration

To diagnose age related macular degeneration (AMD), Dr. Cusumano initially performs a visual acuity exam and a fundus examination with the pupils dilated. If an advanced form of AMD is present or a suspected form of an AMD of the exudative type, it is necessary to perform a fluorescein angiography (FAG) or an indocyanine green angiography (ICG). In both cases, it may also be recommended to have an optical coherence tomography (OCT) in a "spectral-domain" mode in order to optimize the diagnostic process.

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PHARMACOSURGERY

A new therapy has recently been introduced that we have named pharmacosurgery, that consists of using drugs that block a chemical factor promoting proliferation of vascular endothelial cells (called VEGF) resulting in the development of immature neovessels, responsible for the progression of exudative AMD. These pharmaceutical compounds, known as anti-VEGF, derived directly from molecular biology, are injected inside the eye (into the vitreous cavity), allowing the use of minimal therapeutic concentrations with significant reductions of systemic side-effects that may occur if systemically administered.

Anti-VEGF of the new generation are constructed from a humanized anticorpal fragment that binds and blocks all forms of VEGF present in the extracellular space. These are constructed from a smaller molecule that has peculiar properties; in which the smallest has a reduced molecular volume and weight (48 kD) justifies the maximum capacity to penetrate all the layers of the retina. Therefore, their diffusion in the subretinal space after intravitreal administration provides the most effective therapeutic results.

The introduction of the monotherapy with anti-VEGF has represented a historic event in the treatment of this disease, to be compared to the introduction of chemotherapy to treat cancer: the patient does not recover, but the prospects of prolonging the life of the patient, in this case eyesight, is noticeably increased.

Pharmacosurgery is performed with local anesthesia and without pain. The standard protocol for this treatment foresees three consecutive infiltrations one month apart from one another and possibly being repeated in the future. This is related to the response of each single patient to the different existing molecules and the evaluation of the stage of the disease based on the instrumental monitoring [fluorescein angiography (FAG), indocyanine green angiography (ICG), and a high definition optical coherence tomography (OCT) in which the patient must have done throughout the course of the disease.

In some cases, regardless of repeated administration of intravitreal anti-VEGF medicines, the membranes become insensitive and resistant to them and we assist to a progressive evolution of the disease.

For this purpose, a recent discovery has allowed to recognize the growth of some of the lining cells of immature neovessels, dominated pericyte, a sort of "shield" capable to mature pathological neovessels making them non respondent to the anti-VEGF medicines, with an irreducible progression of the disease. The significant result of the preliminary studies have allowed researchers to start a multi center clinical study (phase II), with a new anti-PDGF (Pericyte Derived Growth Factor) molecule that inhibits the growth of pericyte, "stripping" the pathological vessels of their "protection" and exposing them again to the action of conventional anti-VEGF medicines that must always be associated in a combined therapy. In this way, it is possible to recover a majority of patients in whom it was thought that there was nothing left to do, and at the same time improve, with the combined therapy, the efficiency and the duration of the components that are already available to us. In the preliminary study of (phase I), 59% of the patients treated with the association of the anti-PDGF + the most advanced anti-VEGF have obtained a significant improvement in eyesight (improvement minimum of three lines) only just 12 weeks after starting the therapy associated and a medium reduction of 86% of the area of choroidal neovascularization (CNV).

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Future Therapies

At the moment, in the world there exists or are in advanced developing stages various methodological experimentations: (1) intraocular implants non-biodegradable; (2) intraocular implants biodegradable; (3) micro- and nanomolecules; (4) injectable liposomes; (5) cellular micro-encapsulation technology (ECT). Each of these techniques present advantages and disadvantages related to the type of implant as well as to the modality and extent of the molecules being released.

The eye represents an ideal organ to use for devices for the extended release of molecules activated pharmacologically. The presence of an hemato-retinal barrier further contributes to the "seizing" of the medication inside the eye minimizing the systemic absorption and possible side effects.

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Macular Holes

A macular hole is a small tear in the macula. Macular holes happen when the vitreous, a gel-like substance that fills about 80 percent of the eye, begins to shrink and pull away from the retinal surface. This is a normal part of the aging process, but in cases where the vitreous is firmly attached to the retina when it pulls away, it can tear the retina and create a macular hole. The fluid that has replaced the shrunken vitreous can then seep through the hole onto the macula, blurring and distorting central vision.

A macular hole has three stages. Stage I is known as foveal detachment. Without treatment, approximately half of stage I macular holes will progress. Stage II is characterized by partial-thickness holes. Without treatment, about 70% of stage II holes will progress. A full-thickness hole is described as Stage III. Most central and detailed vision can be lost when a Stage III macular hole develops.

Treatment of a macular hole involves a surgical procedure called a vitrectomy. In a vitrectomy, the vitreous gel is removed to prevent it from pulling on the retina, and is replaced with a bubble containing a mixture of air and low absorbable gas . The bubble holds the edges of the macular hole in place as it heals and acts as an internal, temporary bandage. The procedure is generally performed under local anaesthesia, often on an outpatient basis.

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Diabetic Retinopathy

A complication of diabetes and a common cause of blindness, diabetic retinopathy occurs when diabetes damages the tiny blood vessels inside the retina. Diabetic retinopathy often has no early warning signs. People with all types of diabetes should have a comprehensive eye exam at least once a year.

Stages of Diabetic Retinopathy

  1. Mild Nonproliferative Retinopathy – This stage is characterized by microaneurysms, small areas of balloon-like swelling in the retina's tiny blood vessels.
  2. Moderate Nonproliferative Retinopathy - As the disease progresses, some blood vessels that nourish the retina are blocked.
  3. Severe Nonproliferative Retinopathy - Many more blood vessels are blocked, depriving several areas of the retina of blood supply. These areas of the retina send signals to the body to grow new blood vessels for nourishment.
  4. Proliferative Retinopathy - At this advanced stage, the signals sent by the retina for nourishment trigger the growth of new blood vessels. This condition is called proliferative retinopathy. These new blood vessels are abnormal and fragile. They grow along the retina and along the surface of the clear, vitreous gel that fills the inside of the eye. By themselves, these blood vessels do not cause symptoms or vision loss. However, they have thin, fragile walls. If they leak blood, severe vision loss and even blindness can result in the absence of any therapy.

Fluid can leak into the centre of the macula, making the macula swell and causing blurred vision. This is called laser treatment. It can occur at any stage of diabetic retinopathy, but is more likely as the disease progresses.

Treatment

During the first two stages of diabetic retinopathy, no treatment is needed, unless you have macular edema. To prevent progression of diabetic retinopathy, people with diabetes should control their levels of blood sugar, blood pressure, and blood cholesterol. At stage three generally patients need one ore more laser treatment to reduce the risk for progression into proliferative retinopathy. If you are already in the fourth stage of diabetic retinopathy and have severe bleeding, you may need a vitrectomy to remove blood from the centre of your eye.

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Retinal Detachment

When the retina becomes “detached”, it separates from the back wall of the eye, losing its blood supply and source of nutrients. If the retina remains detached, it will degenerate and lose its ability to function. There are three main types of retinal detachment:

Rhegmatogenous retinal detachment is the most common form. It occurs when a tear or hole in the retina allows vitreous fluid to enter the potential space beneath the retina, separating the retina from the layer beneath. This type of detachment generally requires urgent surgery, within 24 hours of diagnosis.

Exudative retinal detachment is caused by leakage from under the retina, which creates fluid that detaches the retina. Tumours and inflammatory disorders are two common causes of exudative detachment.

Traction retinal detachments are caused by a pulling on the retina, usually from fibro-vascular tissue within the vitreous cavity. Proliferative diabetic retinopathy is the most common cause.

At our practice, we offer two types of surgery to reattach the retina:

Scleral buckle surgery uses a flexible band to pull the retina to the back wall of the eye; the doctor often drains off the fluid that is trapped under the retina. The buckle is usually a piece of silicone sponge or solid silicone. Often, scleral buckle surgery can be done with local anaesthetic on an outpatient basis. This procedure has been in use for more than 40 years.

Vitrectomy is a slightly newer procedure that involves removing the vitreous gel and replacing it with a gas bubble, which the body’s fluids will gradually replace. It is most commonly used for traction retinal detachments, but is also used for rhegmatogenous detachments. It can usually be performed as same day surgery with local anaesthesia.

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Glaucoma

Glaucoma is a broad term for a certain pattern of damage to the optic nerve. Glaucoma usually occurs in the presence of high intraocular pressure, but can occur with normal or sub-normal pressure.

There are two main forms of glaucoma: open-angle (which is the most common form and affects approximately 95% of individuals) and closed-angle. There are also several other varieties of glaucoma, including secondary, normal-tension, congenital, juvenile, neovascular, pigmentary, pseudoexfoliation syndrome, and irido-corneal-endothelial syndrome (ICE syndrome).

The different varieties of glaucoma all have slightly different symptoms and risk factors. For early detection of this disease, you should have a dilated pupil eye examination at least every year and if necessary a visual field examination or others, highly specific, instrumental examinations.

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Cataracts

The eye has a natural lens, very much like the lens of a camera, which lies behind the iris and the pupil and focuses images onto the retina at the back of the eye. It works in much the same way as a camera lens, adjusting the eye’s focus. A cataract occurs when this lens becomes cloudy as part of the natural aging process or as a result of complications from other conditions. About half the population has a cataract by age 65, and nearly everyone over 75 has at least one. If the cataract is bad enough to impair vision, corrective surgery is required.

Cataracts are typically removed surgically, and replaced with an intraocular lens. Different types of intraocular lenses exist, some capable of improving vision at one range, and others with multifocal capabilities.

Contact the ophthalmologist for more information about cataracts and intraocular lenses.

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Low Vision

Low vision is a term commonly used to describe partial sight, or vision that isn't fully correctable with surgery, medication, contact lenses, or glasses.

Low vision can range from moderate vision impairment, such as tunnel vision or blind spots, to almost total blindness.

It can have a variety of causes, including injury, diseases and heredity. Sometimes low vision involves a lack of visual acuity, meaning that objects do not come into focus, while other times, it involves the ability to distinguish colours, see contrasts, or determine spatial relationships among objects.

Low vision can describe sight that is hazy with cataracts, blurred or partially obscured in the central visual zone with macular degeneration, and distorted or blurred with diabetic retinopathy. People with glaucoma or retinitis pigmentosa can progressively lose peripheral vision and have difficulty seeing at night.

Children as well as adults can be visually impaired, but it is mostly a problem that afflicts older adults.

If you are having vision problems - such as hazy or blurred vision, light sensitivity, loss of peripheral vision, night blindness, colour confusion, unusual floaters or spots, or difficulty reading - contact Dr. Cusumano. These symptoms could be the first signs of a serious eye disease such as macular degeneration or retinitis pigmentosa. By catching these problems early on, in some cases you can prevent further vision loss.

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Myopia

The way the human eye functions is very similar to the way a camera lens functions. Light enters two lenses of the eye, respectively called the cornea and the lens, and projects an image onto the light sensitive tissue at the back of the eye, called the retina. The iris works just like the diaphragm in a camera, controlling the amount of light that reaches the retina. The retina, made of light sensitive tissue, functions like the film, imprinting the light images projected onto it and sending them to the brain to be interpreted. The most common vision problems such as myopia, hyperopia, and astigmatism may be caused by imperfections in the cornea that cause the images projected on the retina to be distorted.

Myopia, also known as nearsightedness, is caused by a cornea that is too curved or an eye that is too long. These imperfections cause light to focus on the front of the retina, making objects at a distance appear blurry. Myopia typically appears between the ages of eight and twelve years old, and the condition often worsens as the body grows, usually stabilizing in adulthood.

Myopia can be treated with glasses, contact lenses, and refractive surgery, such as PRK. If you suffer from myopia, schedule a consultation with the ophthalmologist today.

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Hyperopia

Hyperopia, also known as farsightedness, is caused by a cornea that is too flat or an eye that is too short. The flattened cornea focuses light at a point beyond the retina, resulting in the blurred appearance of objects at close range. Hyperopia is often left undetected until later in life, because the young eye can compensate for hyperopia by contracting the internal lens of the eye.

Hyperopia can be treated with glasses, contact lenses, and refractive surgery, such as PRK. If you suffer from hyperopia, schedule a consultation with the ophthalmologist today.

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Astigmatism

Astigmatism is caused by a cornea that has an oblong shape. Astigmatism can occur alone, or in conjunction with either hyperopia or myopia. The condition causes light to focus in multiple points on the retina, causing blurry and distorted vision. It can appear in children or adults of any age. Usually astigmatism is hereditary, but it can also result from an eye injury that has caused scarring on the cornea, or from keratoconus, a disease that cases a gradual thinning of the cornea.

Astigmatism can be treated with glasses, contact lenses, and refractive surgery, such as PRK. If you suffer from astigmatism, schedule a consultation with the ophthalmologist today.

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Prof. Dr. med. Andrea Cusumano
Via Donatello 37
Rome, Italy 00196

Phone: +39 06 320 0369
Fax: +39 06 322 7607