Orlick & Kasper, MDs, PA
Vitreoretinal Eye Care Specialists
Saving the gift of sight in the Tampa Bay area since 1991
The leading cause of visual loss in the United States' senior population is age-related macular degeneration. This condition causes deterioration and possible eventual loss of central vision. Macular degeneration is caused by a number of factors including, but not limited to, age, genetics, and increased oxidative stress on the eye. Specific risk factors include advanced age, genetics (heredity), race, smoking, exposure to sunlight, diets high in saturated fats and cholesterol, little exercise, vascular disease, high blood pressure, and farsightedness (hyperopia). While age and family history are unpreventable, one has the ability to reduce some of the other risk factors.
The most common type of macular degeneration is the "dry" form. In this type of macular degeneration, there is progressive thinning (atrophy) and deposition of waste products (drusen) in the retina. Although vision loss can occur, it is usually minimal and only slowly progressive.
The "wet" form of macular degeneration is fortunately only responsible for 10% of macular degeneration cases. In this condition, abnormal blood vessels are stimulated to grow beneath the retina. Leakage and bleeding from these abnormal vessels can destroy central vision.
Because the wet form of macular degeneration is often devastating, we have been searching for ways to prevent it from occurring. The Age Related Eye Disease Study (AREDS) has now shown that vitamin supplementation is important in slowing the progression of macular degeneration in patients with moderate dry macular degeneration or patients with more advanced disease in one eye only. The most benefit was derived from a combination of antioxidants and zinc. Consult with your physician, however, before taking such supplements.
Metamorphopsia (distortion) is the usual presenting first symptom when wet macular degeneration begins and thus this symptom should be evaluated promptly. Such distortion can be easily detected on an Amsler grid. Click HERE to download a copy for your own use. Fluorescein Angiography is used to identify the presence and location of any abnormal new blood vessels. OCT enables noninvasive detection of macular fluid commonly seen in Wet AMD.
We now routinely use drugs called anti-VEGF therapies such as Lucentis, Avastin and Eylea in the treatment of Wet AMD. However, tailoring the use of the drugs, and combining these agents with Photodynamic therapy and thermal laser treatments can achieve significant benefits in certain patients. Tailoring the dosing regimen to achieve the best combination of efficacy and safety is key, and we complete this process for all of our patients.
Despite our best efforts, many patients with macular degeneration and other retinal diseases are left with poor vision. For those patients, evaluation by a Low Vision specialist can be arranged by our office. Special lenses and optical devices can be adapted to enable the patient to optimize their visual abilities.
For further information, http://www.geteyesmart.org/eyesmart/diseases/amd.cfm
Diabetic retinopathy is the leading cause of blindness for adults in the United States. Even with the best control of one's blood sugar, a diabetic can still develop retinopathy. Some patients even have retinopathy at the time that they are first diagnosed with diabetes. Background diabetic retinopathy is an early stage of this condition. This type of retinopathy is manifested by damage of the small blood vessels in the retina, usually around the center of the retina (macula).
Leakage of blood causes hemorrhages in the retina, and leakage of fluid causes edema (swelling of the retina). Swelling of the retina can reduce vision and cause metamorphopsia (distortion), easily identified on an Amsler grid. This condition often necessitates fluorescein angiography in its diagnosis and laser photocoagulation in its treatment.
The more advanced form of diabetic retinopathy is proliferative retinopathy. Progressive ischemia (oxygen deprivation) of the diabetic retina causes the abnormal growth of blood vessels on the retinal surface (neovascularization). Though the blood vessels themselves often cause no change in vision, they can easily rupture and fill the eye with blood (vitreous hemorrhage). This is a major cause of catastrophic visual loss in a diabetic.
Even worse, these abnormal blood vessels can cause tractional elevation of the retina and produce a retinal detachment. Again, laser photocoagulation is the treatment of choice for proliferative diabetic retinopathy. For vitreous hemorrhage and retinal detachment, however, vitrectomy is often necessary. The most important factor in preventing the development and progression of diabetic retinopathy is good control of the blood glucose. Hypertension, hyperlipidemia, and pregnancy can result in more extensive retinopathy and increase the risk of visual loss.
Recent scientific evidence gathered through new multicenter clinical trials have now demonstrated that anti-VEGF agents, often used in macular degeneration, now have a leading role in the treatment of macular swelling secondary to diabeties, both in combination with laser and as monotherapy. We also utilize these therapeutic strategies actively in our clinical practices.
For further information please click on these links: http://www.nei.nih.gov/health/diabetic/retinopathy.asp# and / or: http://www.geteyesmart.org/eyesmart/diseases/diabetic-retinopathy.cfm#
Vitreous Separation, Retinal Tear, and Retinal Detachment
Posterior Vitreous Detachment and Retinal Tear
Once retinal detachment occurs, it is important for the patient to have the condition repaired before the central
As part of the aging process, at some point in our life, the vitreous will shrink and separate from the back of the eye. The onset of the vitreous separation is usually accompanied by symptoms of "flashes and floaters".
Because the retina is an extremely thin and fragile structure, if the vitreous separation produces sufficient force, it can cause a break or tear in the retinal surface. Fortunately, when the retina tears, it usually does so in the far corners of the retina, which therefore does not compromise the patient's vision. However, retinal breaks or tears can over time (days to years) begin to accumulate fluid underneath them, which can gradually cause the retina itself to separate from the wall of the eye with disastrous consequences on one's vision.
It is for this reason, that patients who have symptoms of vitreous separation should be evaluated for the presence of retinal tears. If retinal tears are found, they are usually sealed (using laser or cryotherapy) so as to prevent retinal detachment from occurring.
For posterior vitreous detachment and Floaters, http://www.nei.nih.gov/health/floaters/floaters.asp or http://www.geteyesmart.org/eyesmart/diseases/floaters-flashes.cfm
Once retinal detachment occurs, it is important for the patient to have the condition repaired before the central part of the retina (macula) is itself involved in the retinal detachment. Once the macula is involved, the prognosis for good vision, even after successful repair, is lessened. Methods of repair of retinal detachment include:
Pneumatic retinopexy (in-office)
Vitrectomy and/or scleral buckle (in-hospital)
The type of procedure recommended depends on the characteristics of the retinal detachment.
For Retinal Detachment, http://www.nei.nih.gov/health/retinaldetach/retinaldetach.asp or
http://www.geteyesmart.org/eyesmart/diseases/detached-torn-retina.cfm
Macular hole is an abnormal defect in the central part of the retina. Unlike retinal tears which occur in the peripheral retina, macular holes are usually not precursors to retinal detachment. A macular hole looks like a round punched-out defect. Because of its location, this type of retinal hole can cause severe central vision loss. The normal retinal tissue, which should fill the hole, is usually not missing; rather, it is merely spread out to the edge of the hole. Surgery can close the hole, and allow that tissue to return to a normal position, thereby improving vision. Imagine pushing a pencil through a screen; the wires making up the screen are pushed aside, not punched out. The wires may be pushed back into their normal position to repair the screen. Although trauma or disease can cause macular holes, they are usually seen as an age-related manifestation of an abnormality of the vitreous-retinal interface. For unknown reasons, they occur more frequently in women than in men.
Surgery is necessary for the treatment of most macular holes. Macular hole surgery consists of a vitrectomy (removal of the vitreous gel) and filling of the vitreous cavity with a mixture of air and gas. The patient is then asked to remain in a face-down position for 1-2 weeks following this surgery, to allow maximum air/gas contact with the macula. Usually, the intravitreal air/gas spontaneously absorbs from the eye within 1-2 weeks following the operation. In most cases, a macular hole can be closed in this fashion with at least partial restoration of central vision.
For further information, http://www.geteyesmart.org/eyesmart/diseases/macular-hole.cfm
Macular pucker is caused by a transparent membrane of scar tissue that grows over the surface of the central retina. The eventual contraction and shrinkage of this membrane can wrinkle and distort the underlying macula, impairing central vision. Macular puckers usually arise from age-related changes in the vitreous gel but can result from any type of eye injury, inflammation, disease, or surgery.
Treatment is not necessary if symptoms are mild. However, if there is significant metamorphopsia or visual loss, vitrectomy may be performed. During this procedure, after the vitreous gel is removed, the membranous tissue that is causing the macular distortion is peeled off the retinal surface and removed from the eye.
For further information, http://www.nei.nih.gov/health/pucker/pucker.asp
or http://www.geteyesmart.org/eyesmart/diseases/macular-pucker.cfm
Just like any other portion of our body, the retina in our eyes has both arteries and veins which are responsible for the blood circulation, delivery of oxygen and nutrients, and the removal of wastes.
Sometimes, one of these blood vessels develops a blockage. This more commonly happens in the veins than the arteries. Depending upon location of the vein blockage, visual loss could be central or peripheral, mild or severe. Fluorescein Angiography may be required to help characterize the type of blood vessel occlusion and to guide treatment recommendations.
Laser photocoagulation is often employed if there is any leakage and swelling of the central retina (macular edema) or abnormal blood vessel growth (neovascularization) that has developed as a consequence of a retinal vein occlusion.
The injection of steroids and anti-VEGF agents in the eye has also been demonstrated to be very useful in the treatment of macular edema associated with branch and central retinal vein occlusions. We currently utilize these treatments.
For further treatment, http://emedicine.medscape.com/article/798583-overview
Uveitis specifically refers to inflammation of the middle layer of the eye, termed the "uvea" but in common usage may refer to any inflammatory process involving the interior of the eye. Uveitis is estimated to be responsible for approximately 10% of the blindness in the United States. Uveitis requires a thorough examination by an ophthalmologist.
Types
Uveitis is usually categorized anatomically into anterior, intermediate, posterior and panuveitic forms.
- Anywhere from two-thirds to 90% of uveitis cases are anterior in location (anterior uveitis), frequently termed iritis - or inflammation of the iris and anterior chamber. This condition can occur as a single episode and subside with proper treatment or may take on a recurrent or chronic nature. Symptoms include red eye, injected conjunctiva, pain and decreased vision. Signs include dilated ciliary vessels, presence of cells and flare in the anterior chamber, and keratic precipitates ("KP") on the posterior surface of the cornea.
- Intermediate uveitis consists of vitritis - inflammatory cells in the vitreous cavity, sometimes with snowbanking, or deposition of inflammatory material on the pars plana.
- Posterior uveitis is the inflammation of the retina and choroid.
- Pan-uveitis is the inflammation of all the layers of the uvea.
Symptoms
Depending on which part of the eye is inflamed in uveitis different combinations of these symptoms may be present.
- Redness
- Light sensitivity
- Floaters
- Blurry vision
- Pain
These symptoms may come on suddenly, and you may not experience any pain. The symptoms described above may not necessarily mean that you have uveitis. However, if you experience one or more of these symptoms, contact your eye doctor for a complete exam.
Treatment
Treatment may include steroid eyedrops, injections, or pills, as well as eyedrops to dilate the pupil and reduce pain. More severe cases of uveitis may even require treatment with chemotherapeutic agents to suppress the immune system.
For further information, http://www.geteyesmart.org/eyesmart/diseases/uveitis.cfm
Malignant tumors can metastasize to the eye, just as they can metastasize to any other part of the body. The most common cancers that spread to the internal structures of the eye, originate in the breast, lung, prostate, or bone marrow (leukemia). Metastatic tumors within the eye are usually treated with systemic chemotherapy, targeting the origin of the cancer as well as the eye itself. Occasionally, radiation therapy has been used to treat the eye more directly.
However, the eye can also be the primary location for a cancerous tumor, the most common being choroidal malignant melanoma (see photo on the left). The average onset age for this type of melanoma is 55 or older and it appears that Caucasians are at highest risk of development.
Most people, today, are familiar with melanoma as the most dangerous type of skin cancer. Melanoma refers to cancer of the melanocytes, which are the cells responsible for giving skin color. Skin melanomas are associated with unprotected sun exposure, especially during youth. Choroidal melanomas, on the other hand, have not been linked to sun exposure, despite their increased occurrence in individuals with lighter skin. However, similar to skin cancer, intraocular melanomas are believed to arise from small benign pigmented areas called nevi and are best detected through pupil dilation and examination of the eye with special lenses. Photographs, including specialized digital imaging techniques, may be taken at each visit so that a patient’s progress can be visually documented, over time. If a pigmented area, within the eye, becomes larger and thicker, an ultrasound is usually performed to measure the area and check for suspicious characteristics.
Orlick & Kasper, MDs, PA
Vitreoretinal Eye Care Specialists