The eye is shaped like a ball. The retina is the light sensitive membrane at the back of the eye. Rays of light enter the eye and are focused onto the retina by the cornea and the lens. The retina produces a picture which is sent along the optic nerve for the brain to interpret. The eye and the brain together produce the images that we see. If the cornea becomes scarred, or the lens becomes cloudy (as in a cataract), the image projected onto the retina becomes degraded and the vision is effected. Similarly, if the retina is unhealthy, either by age-related macular degeneration, macular hole, or other retinal problem the vision may also be reduced.
The retina is the light sensitive membrane at the back of the eye. It converts light, coming from the front of the eye through the cornea and lens, into electrical impulses which are then relayed to the brain via the optic nerve.
The macula is the central area of the retina, and is responsible for fine vision. When you read, look at someone's face, or thread a needle, you use the macula area to give you fine vision. Problems with the macula give blurring or distortion of central vision.
The posterior cavity of the eye is filled with vitreous jelly. The vitreous is a clear jelly-like substance within the eye which takes up the space behind the lens and in front of the retina, the light sensitive layer at the back of the eye. It is 99 per cent water. The other 1 per cent consists of substances which are important in maintaining the shape of the vitreous. The outer part of the vitreous (the cortex) has the highest concentration of protein called collagen. The vitreous is attached to the retina, more strongly in some places than others.
The crystalline lens in the eye helps to focus light coming from outside the eye onto the retina. It is usually entirely clear. However as patients get older, or for other reasons such as previous eye surgery or injury, the lens may go cloudy and form a cataract
Your risk of complications is greater if you have another eye disease or a serious medical condition affecting any part of your body. Occasionally, cataract surgery fails to improve vision because of underlying eye damage from other conditions, such as glaucoma or macular degeneration. If possible, it may be beneficial to evaluate and treat other eye problems before making the decision to have cataract surgery.
To prepare for your cataract surgery, you may be asked to:
Understanding cataract surgery will help you feel more confident about your decision. Here are some facts about cataract surgery:
Nearly half of people with diabetes have some degree of diabetic retinopathy, a complication of diabetes that can result in blindness. After 20 years with diabetes, most patients have diabetic retinopathy. Treatment depends on the severity of the condition
When people have diabetes, excess glucose in the bloodstream can cause the tiny capillaries in the back of the eye to swell and leak fluid. This causes blurry vision. Tiny new blood vessels grow out of the retina as the disease advances. These blood vessels may break and bleed into the vitreous, further impairing vision.
Initially, you may not notice changes in vision even though you may have the early stages of diabetic retinopathy. However, as the retinopathy progresses, you may start to notice a decline in vision, usually in both eyes. With advanced retinopathy, you may have severe vision loss or blindness.
There are two types of diabetic retinopathy; proliferative diabetic retinopathy is the more serious and should be treated promptly.
Nonproliferative diabetic retinopathy (NPDR): This is the early stage of the disease. Symptoms often are mild or nonexistent. However, blurred vision may occur from swelling of the retina. This swelling occurs because the damaged blood vessels can ooze fluid.
You may not need treatment immediately. Your eye doctor will closely monitor changes in the retina. You need to work with your general medical doctors to control your glucose, blood pressure and cholesterol.
Proliferative diabetic retinopathy (PDR): This is the more advanced form of the disease, where abnormal new blood vessels grow on the surface of the retina or into the vitreous cavity. These new vessels may bleed into the vitreous, clouding or blocking vision. The blood vessels can pull on the retina, leading to retinal detachment.
Macular edema/clinically significant macular edema (CSME): This is responsible for diminition of vision and happens due to leakage of fluid from the damaged blood vessels and needs immediate treatment. It may coexist with either NPDR or PDR.
Who is at risk for diabetic retinopathy and what preventative measures can be taken ?
Individuals with Type I, Type II, and gestational (during pregnancy) diabetes are all at risk. As there are no symptoms in the early stages of diabetic retinopathy, individuals with diabetes should have a comprehensive dilated exam once a year.
However, depending on the stage of diabetic retinopathy, your optometrist or ophthalmologist may examine your eyes more often. If you are pregnant and diabetic, you should have the examination as soon as possible. Whether or not symptoms are present, early detection and appropriate timely treatment can prevent vision loss.
The Diabetes Control and Complications Trial (DCCT) have shown that tight control of blood sugar levels may slow down the onset and progression of retinopathy. If blood sugar levels are kept in normal ranges, you are not only at a lower risk for diabetic retinopathy complications but also for developing nerve and kidney complications. Good blood sugar, blood pressure, lipid control and exercise and diet can significantly decrease the progression of retinopathy and are an important part of managing diabetic retinopathy.
Diabetic retinopathy often has no early warning signs, which is why it important to have your eye thoroughly checked yearly.
As the diabetic retinopathy advances, you may experience blurred vision or distortion of images, which will make it difficult for you to read and drive. This is often attributed to the swelling of the macula, which is the part of the retina that provides sharp central vision. This condition is called macular edema.
With diabetic retinopathy, new blood vessels may grow on the surface of the retina. These vessels are fragile and may bleed (hemorrhage) into the eye, which may blur the vision. You may see spots or speck of blood "floating" in your vision. If this occurs, consult your ophthalmologist immediately.
Sometimes, the spots may resolve resulting in an improvement in vision. However, due to the fragile nature of the blood vessels, more bleeding may occur. This can cause severe blurring of vision. If left ignored, vision loss and potential blindness may occur. Again, if any of these symptoms occur, visit your eye care specialist immediately. The earlier you receive treatment, the more likely you will be able to save your vision.
Diabetic retinopathy and macular edema are detected during a comprehensive eye examination which includes:
Visual Acuity Testing: The eye chart measures how well you see at various distances.
Tonometry: This test determines the fluid pressure of your eye. Elevated eye pressure could be a possible sign of glaucoma, which may be a complication of diabetic retinopathy.
Dilated Eye Exam: During this part of the examination, the ophthalmologist or optometrist uses a special magnifying lens to examine you retina and optic nerve for signs of damage, such as leaking blood vessels, macular edema, fatty deposits, areas of ischemia, new blood vessel formation, and any change in shape to the blood vessels.
If the eye specialist suspects macular edema or leaking of vessels, additional testing may be performed. These tests include:
Fluorescein Angiography: In this test, a special dye is injected into your arm. As the dye passes through the blood vessels in your retina, pictures are taken. This test allows the ophthalmologist to find areas of leaking vessels and determine the best treatment.
OCT: OCT, which stands for Optical Coherence Tomography, is a highly specific diagnostic test that allows the ophthalmologist to examine the cell layers of the retina and optic disc in detail. This diagnostic test is very useful in the diagnosis of macular edema.
No treatment is typically needed during the first three stages of diabetic retinopathy (i.e. NPDR), unless macular oedema is present. The best way to prevent progression of diabetic retinopathy is to control levels of blood sugar, blood pressure, and cholesterol.
Macular oedema can be treated with
Intravitreal injections: of Anti-VEGF (avastin) or Steroids (Triamcinolone / IVTA/ Ozurdex)
Focal Grid Laser : Your ophthalmologist will place up to several small laser burns in the areas of retinal leakage surrounding the macula. These burns slow the leakage of fluid and reduce the amount of fluid in the retina. Focal laser treatment stabilises vision. It can reduce the risk of vision loss by 50 percent. This treatment is usually completed in one session, however, further treatment may be needed.
Although both treatments have high success rates, they are not a cure for diabetic retinopathy.
Scatter Laser treatments shrink the abnormal blood vessels and prevent further bleeding. Your doctor places laser burns in the peripheral areas of the retina, causing the abnormal vessels to shrink. Due to the high number of laser burns, several treatment sessions are necessary.
Although you may notice some loss of your side vision, laser treatments can preserve the rest of your sight. Laser treatment may slightly reduce your color and night vision.
If there is severe bleeding in the retina, a vitrectomy may be performed. During a vitrectomy, blood is removed from the center of the eye. A vitrectomy is performed under local anesthesia. Your doctor makes are tiny incision in your eye and inserts a small instrument which is used to remove the vitreous gel that is clouded with blood. The vitreous gel is replaced with salt solution.
Avastin (Bevacizumab) is an anti-growth factor drug that is delivered through an intravitreal injection. This drug is used to reduce macular oedema associated with diabetes and also to reduce new vessel growth.
Usually, treatment helps slow or stop the progression of diabetic retinopathy. Treatment doesn't cure the underlying disease. Careful diabetes management is important to reduce the risk of further eye damage.
Age-Related Macular Degeneration (AMD) is one of the most common causes of vision loss and blindness. AMD is a retinal eye disease that causes progressive loss of central vision, but leaves the peripheral vision intact. This progressive degeneration affects the macula, which is responsible for fine detail and color. This can make it difficult to read, drive, write, recognize faces, or perform daily tasks.
AMD can be divided into two general types: Dry (Atrophic) and Wet (Exudative).
Dry (Atrophic): The "dry" form of AMD results from a slow wearing away of the layers of the macula, and occurs over many years. As dry AMD progresses, you may notice a central blurring in your vision.
Wet (Exudative): The "wet" form of AMD is due to leakage of blood or fluid from an abnormal blood vessel that grows in the macula. This can lead to sudden distortion or loss of central vision in a short period of time. Wet AMD is responsible for the majority of cases of severe vision loss in AMD.
Symptoms of Wet AMD may include:
Visual distortions such as:
Currently there is no treatment for dry AMD: However, there are various ways to help slow down the progression of macular degeneration. These include:
When the retina detaches, it separates from the back wall of the eye and is removed from its blood supply and source of nutrition. The retina will degenerate and lose its ability to function if it remains detached. Central vision will be lost if the macula remains detached. The causes of retinal detachment can be divided into three main categories:
1. Rhegmatogenous retinal detachment (most common): This detachment is due to a retinal break or tear which allows the liquid vitreous (the fluid that fills the center of the eye ball) to pass through the break and lift off the retina. This is the most common type of detachment.
2. Exudative retinal detachment: This detachment is due to leakage of fluid from under the retina. The fluid is called exudate. Tumors and inflammatory disorders can create exudative detachments.
3. Traction retinal detachments (TRD): This type of detachment is due to pulling on the retina usually from fibro-vascular tissue within the vitreous cavity. Proliferative diabetic retinopathy (PDR) is the most common cause of traction retinal detachments.
The retina is the light sensitive membrane at the back of the eye. If a tear forms on the retina (which can occur after a posterior vitreous detachment), fluid can collect underneath the retina, which then proceeds to detach, rather like wet wallpaper coming away from a wall.
What are the symptoms of a retinal detachment ?
Patients usually have symptoms with an onset of floaters in the vision, and sometimes flashing lights, followed by the development of a shadow which extends from the peripheral vision towards the centre until reading vision is lost. Without treatment of a retinal detachment the eye will usually become blind. Occasionally patients have no symptoms at all, so-called asymptomatic retinal detachments. These may be treated differently, and if very longstanding, no treatment may be required. However this is unusual.
Overall retinal detachment is uncommon, affecting only about one in ten thousand people. However certain groups are at increased risk:
Retinal detachments can be treated. Surgery is usually successful in reattaching the retina in one operation in 9 out of 10 patients. However this means that further surgery is occasionally required in some patients. There are 3 ways of treating retinal detachments. The appropriate technique used depends on the features of the retinal detachment and age of the patient:
Scleral buckle: This surgical procedure has been in use for more than 30 years, and, until approximately 20 years ago, was the only procedure available. It is still commonly used for rhegmatogenous retinal detachments, especially when there are no complicating factors. The procedure involves localizing the position of all the retinal breaks, treating all retinal breaks with the cryoprobe and supporting all the retinal breaks with a scleral buckle. The buckle is usually a piece of silicone sponge or solid silicone. The type and shape of the buckle varies depending on the location and number of retinal breaks. The buckle is sewn onto the outer wall of the eyeball (sclera) to create an indentation or buckle effect inside the eye. The buckle is positioned so that it pushes in on the retinal break and effectively closes the break. Once the break is closed, the fluid under the retina (subretinal fluid) will usually spontaneously resolve over 1-2 days. Sometimes the surgeon elects to drain the subretinal fluid at the time of surgery. Most often, a scleral buckle procedure can be done with local anesthesia and as same day surgery ( in and out of the hospital on the same day). Postoperatively, there are usually no positioning requirements and one can resume most activities within several days (except for anything that would jar the head).
Vitrectomy: Usually referred to as a trans pars plana vitrectomy (TPPV), this procedure was first used ~ 20 years ago and has been continuously refined and improved since then. It is most commonly used for traction retinal detachments from diabetes but is also used for rhegmatogenous detachments especially if they are associated with vitreous traction or vitreous hemorrhage. The procedure involves making small incisions into the wall of the eye to allow the introduction of instruments into the vitreous cavity (the middle of the eyeball). The first part of the procedure usually is the removal of the vitreous using a vitreous cutter. Then, depending on the type and cause of the detachment, a variety of instruments (scissors, forceps, pics, lasers, etc…) and techniques (excision of tractional bands, air-fluid exchange, silicone oil fill, etc…) are used to reattach the retina. A TPPV can also usually be done as same day surgery and with local anesthesia. It is sometimes important to maintain a specific head position after surgery to keep the retina attached. More information regarding vitrectomy surgery can be found on the
Pneumatic retinopexy: Over the past 10 years, this has become a popular way to repair a straight-forward rhegmatogenous retinal detachment, especially if there is a single break located in the superior portion of the retina. This procedure involves injecting a gas bubble into the middle part of the eye (vitreous cavity). It is then critical to position oneself so that the gas bubble covers the retinal break. If the break can be covered by the bubble, the subretinal fluid will usually resolve within 1-2 days. The retinal tear is either treated with cryopexy before the bubble is injected or with laser after the retina has flattened. The main advantages of this approach are that it can be done in the office, thus avoiding hospitalization and that it avoids some of the complications of scleral buckling surgery, although it has its own set of complications. The main disadvantages are the requirement for precise head positioning for up to 7-10 days following the procedure and a slightly lower initial success rate as compared to a scleral buckle. If the retina is not reattached by a pneumatic retinopexy procedure, a scleral buckle and/or TPPV can be done at that point.
The vision is blurred if there is a gas bubble in the eye, rather like having your eyes open under water. As the gas bubble gets smaller patients notice it's edge as wobbly line in the upper field of vision. This will then drop across the field of vision, the bubble then being seen as a round blob before it disappears.
The gas bubble, by it's buoyancy, is used to seal the retinal break while the laser treatment or cryotherapy forms a scar, which takes about 5-7 days. To make sure that the bubble is pressing on the retinal tear, you will be asked to position your head so that the tear is uppermost. If the tears are at the top of the eye it is enough to have your head in a normal upright position after surgery. You may however be asked to have your face pointing down at the floor or lying on one side, depending on where the retinal tears are. The best position to treat your detachment will be discussed with you after surgery. You do not need to be in position continuously: we recommend 50 minutes in the hour, day and night for 7 days, although some patients may need to posture for shorter and some longer.
It is important to appreciate that there are 2 parts to vision: central (ie: reading) and peripheral vision. Peripheral vision tends to return to normal after successful retinal detachment surgery. How much the central, or reading, vision returns depends on whether or not the central part of the retina, the macula, was detached prior to surgery (a "macular –off" detachment), and for how long. If the macula was attached prior to surgery (a "macular-on" detachment) the outlook is very good and central vision should return to normal. If the macula was detached for more than a few days prior to surgery then it is unlikely that it will entirely return to normal. The longer the macula is detached prior to surgery then less visual improvement can be expected after surgery. Therefore it is important to have a retinal detachment treated as soon as possible, before the macula detaches.
Your vision will be blurred until the gas bubble has gone. You should not fly or drive while the gas bubble is present. The eye will be uncomfortable and scratchy if sutures have been used for the first few days. You should take things easy for the first few weeks, with only gentle exercise. Having a retinal detachment is a very stressful time for patients and you may feel tired for 2 to 3 weeks after surgery. You should not be working while you are meant to be positioning. I would not recommend swimming until 4 weeks or so after surgery. However when everything has settled down there should be no limits on your activities: as long as it is legal of course!!
If you have had a retinal detachment in one eye, then there is a small risk of developing retinal detachment in the other eye. We will carefully examine your fellow eye. If there are weak areas then laser treatment to strengthen the retina may be recommended. However if the fellow eye has already had a posterior vitreous detachment then you should be at low risk of developing a retinal detachment.
Symptoms of retinal tear or retinal detachmentThese are dark specks, strands, spots, dots or cobwebs moving in your field of vision. People with floaters will notice that they are more apparent when looking at a plain background or sky. Although floaters seem to be in front of the eye, they are infact opacities floating inside the eye. Floaters are not imaginary and can be viewed by your ophthalmologist using special equipment
The eye contains a jelly like substance, known a vitreous, which fills the central cavity of the eye. As we grow older the vitreous can shrink, thicken, or become more fluid, forming clumps or strands inside the eye. Floaters often occur when the vitreous gel pulls away from the retina, condition known as posterior vitreous detachment (PVD).
Besides PVD and ageing, floaters can also be associated with certain eye diseases (like blood in the vitreous gel- vitreous hemorrhage) and with other conditions such as migraine.
Flashes are seeing lights going on and off, especially on one side of the field of the vision, even when the eyes are closed.
When the vitreous gel inside the eye pulls on the retina, it may cause you to see flashing of lights. This usually happens during PVD
If you see jagged lines of light that last 10 to 20 minutes and happen in one or both eyes, this is probably a migraine caused by the spasm of blood vessels in the brain.
Posterior Vitreous Detachment (PVD) is a common condition which occurs in about 75 per cent of people over the age of 65. As people get older the vitreous, a jelly-like substance inside the eye, changes: the central part of the vitreous becomes more liquid and the outer part (cortex) peels away from the retina. As it comes away from the retina it can cause the symptoms of posterior vitreous detachment
Do floaters and flashes cause any harm ?Floaters and flashes themselves are harmless; the changes that are occurring in the eye can potentially be causing damage, which if untreated may lead to loss of vision.
Most of the times the vitreous separates from the retina (PVD) without causing any symptoms. In some cases the retina can tear if the shrinking vitreous gel pulls away from the wall of the eye. A torn retina is always a serious problem, since it can lead to a retinal detachment.
Sometimes, there is a sudden occurrence of flashing lights with many new floaters or even with a blacking out of part of the field of vision. If this happens, you should see your ophthalmologist right away to find out if you have a retinal tear or retinal detachment.
Approximately 15% of patients with acute symptoms of PVD have a retinal tear at the time of the initial examination. Patients with acute PVD who have no retinal breaks on presentation have a 2% to 5% chance of developing them in the weeks that follow. In patients who present with substantial vitreous hemorrhage following, the chances of having retinal tears increases to about 70%.
The treatment for floaters and flashes depends upon the underlying condition. Most of the flashes and floaters are not serious but you should always have an eye examination by an ophthalmologist to make sure there has been no damage to your retina.
Although some floaters may remain in your vision, but most of them usually fade over the time and gradually become less bothersome.
However if the floaters become bothersome and you think you are not able to cope with your day to day life because of the annoying floaters, then floater correction surgery can be considered. The surgery involves removal of the jelly from the eye (Vitrectomy).
If retinal tears are found on examination then laser/cryotherapy or surgery are the options.
Your vision will be blurred until the gas bubble has gone. You should not fly or drive while the gas bubble is present. The eye will be uncomfortable and scratchy if sutures have been used for the first few days. You should take things easy for the first few weeks, with only gentle exercise. Having a retinal detachment is a very stressful time for patients and you may feel tired for 2 to 3 weeks after surgery. You should not be working while you are meant to be positioning. I would not recommend swimming until 4 weeks or so after surgery. However when everything has settled down there should be no limits on your activities: as long as it is legal of course!!
If you have had a retinal detachment in one eye, then there is a small risk of developing retinal detachment in the other eye. We will carefully examine your fellow eye. If there are weak areas then laser treatment to strengthen the retina may be recommended. However if the fellow eye has already had a posterior vitreous detachment then you should be at low risk of developing a retinal detachment.
Symptoms of retinal tear or retinal detachment
Lattice degeneration is a condition that causes thinning and weakening of the peripheral retina, the light-sensitive layer of cells lining the back of the eye, which can lead to a retinal tear.
The vitreous, a clear, gel-like substance that fills the inside of the eye, is contained in a sac loosely attached to the retina. As one ages, the vitreous takes on a more fluid consistency, and the sac sometimes separates from the retina. In lattice degeneration, there are places where the sac is strongly attached to the retina and pulls on it. This pulling weakens the retina and creates "lattice" lesions, which look like white, crisscrossing lines on the retina.
If part of the vitreous sac becomes detached from the retina, the friction and pulling at the attachment site can create a tear in the retina. Lattice degeneration can sometimes cause retinal detachments when holes or tears in the lattice formation permit vitreous fluid to flow under the retina.
Fortunately, most people with lattice degeneration do not develop a retinal detachment. Preventive treatment of lattice degeneration is indicated in some cases, but usually, the ophthalmologist will only need to monitor the condition. If you have a history of lattice degeneration, you should be aware of the symptoms of retinal tears and detachment.
Patients with significant lattice lesions may be at slightly increased risk for vision loss due to retinal detachment. These high risk patients should have regular follow-up examinations of the retina. Patients with lattice degeneration should be aware of the signs and symptoms of retinal tear or detachment and seek urgent ophthalmic care when needed.
The term colour blindness is a common but misleading term that implies total loss of colour vision. In most cases the defect is usually only partial and the term "colour defective vision" is more appropriate. The commonest defect is in the red/green part of the visual spectrum. Males are more commonly affected; about 8% of all males and 0.5% of females are affected to a varying degrees.
There are other defects due to failure in the blue receptors, a total failure of all receptors and a failure of the other retinal receptor, the rod. These are all rare and not suitable for discussion here.
All colours can be made by mixing the three primary colours; red, green and blue in varying amounts and the eye sees colours by detecting the amounts of these primary colours. This processing is done by special nerve endings in the retina of the eye. One type of nerve ending, the cone, has three special pigments which detect one colour, either red, green or blue. If one of these nerve types is impaired there is a colour defect.
Males are more affected because the genes that control the development of these colour sensitive nerve endings are carried on the X chromosome. Males have an X and a Y chromosome and women have two X chromosomes. Women have two copies of the genes for colour vision, one set on each X chromosome. Males have only one set of genes for colour vision and if they are not working properly, males do not have the back up of the other set of genes on the other X chromosome that women have. This is known as X-linked recessive inheritance.
Colour defects can also be acquired and a common cause in our community is cataracts. As the cataract becomes more dense it filters out all colours, but the bright reds, yellows, greens and blues are more affected. It has been said that the changing colour choices of many famous painters has been due to the affect cataracts have had on their colour vision. Other diseases affecting the optic nerve and the retina also affect colour vision but these are rare and often only affect one eye.
The defects are named after the Greek words for the three primary colours: Protos for red, Deutros for green and Tritos for blue. Someone who has a complete red defect is said to have Protanopia and if he only has partial defect he is said to have Protanomaly. The commonest defect involves the green receptors and it accounts for over half of the defects; 4% of all males have a partial defect and 1% have a complete defect. As the loss of colour vision is in the middle of the visual spectrum this defect causes the least awareness. The problem is the inability to distinguish red and green but they are sensitive to red light.
The next most common defect is due to failure in the red receptors, and it affects 1% of males. These people also confuse red and green but are not sensitive to red light.
There are other defects due to failure in the blue receptors, a total failure of all receptors and a failure of the other retinal receptor, the rod. These are all rare and not suitable for discussion here.
A number of tests have been devised to detect colour vision defects. The most basic of these is to show the patient a number of coloured discs on a screen and ask him or her to identify the colours.
The commonest test and one of the most efficient is the use of special test plates called "pseudo isochromatic" plates or confusion plates. The Ishihara or H-R-R are the most commonly used ones in this country.
It can be seen that these plates are made up of a series of spots of varying colours and hues so that the central number or letter stands out from the background. Patients with normal colour sense can pick out the central figure from the background, but those with a defect are unable to make this distinction. These people either see no figure at all, or see a different figure due to different appreciation of the hues. By changing the colour and hues of both the figures and the background all basic types of defective colour vision can be recognised and classified.
For more subtle defects in colour vision more complicated tests are available. These are conducted by asking the patient to match a fixed colour with a mixture of other colours, or by trying to put coloured objects in a correct sequence. The lantern test is an old test that is used to check colour vision when applying for certain forms of work e.g. train engine drivers, signal men in the Navy, and pilots. This test mainly picks up red/green defects by asking the patient to pick and match seven colours on three discs.
Most defective colour vision does not seriously handicap those suffering from it. This is because the patients have normal visual acuity and then they adapt, for example, they know that the red traffic light is at the top and the green at the bottom. They also see some colour but in different intensity and hues to those with normal colour vision.
There are restrictions on certain occupations such as train drivers, service personnel and pilots, as these occupations cannot afford to rely on associations to make correct decisions about colours of signals or signs. In fact, people with defective green receptors are very useful in the military services as they can very easily detect camouflage as they have the ability to pick up different hues.
There is no known treatment for defective colour vision and there is no test to determine who are carriers of the defect. Although 8% of all males suffer from some defect in colour vision, many of these are only minor defects and these people are unaware of the problem; it is only a minority of this group that have more severe manifestations and as was said before most of these people adapt without any serious inconvenience or problems.
A retinal vein occlusion means that a vein in the retinal circulation has become blocked. Retinal veins carry blood from the retina back to the heart for re-circulation. If one of these veins becomes blocked a pressure build up causes leakage of blood and fluid in the retina. This blockage can cause haemorrhages, swelling, and ischemia (lack of oxygen) of the retina.
There are two types of retinal vein occlusions:
1. Central Retinal Vein Occlusion (CRVO)
Occurs when the main retinal vein is blocked. This results in poor blood flow throughout the entire retina and can cause severe visual loss, particularly in older people.
2. Branch Retinal Vein Occlusion (BRVO)
Occurs when a smaller branch of the main retinal vein is blocked. This results in damage to the area of the retina drained by this branch. Visual loss varies but is not as severe as with a central retinal vein occlusion.
Blurred vision is the main symptom of a retinal vein occlusion. This occurs when the excess fluid leaking from the blocked vein collects at the macula (the area of the retina responsible for central vision).
Floaters can be another sign of a retinal vein occlusion. They appear as 'spots' which float through the visual field. When an area of the retina is not working properly abnormal blood vessels may grow (neovascularisation). These abnormal blood vessels are fragile and can cause bleeding or leakage of fluid into the vitreous (gel-like fluid which fills the eye). Floaters may be noted when this occurs.
Pain in the eye can occur as a complication of a central retinal vein occlusion. This is caused by excessive eye pressure called neovascular glaucoma.
Your ophthalmologist may perform fluorescein angiography to diagnose and monitor your retinal vein occlusion.
Fluorescein angiography involves intravenous administration of a diagnostic dye called fluorescein. As the dye circulates through the retinal blood vessels a series of photographs are taken. The test is performed to highlight the occlusion as well as areas of swelling and assess the amount of accumulated fluid.
OCT is also performed to measure macular oedema (swelling).
Blood tests may also be ordered to determine the cause of the occlusion.
Your Ophthalmologist will discuss the different treatment options available. Treatments may include:
People who have minus number glasses more than 6 diopter in power are said to have high or pathologic myopia. The glasses number of such patients may even be as high as 15 to 20 diopters. The eyeball in such cases is enlarged leading to thinned out coats of the eyeball so the central area may be very weak (chorioretinal degeneration) leading to poor vision. The retina in these eyes is weak in the periphery also and usually has some degeneration, atrophic holes, or even retinal tears. These retinal holes or tears may sometimes lead to a serious condition of retinal detachment, leading to sudden loss of vision, and may require major surgery urgently to settle the retina.
So a regular retinal checkup is very essential in these patients to look for the holes and to treat them with laser or else they might lead to a retinal detachment, which needs surgery. Also, whenever the patient with high number develops symptoms like flashes or floaters, he/she must immediately get the eyes examined to look for retinal hole, tear or retinal detachment.
High myopes are also predisposed to develop abnormal new vessels in the central area (macula) called Choroidal Neovascular Membrane (CNVM), which leads to sudden marked fall in vision due to hemorrhage or fluid leakage. The treatment modalities being tried out for myopic CNVM are anti-VEGF agents like Lucentis, Avastin and Macugen, photodynamic therapy (PDT) with verteporfin, Transpupillary Thermo Therapy (TTT) laser and surgical options like macular translocation.
The doctors are expert practitioners dedicated to providing the best eye treatment in India. Our doctors offer highly specialized services in the field of vitreo-retina service, ensuring that the latest technologies are made available to provide effective solutions to patients at Save Sight Centre. Above all, every doctor at Save Sight is dedicated to ensuring that the patients receive individual attention and care when it comes to their treatment needs. This dedication to service is what gives Save Sight Centre its reputation. It is vital to choose the best eye doctors in India, for the best treatment.
Our department has one of the best vitreoretinal services in Delhi. Save Sight is well equipped with the latest types of equipment for evaluation & management of the EYES. Individual personal care is achieved at our centre with the help of highly qualified personnel, modern diagnostic equipment, and the latest surgical facilities of international standards.
With India becoming the diabetic capital of the world, managing complications related to diabetes is a major concern. One of the complications is diabetic retinopathy, which is fast gaining importance as a cause of visual impairment among a large population of individuals. If left untreated, it can get worse and cause some loss of vision, or blindness in severe cases. Save Sight Centre is one of the best eye hospitals for diabetic retinopathy treatment. Save Sight with its highly experienced professionals and ultra-modern technologies provide tons of patients with a better vision.
Reasons to choose Save Sight Centre for Retina Treatment-
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