Retina Insight
Super-speciality Eye Hospital

Diabetes is a disease not limited to a single organ. It’s a systemic disease which affects various organs in the body like eye, kidney, brain, heart. In eye diabetes causes damage to the back portion of the eye called the retina which is called Diabetic retinopathy. It can lead to swelling or bleeding in the retina and adjacent structures resulting in decreased vision. It is divided into 5 stages; stage 1 is mild where systemic sugar control should suffice to stage 5 (advanced stage) where surgical procedure may be required. Patient starts experiencing symptoms generally around stage 3 when swelling of the retina (macular edema) starts.

Macular degeneration could be due to various causes the most common among which is Age related macular degeneration (ARMD). Diabetic retinopathy is different from ARMD as ARMD is generally limited to loss of central vision alone while diabetic retinopathy in advanced stages may lead to decrease in central as well as peripheral vision.

The prevalence of diabetic retinopathy in India is about 20% which means 1 in 5 patients of Diabetes has diabetic retinopathy. The duration of disease is the most important risk factor which means that the longer the duration of disease in your body the more likelihood of having diabetic retinopathy.

Diabetes leads to hyperglycemia (raised sugars) which causes damage to the small blood vessels in the body including retina. Therefore, patients with uncontrolled sugars there is increased damage to these small blood vessels leading to damage of retinal cells

There is no fixed timeline for the occurrence of diabetic retinopathy but around 5% of patients have diabetic retinopathy at the time of diagnosis of diabetic retinopathy. Diabetic retinopathy will occur earlier in patients with uncontrolled sugars compared to patients with controlled sugars.

There is increasing evidence that diabetic retinopathy has genetic component as well. While all patient with diabetes are at risk of developing diabetic retinopathy, genetic factors can play an important role in further increasing the risk in predisposed individuals.

Diabetic retinopathy affects the retina (back part of the eye) and unfortunately cannot be detected without a complete eye examination. An eye of a patient with diabetic retinopathy shows no changes on the outside compared to normal eye. The symptoms also may start much later after the onset of diabetic retinopathy. Therefore, it is important for a regular screening for diabetic retinopathy.

Screening for diabetic retinopathy means a detailed evaluation of the retina (back part of the eye) after dilating the eye with dilating drops. No additional tests are required to screen a patient for diabetic retinopathy and the examination itself takes about 5 minutes. Every diabetic patient should get his screening done once a year to look for retinopathy changes even before symptoms arise.

Diabetic retinopathy is generally not painful. In some cases with very advanced disease it can become painful if the new vessels develop on the Iris causing neovascular glaucoma.

Diabetic retinopathy can affect vision in mainly 2 ways. It can lead to swelling of the retina causing difficulty in reading, using mobile or can lead to bleeding inside the eye which will cause sudden decrease in vision. Some patients may experience black clouds floating in front of the eye due to bleeding. Swelling of retina (Diabetic macular edema) is the most common cause of decreased vision in diabetic patients

Diabetic retinopathy can be diagnosed with retina evaluation by a trained retinal surgeon. A diagnosis of diabetic retinopathy can be made by clinical evaluation alone in majority patients. There are many adjuvant tests like OCT, fundus photography, FFA etc which play a role in certain cases and are used as and when required. OCT is used to assess the presence and severity of macular edema. FFA is used to evaluate diabetic retinopathy changes not visible on clinical evaluation.

Diabetes is treatable in a way that medicines can help keep blood sugar under control but as of now there is no cure for diabetes. Similarly, diabetic retinopathy treatment is aimed at keeping the condition under control, complete cure is not possible. We can treat the vision threatening complications of diabetic retinopathy with systemic care along with targeted eye care.

Diabetic retinopathy screening and treatment is done by ophthalmologist who specializes in Retinal diseases. However, systemic control of diabetes in consultation with a physician also plays an important role in management of diabetic retinopathy.

The symptoms due to diabetic retinopathy like vision loss can be reversible to certain extent provided we catch the disease at an early stage and undergo adequate and timely treatment. In advanced stages of diabetic retinopathy vision recovery is difficult and not always possible. Diabetic retinopathy is not completely reversible or will not go away completely but the progression of disease can be slowed with adequate control of systemic disease and regular eye checkup.

There is no scientifically proven treatment that can prevent diabetic retinopathy. Studies have shown that tight sugar control since the onset of diabetes is the most effective method of preventing or delaying the onset of diabetic retinopathy. Systemic control of sugars is the most important factor in relation to onset of diabetic retinopathy, severity of diabetic retinopathy and also treatment response.

Diabetic retinopathy treatment is divided into two parts – systemic treatment to control sugars by physician and ocular treatment for ocular complications. It is important to understand that ocular treatment will be effective only if blood sugar is under control. The treatment will be less effective if patient continues to have uncontrolled diabetes. Therefore, systemic control and ocular treatment both have equal role to play in treatment of diabetic retinopathy. Ocular treatment of diabetic retinopathy involves 3 steps: Step 1: Intravitreal injections. These injections help to control the swelling in the retina (macular edema) as well as take care of early stage new vessels (flat neovascularization) that can form in diabetic retinopathy Step 2: Laser. If the disease has progressed beyond the scope of intravitreal injections (Fibrovascular proliferation) then the patient may need laser (light) treatment in addition to intravitreal injections Step 3: Surgery. If the diabetic retinopathy is in advanced stage (Tractional retinal detachment, Vitreous hemorrhage) then surgical procedure is the only option. The aim of regular screening and follow up is to prevent the disease to progress to a stage where surgical procedure is required

Age related macular degeneration (ARMD) is the leading cause of central vision loss. It is due to age related changes in the central part of retina which is important for reading, writing and recognising faces. Consider eye as a camera, the front part of the eye is the lens of the camera. If this lens is not working properly that means you have a cataract where we remove the lens and put another lens. Now, In ARMD the lens of the camera is fine but the film of the camera (retina) at the back is damaged. Therefore the light enters the eye but the image is not formed on the film (retina)

Age is the most common cause for ARMD. As we cannot reverse ageing so completely preventing this disease is not possible. Genetic link also plays an important role which means if your parents have ARMD then the chances of you developing it in the future are higher as compared to general population. We cannot alter age or genetic link but one important risk factor to develop ARMD which we can stop is SMOKING. Smoking doubles the risk of ARMD. Hypertension and obesity are also associated with ARMD.

ARMD generally starts after 55 years of age. However, it may start earlier in patients who have other risk factors like genetic predisposition, smoking, obesity.

The most common cause for ARMD is age. Old age is not reversible/curable so similarly the disease is not reversible or completely curable. We should try to control other risk factors like smoking, obesity, hypertension. We can delay the progression and limit the loss of vision or even regain meaningful vision back if diagnosed early and treated appropriately. It is therefore important to get regular retina checkup done for patients who are at risk of ARMD.

This question is most commonly asked by patients who have lost significant central vision already in one eye. The answer to this question is unfortunately YES. The risk of developing ARMD if one eye is already affected is 50 % in next 5 years. We cannot stop the disease completely as of now but it is important we diagnose it early so we can limit vision loss in this eye and prevent damage to the extent possible.

We have 2 types of vision – central vision (important for reading, writing, recognizing faces) and peripheral vision (Crossing road, walking). ARMD affects only central vision and therefore it creates problem in reading and recognizing faces. Patients generally complain of straight lines appearing wavy to them.

This is the question most asked by patients in the clinics as soon as they are diagnosed with ARMD. This question has immense implications on the psyche of patient and is often the only information they are seeking. I cannon emphasize enough that no ARMD WILL NOT CAUSE COMPLETE BLINDNESS. Even if the disease progresses, it affects only central vision. Patient will not have problem while walking in the house or going to washroom. They will have difficulty in watching TV or focusing on objects but will not be completely dependent on others for their daily activities.

ARMD is broadly divided in two types wet and dry. To put it in simple terms, Wet AMD is associated with edema and/or bleeding and needs treatment in the form of intravitreal injections. Dry ARMD is associated with irreversible damage to cells and does not need aggressive treatment.

The initial diagnosis of ARMD is based on clinical evaluation. The diagnosis is confirmed with tests like OCT, OCT angio, FFA. The detail features of these are beyond the scope of this document. The most common test done is OCT which allows us to assess the presence of edema in the retina and plays an important role in deciding treatment / re treatment.

The treatment of ARMD is primarily intravitreal Anti VEGF injections. The two most important questions regarding anti VEGF injections are: i. How many injections will I need? ii. Will my vision come back to normal with treatment? To answer the first question there is no fixed number of injections that are required. Each patient responds differently and the number of injections depends on how the eye responds to treatment. I generally give an estimate of 3-4 injections as most patients need 3-4 injections to stabilize. However, some patient may need less injections and some may need more. The injections are usually given at 1 month intervals. The injection is given inside the white part of the eye and is not painful. You can resume your daily activities immediately following the injection with no additional restrictions post injection, no admission required. To answer the second question, the aim of treatment is not complete visual recovery as that is not possible in most cases. The aim of treatment is to prevent further visual loss and try to regain some meaningful vision back. The disease is age related and will progress eventually but with treatment we slow down the progress or in some patients we are even able to halt the progress.

Retina is the back part of the eye. The light enters the eye and falls on retina forming an image which helps us to see. This layer can detach or fall from its place if there is any break or tear in this layer causing retinal detachment. If the retinal gets detached from its place, the blood supply gets affected and it can not function properly. Therefore, in retinal detachment even if the light enters the eye, the image is not formed and vision is severely affected. Retinal detachment can involve the entire retina or only part of it depending on location of break or tear. If retinal detachment is not treated in time then there is an increased chance of proliferative changes to occur leading to PVR. These PVR changes if very extensive prevent the retina from going back to its normal place and therefore reduce the success rate of treatment and also affect the final visual recovery.

Retinal detachment can occur due to multiple reasons like trauma, inflammation but in most cases it is idiopathic (no particular cause). The most common mechanism of retinal detachment is due to a break in retina which allows the fluid/water to enter under the retina causing it to detach. The break could be at a preexisting weak area in retina or could even be at a previously normal area. So, the question arises what causes these breaks? To better understand imagine removing an adhesive tape from the wall and how while peeling it from the wall, the underlying colour or layer also comes out with the tape. Similarly, there is a vitreous gel inside the eye which is firmly adherent to the retina normally. It slowly separates from retina with age and while separating sometimes it rips a part of retina causing a break.

The lifetime risk of retinal detachment is about 1 in 300 people. Retinal detachment is more common in middle aged and elderly population. There are certain people who are predisposed to retinal detachments like patients with high myopia, patients with syndromes like marfans and patients who have retinal degeneration like lattice. Retinal detachment is seen more commonly in some families which could be due to the genetic factors predisposing to retinal detachment.

Yes, retinal detachment can happen in both eyes. It is therefore important to not only treat the eye with retinal detachment but also to screen the other eye for any risk factors. Prophylactic barrage laser can help reduce the chances of retinal detachment in the other eye of predisposed individuals.

Retinal detachment is a relative emergency and can be corrected with good outcome if treated in time. If the treatment is delayed for too long then it may lead to permanent damage to cells that leads to reduced vision or even blindness in severe cases.

It is important to note that the patient may not find any difference or abnormality in the external appearance of the eye. The eye looks normal from outside and generally does not show any symptoms of underlying retinal detachment. Retinal detachment generally begins in the periphery where it may cause milder symptoms like decrease in peripheral vision, floaters, flashes. The vision loss will be severe when the retinal detachment extends towards the centre of the retina (macula). Some patients may experience a feeling like a curtain has fallen in front of their eye. Retinal detachment is unlikely to be painful in the initial stages but can become painful later on due to development of secondary complications because of non-treatment.

A patient with retinal detachment generally comes with the symptoms discussed earlier. On dilated fundus (retina) evaluation, detached retinal can be visualised by a trained professional. The break or tear in retina leading to retinal detachment can also be identified in most cases

Retina (back part of the eye) receives its blood supply through a single artery and vein called central retinal artery and vein respectively. This artery and vein or one of its branch can get blocked in some patients similar to stroke seen in brain or heart. This blockage could be in one of the branches (Branch retinal vein occlusion, BRVO) or may block the central vein itself (Central retinal vein occlusion, CRVO). Any blockage in the branch of the vein leads to blockage of the exit path of blood leading to a scenario similar to a traffic jam. Due to this blockage, the part of the vein involved becomes dilated and eventually may rupture leading to bleeding and swelling. This swelling gets collected at the center of retina called macula causing macular edema. This macular edema leads to decreased vision. The superotemporal branch of the vein is the most common branch to get blocked.

BRVO develops from a blood clot or decreased blood flow in the affected branch of central retina vein. BRVO can be caused by multiple factors. Age is the most important risk factor. The other risk factors associated with BRVO are Hypertension, Diabetes, Smoking, Glaucoma (Raised eye pressure) etc. The specific cause for the clot to form is unknown.

BRVO is one of the leading retinal vascular diseases causing decreased vision after diabetic retinopathy. It is the most common type of vein occlusion followed by CRVO. It is commonly seen in patients with risk factors like hypertension, smoking, diabetes and old age.

BRVO leads to sudden decrease in vision. However, with adequate treatment patient has high probability of gaining good vision back. The recovery in vision depends on the underlying nerve cell damage and the duration of the disease.

BRVO generally presents as sudden painless decrease in vision in the acute stage. Some patients may have distorted / wavy vision where objects appear distorted. BRVO is not associated with pain. Some patients may develop new vessels which may lead to bleeding in the absence of treatment.

BRVO can be diagnosed clinically with the presence of retinal bleeding, swelling in the retina and dilated and tortuous vessels in the affected area. OCT helps to assess the extent of swelling of retina and also treatment response. FFA is occasionally required to look for new vessel formation.

BRVO is like a stroke of the eye where the blood vessel in the retina gets occluded partially or completely. It is important to identify the cause for this blockage so as to prevent the stroke in other eye or elsewhere in the body. Therefore, systemic workup in the form of blood tests like CBC, blood sugar, lipid profile, homocysteine levels is essential to identify the underlying pathology.

In the acute stage, the treatment is aimed at resolution of swelling in the retina. The treatment includes intravitreal anti VEGF injection. The two most important questions regarding anti VEGF injections are: i. How many injections will I need? ii. Will my vision come back to normal with treatment? To answer the first question there is no fixed number of injections that are required. Each patient responds differently and the number of injections depends on how the eye responds to treatment. The treatment is to be continued till the patient shows visual improvement with reduction in swelling. I generally give an estimate of 3-4 injections as most patients need 3-4 injections to stabilize. However, some patient may need fewer injections and some patients may need more. The injections are usually given on 1 month intervals. The injection is given inside the white part of the eye and is not painful. You can resume your daily activities immediately following the injection with no additional restrictions post injection, no admission required. To answer the second question, the aim of treatment is to decrease the swelling in the retina. Usually patients show good improvement in vision with treatment with some patients regaining near normal vision back. In patients who do not undergo adequate treatment or do not follow up regularly as advised, secondary complications may develop in the form of neovascularization. In such patients laser therapy may be required in addition to intravitreal injection.

There is no cure for the occlusion in BRVO. Unlike in other strokes, we cannot lyse or remove the clot as the blood vessels in the retina are very narrow. The treatment is primarily aimed at preventing vision loss and treating any complications that may arise.

Retina (back part of the eye) receives its blood supply through a single artery and vein called central retinal artery and vein respectively. This artery and vein can get blocked in some patients similar to stroke seen in brain or heart. This blockage could be in one of the branches (Branch retinal vein occlusion, BRVO) or may block the central vein itself (Central retinal vein occlusion, CRVO). Any blockage in the central retinal vein blocks the exit path of blood leading to a scenario similar to a traffic jam. Due to this blockage, the vein becomes dilated and eventually may rupture leading to bleeding and swelling. This swelling gets collected at the center of retina called macula causing macular edema. This macular edema leads to decreased vision.

CRVO develops from a blood clot or decreased blood flow in the central retina vein. CRVO can be caused by multiple factors. Age is the most important risk factor. The other risk factors associated with CRVO are Hypertension, Diabetes, Smoking, Glaucoma (Raised eye pressure) etc. The specific cause for the clot to form is unknown.

There is no significant link between hereditary factors and CRVO. However, certain hereditary diseases like thrombophilia, spherocytosis, sickle cell disease increase the risk of CRVO.

CRVO is one of the leading retinal vascular diseases causing decreased vision after diabetic retinopathy. It is commonly seen in patients with risk factors like hypertension, smoking, diabetes and old age. If one eye develops CRVO then the risk of other eye also developing CRVO is 6 – 17 %.

CRVO causes sudden decrease in vision. The severity of vision loss depends on the type of CRVO and extent of swelling of retina. There are 2 types of CRVO: i] Non Ischemic CRVO (81%): The vision loss in this type is reversible with treatment. 5% patients may improve without treatment also however majority will worsen without adequate treatment. If it is not treated for many months, the edema may cause degenerative changes in retina leading to permanent decrease in vision. With treatment patients with non ischemic CRVO generally show significant vision improvement. ii] Ischemic CRVO (19%): This is the more serious variant of CRVO where the vision is very poor with less chance for improvement even with treatment. The rate of complications are also higher in this type.

CRVO patients have sudden drop in vision. It needs prompt retinal evaluation and treatment by retina specialist. However, it is not an emergency where we need to treat it immediately the same day. A prompt evaluation and treatment helps limit the damage to eye.

The acute signs resolve over 6 - 12 months with disc collateral and pigmentary changes at macula as residual changes. In some patients (more commonly in Ischemic type) long term complications in the form of neovascularisation with secondary glaucoma may develop. In acute stage, patient may need frequent follow ups and treatment.

CRVO generally presents as sudden painless decrease in vision in the acute stage. Some patients may have distorted / wavy vision where objects appear distorted. Occasionally patients may complain of painful red eye if neovascular glaucoma has developed due to ischemic CRVO / inadequate treatment or follow up. Pain in CRVO generally happens only in the later stages as a result of complication (Neovascularisation) secondary to CRVO. Therefore, it is important to have regular follow up to identify and treat these complications at an early stage and prevent severe pain and blindness. CRVO can cause headache if ocular pressure increases as a result of neovascular glaucoma.

CRVO can be diagnosed clinically with the presence of retinal bleeding, swelling in the retina and dilated and tortuous vessels. OCT helps to assess the extent of swelling of retina and also treatment response. FFA is occasionally required to look for ischemic CRVO.

CRVO is like a stroke of the eye where the blood vessel in the retina gets occluded partially or completely. It is important to identify the cause for this blockage so as to prevent the stroke in other eye or elsewhere in the body. Therefore, systemic workup in the form of blood tests like CBC, blood sugar, lipid profile, homocysteine levels is essential to identify the underlying cause.

In the acute stage, the treatment is aimed at resolution of swelling in the retina. The treatment includes intravitreal anti VEGF injection. The two most important questions regarding anti VEGF injections are: i. How many injections will I need? ii. Will my vision come back to normal with treatment? To answer the first question there is no fixed number of injections that are required. Each patient responds differently and the number of injections depends on how the eye responds to treatment. The treatment is to be continued till the patient shows visual improvement with reduction in swelling. I generally give an estimate of 3-4 injections as most patients need 3-4 injections to stabilize. However, some patient may need fewer injections and some patients may need more. The injections are usually given on 1 month intervals. The injection is given inside the white part of the eye and is not painful. You can resume your daily activities immediately following the injection with no additional restrictions post injection, no admission required. To answer the second question, the aim of treatment is to decrease the swelling in the retina. Usually patients show good improvement in vision with treatment with some patients regaining near normal vision back. However, in ischemic CRVO the patient may not have significant improvement in vision with treatment and thus may need treatment to be stopped. Rarely, some patients show improvement in the initial stage of treatment but then do not improve further with treatment due to conversion of non ischemic to ischemic CRVO. In patients who do not undergo adequate treatment or do not follow up regularly as advised, secondary complications may develop in the form of neovascularization. In such patients laser therapy may be required in addition to intravitreal injection.

There is no cure for the occlusion in CRVO. Unlike in other strokes, we cannot lyse or remove the clot as the blood vessels in the retina are very narrow. The treatment is primarily aimed at preventing vision loss and treating any complications that may arise.

Optimal control of known risk factors and systemic diseases may reduce the incidence of CRVO. There is some evidence that controlling ocular pressure can also lead to decreased chance of CRVO.