Central Serous Retinopathy (CSR) causes painless blurring of central vision, primarily in young men ages 20-45. Common symptoms include distortion, color vision changes, micropsia (objects look smaller), and a central blind or gray spot. These symptoms are caused by a blister of fluid that collects under the center of the retina. The retina is the “film” of the eye’s camera and the symptoms are related to the size and duration of the fluid blister. The fluid collection usually resolves spontaneously but may recur in the same or fellow eye months or year later.

CAUSES OF CSR. The exact cause of central serous retinopathy is controversial. Fluid appears to leak from the choroid (a layer of tissue behind the retina) into the space under the retina, but it is unclear whether the underlying problem is in the choroid or the retinal pigment epithelium (RPE), a layer that sits between the retina and the choroid. In most cases, CSR is not related to an underlying medical condition or use of medications. Stress and “Type A” personality traits have been associated with CSR. Steroid use is a common trigger for CSR, regardless of whether the steroids are taken by mouth, by inhaler, or by topical application. Other associations include organ transplantation, Cushing syndrome, hypertension, systemic lupus erythematosus, pregnancy, and use of some medications.

EVALUTION. The blister of fluid under the retina is usually visible on clinical examination by an eye professional, but additional testing is helpful to confirm the diagnosis (other conditions may also cause fluid collections) and monitor change over time. Optical coherence tomography (OCT) is a non-invasive scan of the retina which measures and illustrates the subretinal fluid in cross-section. Fluorescein angiography involves a small intravenous injection of dye (fluorescein) followed by a series of photographs of the retina. The images can differentiate between various causes of subretinal fluid and can also identify the precise source of fluid leakage.

TREATMENT. Initially, the pocket of subretinal fluid in CSR is measured and usually observed, since the fluid reabsorbs spontaneously in the vast majority of cases. If imaging shows improvement, continued observation is usually most appropriate. In some cases, particularly those in which the fluid fails to reabsorb within three to six months, treatment may be recommended to facilitate resolution of the fluid. Current treatment options include photodynamic therapy and intravitreal injection. Photodynamic therapy treats the source of leakage with a “cold” laser after intravenous injection of a medication called Verteporfin. Intravitreal injection involves the injection of a medicine into the eye after numbing drops are given in the office. If treatment is advised, your retina specialist will discuss the various options and make recommendations based on your particular case. While most cases of CSR resolve without treatment, and those cases that require treatment tend to resolve as well, it is important to understand that CSR is often a chronic disease. Repeat episodes are common and may occur in the same eye or the other eye. Even after the fluid reabsorbs, vision may not return to normal due to damage in the retinal tissue. When a trigger such as steroids is identified, avoiding that trigger in the future will help reduce the chance of a recurrence.

Diabetes affects about one fifth of the American adult population, and diabetic retinopathy is the leading cause of legal blindness in this group. Diabetes affects the eyes in the same way that it affects the kidneys and other organs: small blood vessels are damaged and over the years, this can result in permanent tissue damage. Vision loss in diabetes is due primarily to damage in the retina.

The retina is like the film of the camera. Just as focusing the lens of a camera will not create a clear picture if the film is damaged, getting a pair of glasses will not improve the vision if diabetes has damaged the retina.

Diabetic retinopathy causes vision loss in the following ways:

Diabetic macular edema (DME) is swelling of the macula, or central retina, in patients with diabetes.  Diabetes affects the blood vessels in the eye and may cause them to leak. When fluid leaks out of the retinal blood vessels, it collects in the retina and causes the retina to swell. When the retina is swollen, central vision may be blurred or distorted. Diabetic macular edema is the leading cause of vision loss in patients with diabetes. DME is more likely to occur with longer duration of diabetes and poor control of diabetes. High blood pressure also increases the risk of DME. Vision loss from diabetic macular edema tends to occur gradually over time.  Regular eye examination of the retina is important for all diabetic patients. It is easier to maintain good vision by preventing DME in the first place rather than treating it after it occurs.

Evaluation. Your retinal surgeon may order diagnostic tests in the office to determine the degree of diabetic swelling and damage to the retina. Optical coherence tomography (OCT) is a scan of the retina that locates and measures swelling. Fluorescein angiography identifies poor blood flow and fluid leakage in the retina.

Treatment.  Treatments for diabetic macular edema include laser as well as injections of medications. In many cases, treatment involves a combination of these therapies. Your retinal surgeon is trained in the most effective use of these treatments and will tailor the treatment to your individual eyes. It is important to understand that the first goal of treatment is the prevention of further vision loss, which is likely to happen without treatment. The second goal of treatment is improvement of the vision. Modern treatments are very effective at both of these goals, particularly when diabetes and high blood pressure are well controlled. With a combination of the best treatments available, we can reduce the risk of further vision loss by at least half. 

Proliferative diabetic retinopathy is a serious complication of diabetes. Damage to the retinal blood vessels causes release of a hormone known as VEGF which causes abnormal new blood vessels to grow. These new blood vessels may leak and bleed, causing vision loss. If these abnormal blood vessels continue to grow, they may cause scar formation and pull the retina off the wall of the eye. Proliferative Diabetic Retinopathy (PDR) often occurs without any early warning signs, which is why regular retinal examination is critical in patients with diabetes. Bleeding from abnormal blood vessels may be seen as floaters in the vision, or as dramatic vision loss if a large amount of bleeding occurs suddenly. This blood may clear on its own over weeks or months, and sometimes the blood may not clear in which case surgery is required. Gradual vision loss may occur from scar formation on the retina. The scarring can cause traction on the retina resulting in loss of vision. Surgery may be required to remove the scar tissue.

Evaluation. Diagnostic imaging is sometimes needed. This testing may include ocular ultrasound (a probe is placed on your eyelid and reflected sound waves produce images on a screen) and optical coherence tomography and fluorescein angiography

Treatment. There are various methods of treating proliferative diabetic retinopathy. These methods may be employed individually or together.

Laser Treatment: Panretinal photocoagulation (PRP) laser treatment creates hundreds of small laser burns throughout the peripheral retina, thereby improving the flow of oxygen to the central retina, which is most important for everyday vision. The application of laser also decreases the stimulus for new blood vessel growth. This treatment may be done in one or more sessions. 

Vitrectomy surgery: This procedure is recommended in cases of advanced bleeding or scarring inside the eye. Vitrectomy surgery is performed in an operating room. The surgeon views the interior of the eye through a microscope  while using fine instruments to remove blood, scar tissue, repair the retina and perform laser treatment.

Anti-VEGF therapy: This form of therapy causes stabilization and temporary shrinkage of the new blood vessel formations, thus decreasing the likelihood of bleeding. The medicine is injected into the eye in the office after numbing medicines are given. The anti-VEGF medication has a temporary effect and may need to be repeated periodically depending on the response to treatment. This treatment is sometimes used prior to vitrectomy surgery or in combination with laser.

Diabetes causes even more damage when combined with high blood pressure, so controlling both is important to prevent blindness. Diabetic retinopathy is more common in patients with poorly controlled diabetes and patients with more years of diabetes. Diabetic retinopathy may already be present at the time of diagnosis of adult onset (Type II) diabetes. Diabetic retinopathy begins long before the vision is affected. Regular examination of the retina is important to identify and treat diabetic retinopathy before vision loss occurs. Once the vision is affected, treatments can often improve the vision, but it may never return to normal even with treatment.

Epiretinal membrane (ERM), also known as macular pucker, is a common disorder of the central retina (macula) which may cause a central blur or distortion in the vision. An ERM is a layer of scar-like tissue on the surface of the retina. Most eyes with ERM are asymptomatic, but ERMs may require intervention if the vision is significantly affected due to distortion or lack of clarity. In some cases, an epiretinal membrane develops as a response to injury or swelling in the eye. An ERM may form after a retinal tear or detachment, after cataract surgery, or after swelling in the eye from a variety of diseases such as diabetes or uveitis. However, in most cases there is no identifiable cause of the epiretinal membrane.

EVALUTION. A visually significant ERM is usually first identified on clinical examination of the eye. An ERM may cause only a slight wrinkle in the retina, or it may pull on the retina and cause swelling or distortion with decreased vision. Imaging tests such as optical coherence tomography (OCT) and fluorescein angiography (FA) can be helpful in demonstrating the degree to which an ERM is distorting or damaging the underlying retina.

SURGERY. Vitrectomy is the surgical removal of the gel in the eye, or vitreous. Membrane peeling, or removal of the scar tissue, is then performed using microscopic instruments. Vitrectomy with membrane peeling is an outpatient procedure that usually takes less than an hour. Surgery is most often performed under local anesthesia, but can be done under general anesthesia as well. Visual improvement after surgery for epiretinal membrane is gradual, since the retina does not immediately return to its normal configuration after surgery. Significant visual improvement is usually seen by 6-8 weeks after surgery, but vision may continue to improve for 6 months or more. Vitrectomy with membrane peeling can lead to visual improvement in 75-90% of eyes with enough distortion and blur to warrant surgery. The average postoperative visual acuity is half way between preoperative vision and 20/20. It is important to consider that postoperative vision may not be perfect, but most eyes that undergo this surgery have a decrease in distortion. Eyes that have had a prior retinal detachment in the macula are less likely to have return of fine vision. Rare complications after vitrectomy surgery include bleeding, infection, retinal tear and retinal detachment. These complications occur in 1 out of several thousand patients. More commonly, cataract may advance at a faster pace following vitrectomy. Patients who have not previously undergone cataract surgery should expect to need cataract surgery within 1-2 years of vitrectomy surgery.

Cataract surgery is one of the most common and successful surgical procedures performed today. During the surgical procedure, the patient’s cataract (cloudy lens) is removed, and a clear intraocular lens (IOL) is placed inside the capsular bag that previously held the cloudy lens. On rare occasion, days to years later, the intraocular lens moves out of place either due to the result of factors during the original surgery, trauma to the eye, or due to diseases that affect the stability of the capsular bag that holds the intraocular lens in place. The most common symptom of a dislocated IOL is a change in vision. The degree to which vision is affected depends upon the severity of the dislocation. Blurring, double vision, and seeing the edge of the lens implant are other symptoms that can appear. IOL dislocation can also lead to other complications such as retinal detachment, bleeding, intraocular inflammation, macular edema, increased eye pressure and corneal edema. Diagnosis of a dislocated IOL includes a dilated eye examination and photographs to document the extent of the problem.

Lattice degeneration is a common peripheral retinal degeneration, with oval or linear patches of retinal thinning. Lattice degeneration affects about 10% of the population and is bilateral in 30 to 50% of those patients. It may run in families and it is more common in near-sighted eyes. Patients with lattice degeneration are typically asymptomatic, and the lesions are usually an incidental finding of dilated eye exam. Lattice lesions usually develop during the teenage years and may continue to develop over many years. Lattice degeneration may predispose the retina to tears or atrophic holes which may lead to retinal detachment. For this reason, the acute onset of floaters, flashes of light, peripheral field loss, or central vision loss should be taken seriously and a detailed retinal examination is appropriate. Lattice lesions may be single or multiple and are usually located near the periphery of the retina. The back part of the eye is filled with a gel called the vitreous. Condensed vitreous gel is adherent at the margins of lattice and may pull on the retina. Lattice lesions appear to be caused by loss of peripheral retinal capillaries (fine blood vessels), which leads to thinning of all retinal layers and in some cases a full-thickness retinal hole. Lattice degeneration and associated retinal holes or breaks can be detected by peripheral retinal examination with scleral depression, a technique in which the doctor pushes on the edge of the eye with an instrument to clearly visualize the periphery of the retina.

TREATMENT. Mild lattice does not interfere with vision and does not present a high risk for future retinal detachment. Prophylactic treatment is indicated only in specific circumstances. Lattice degeneration complicated by retinal tear or an increasing cuff of fluid under the retina constitutes an urgent indication for treatment with laser retinopexy or cryoretinopexy. Both of these techniques create a controlled scar around the tear to seal it and prevent a vision-threatening retinal detachment from occurring. Lattice lesions in fellow eyes of patients who have retinal detachment in the other eye may be treated prophylactically, but there is still a small chance of retinal detachment even after treatment. 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.

A macular hole is a full thickness defect in the central retina (macula). Since the macula is responsible for reading vision, patients who develop a macular hole complain of distorted vision and loss of central vision in the affected eye. The incidence of macular hole is 3.3 cases per 1000 in the population. The risk for developing a macular hole in the fellow eye is 10% – 15%. Small macular holes occasionally resolve spontaneously but the majority will persist. Once a macular hole develops, vision usually stabilizes at 20/200 if left unrepaired. Changing eyeglasses will not correct the blur and distortion caused by the macular hole. The vitreous is the gel that fills the eye. The majority of macular holes are caused by a spontaneous separation of the vitreous overlying the center of the retina (macula). The vitreous has a strong natural adhesion to the macula. Due to age-related changes in the vitreous gel, contraction of the vitreous overlying the macula may pull open a defect in the macula creating a macular hole. Less common causes of a macular hole include blunt trauma to the eye, contraction of a pre-existing epiretinal membrane (macular pucker), or extreme near-sightedness (high myopia).

EVALUATION. Macular holes are frequently identified by an eye care professional using a slit lamp microscope. Fluorescein angiography (a dye test to evaluate blood flow) is often performed to evaluate a macular hole and rule out other conditions. Optical coherent tomography (OCT) is a type of imaging test used to produce high-resolution cross-sectional images of the macula to confirm the diagnosis, exclude other conditions, and monitor the macular hole before and after surgical repair.

SURGERY. Macular holes can be repaired by a surgical procedure called vitrectomy with membrane peeling and fluid gas exchange. This operation is performed in a hospital or surgery center on an outpatient basis. During surgery, the retinal surgeon removes the vitreous gel and then releases all forms of traction by separating the back of the vitreous from the retina and peeling any membranes surrounding the macular hole. The eye is filled with a bubble of sterile air mixed with a long-acting gas. After surgery, the patient must stay in a face down position to keep the gas bubble over the macular hole at the back of the eye. Patients may sit upright for meals, to shower and use the bathroom but should otherwise stay and sleep in the face down position for a period of time determined by the surgeon, usually 3-5 days. Eighty to ninety percent of macular holes can be successfully repaired with this technique. The majority of patients will notice an improvement in the distortion and vision. With a gas bubble in the eye, one should never travel to a higher elevation or fly in an airplane until the gas bubble has disappeared. Otherwise, the gas bubble may expand in the eye at the higher altitude causing acute glaucoma and permanent blindness. Rare complications of surgery include bleeding, the development of a retinal tear or detachment, and infection. These complications occur in 1 out of several thousand patients. More commonly, a cataract may develop following macular hole surgery if cataract surgery was not previously performed.

Between the lens in the front and the retina in the back of the eye lies a clear gel called the vitreous. A posterior vitreous detachment (PVD) is a separation between the vitreous gel and the retina. At birth, the vitreous gel is clear and firm, and it is attached to the retina. With age, the vitreous gel becomes liquefied and some of the proteins in the gel clump together—these are the small floaters that most people see. Eventually the back surface of the gel may separate from the retina, beginning near the optic nerve and macula (central retina) and continuing towards the edges of the retina. The incidence of PVD increases with age. Most of the time, a PVD occurs without any sudden new symptoms. Some of the time, however, a PVD is marked by the sudden onset of new flashes or floaters in the affected eye. Posterior vitreous detachment usually occurs spontaneously but may occur acutely in the setting of trauma.

Flashes and Floaters. As the separation of the vitreous gel from the retina moves from the center out towards the edges of the retina, the gel may pull on the retina at the leading edge. This traction on the retina may cause retinal neurons to fire, resulting in transient colorless “flashes” in the vision. Once the gel separates from the retina, clumps of protein on the back surface of the vitreous gel may be seen as large new floaters. Floaters in the setting of a PVD may also represent blood (hemorrhagic PVD) or pigment cells (retinal tear).

Hemorrhagic PVD. As the vitreous gel pulls away from the retina, the gel may tear a blood vessel on the retinal surface. A few drops of blood may leak out of the blood vessel into the gel and be seen as new floaters. While these floaters may be annoying, the blood generally does not cause any damage to the eye tissues. Hemorrhagic PVD is concerning because in the presence of blood there is a high likelihood of a retinal tear. If a tear is present, the blood may obscure it, therefore frequent retinal examinations are appropriate to identify a retinal tear as early as possible and prevent a vision-threatening retinal detachment. In cases of dense hemorrhage that does not clear quickly on its own, surgery may be recommended to remove the blood and identify and treat the underlying source of bleeding.

Retinal tear. When a PVD occurs with flashes or floaters, there is about a 10% chance of developing a retinal tear. Most of these tears occur within 6 weeks of the initial symptoms. Tears occur because of the traction at the leading edge of the gel separating from the retina. An untreated retinal tear may lead to retinal detachment with severe vision loss.

What to expect after a PVD occurs: Detailed examination by a retinal specialist may be necessary after a PVD, depending on the findings at the time of examination. The primary purpose of examination is the detection of a retinal tear, which would be treated without delay to prevent severe vision loss. In most cases, the new floaters from a PVD will not go away entirely. However, the brain often learns to ignore the new floaters, and the floaters may become more mobile and move away from the central vision as the vitreous gel continues to liquefy with time. In cases of hemorrhagic PVD, the floaters may decrease over time as the blood breaks down and disappears. Flashes usually decrease and stop as the process of vitreous separation completes itself. This may take days, weeks or even months depending on the characteristics of the gel. If you experience a sudden increase in flashes, the onset of additional new floaters, or a shadow in the vision, contact your eye care provider immediately, as these may be symptoms of a retinal tear or detachment.

The eye is like a camera, it has a lens in the front that focuses light, and film in the back that captures light. The retina is the “film” inside the human eye and contains over a million neurons as well as a network of blood vessels that keep the tissue healthy. Between the lens in the front and the retina in the back of the eye lies a clear gel called the vitreous. A retinal detachment occurs when the retina pulls away from the wall of the eye. The retina cannot function normally when it is detached from the wall of the eye, which is why a retinal detachment can limit the vision to varying degrees depending on how much of the retina is detached. There are different kinds of retinal detachments: rhegmatogenous, tractional and exudative. The most common kind, a rhegmatogenous retinal detachment, occurs when fluid moves through a retinal hole or tear into the space under the retina, causing the retina to detach. The remainder of this information deals specifically with rhegmatogenous retinal detachment.

PROCEDURES. The goals of the procedure are to get the fluid out from under the retina and seal the tears or holes that caused the detachment. Removing the fluid allows the retina to reposition itself (reattach) against the wall of the eye and thereby regain its nourishing blood supply and restore vision. Sealing the tears or holes in the retina prevents the retina from re-detaching in the future. Fortunately, over eighty to ninety percent of retinal detachments can be repaired with only one procedure. The following are the most commonly used methods to repair a retinal detachment.

SCLERAL BUCKLE. Scleral buckling entails sewing a silicone band to the outside wall of the eye. This material may be sewn to a section of the outside eye wall, or it may go around the eye for 360 degrees forming a “belt” around the eye. The silicone material indents the wall of the eye (buckles) and pushes the wall of the eye closer to the retinal tear. The tear is treated with freezing therapy which causes local tissue damage and controlled scarring which seals the tear. The fluid already under the retina is either absorbed by the body or actively drained from under the retina and the retina is thereby reattached. 

VITRECTOMY. Vitrectomy is a type of surgery that takes place primarily inside the eye. The surgery takes place through three very small openings in the white part of the eye. The surgeon uses fine instruments and an operating microscope to remove the vitreous gel inside the eye and drain the fluid from under the retina. The surgeon may use a laser to seal the retinal tears or holes. A bubble of gas is commonly placed inside the eye to hold the retina in place while it heals. The patient may be asked to maintain a specific head position for several days after surgery to position the gas bubble correctly.

PNEUMATIC RETINOPEXY. Unlike scleral buckling and vitrectomy, which are performed in the operating room, pneumatic retinopexy is performed in the office with only local anesthesia. The surgeon will determine whether this is an option based on the characteristics of the retinal detachment. Pneumatic retinopexy consist of at least three parts. 

1. The tear in the retina needs to be sealed to the eye wall. This is usually done with cryotherapy, a freezing treatment applied to the outside of the eye after numbing medications are given.

2. Gas is injected into the back part of the eye (vitreous cavity). When the head is later positioned appropriately, this bubble pushes the fluid out from under the retina and pushes the retinal tear closed. Proper positioning by the patient immediately after this procedure is critical.

3. Fluid is removed from the eye to make room for the gas. This can be done before the gas is injected, after the gas is injected, or both before and after.

LASER SURGERY. In certain selected cases it may be advisable to “wall off” the detachment to prevent the retinal detachment from spreading within the eye. In cases such as these, a barrier of scar tissue forms as a result of laser (or freezing treatment) and the detachment remains fixed in its position. This technique is most often used when the area of detachment is very small and located at the far edge of the retina so that vision is not significantly affected. This technique is also sometimes used for patients who cannot safely undergo any other procedure due to other medical conditions

RESULTS OF TREATMENT. Results of retinal reattachment surgery are divided into two categories: anatomic results and visual results. The overall anatomic success rate of retinal detachment repair is greater than 90%. This means that the surgeon can successfully put the retina back into place 9 out of 10 times. Sometimes more than one procedure is required to achieve anatomic success. The visual result depends on the patient’s pre-operative vision as well as the body’s ability to heal. If the center of the retina is attached prior to the surgery, then post-operative vision tends to be similar to pre-operative vision. However, if the central retina is detached prior to the surgery, there may be some degree of permanent vision loss even after successful reattachment. Some procedures will accelerate cataract formation, in which case cataract surgery is needed later to achieve the best possible vision.

The eye is like a camera: it has a lens in the front that focuses light and film in the back that captures light. The retina is the “film” inside the human eye and contains over a million neurons as well as a network of blood vessels that keep the tissue healthy. Between the lens in the front and the retina in the back of the eye lies a clear gel called the vitreous. As the vitreous gel changes with age, it may pull away from the retina in the back of the eye. This process usually starts near the back and continues towards the front of the eye, with traction on the retina at the leading edge. If the retina is unusually thin or damaged, the gel pulling may be enough to cause a full thickness tear in the retina. Retinal tears are more common in patients who are very near-sighted; patients with a family history of retinal tear or retinal detachment; or patients with a prior retinal tear or detachment in the same or other eye. Retinal tears may also occur after trauma or surgery in the eye.

TREATMENT. The goal of treatment is the creation of a controlled scar surrounding the retinal tear. This scar serves to weld the retina and seal it to the underlying tissues, thereby preventing fluid from moving through the retinal tear into the space under the retina (retinal detachment). The scar can be created by either laser treatment or a freezing treatment, depending on the location and characteristics of the tear.

Laser Retinopexy. Laser treatment is delivered through the front of the eye using either a head-mounted apparatus or a laser apparatus connected to a slit lamp in conjunction with a contact lens. While this treatment is generally not painful, some patients may have a mild headache after treatment, which is easily remedied with over-the-counter acetaminophen.

Cryoretinopexy (cryotherapy). Cryotherapy involves the application of a probe to the outer wall of the eye corresponding to the location of the retinal tear. A freeze is created at the tip of the probe, extending inwards to the retina. Some patients have a headache or eye ache afterwards, which can be treated with over-the-counter acetaminophen. Many patients with retinal tears initially present with symptoms such as flashes of light or new floaters. It is important to understand that treatment is not meant to get rid of these symptoms. The flashes occur because the vitreous gel is pulling on the retina. This process usually resolves spontaneously within days or weeks but in some cases will last much longer. The continuation of intermittent flashes after treatment is usually not concerning unless the flashes increase in frequency or are associated with new floaters or other vision changes. Floaters in the setting of a retinal tear may occur for two reasons. When the vitreous gel pulls away from the back of the eye (a normal, age-related process), small condensations in the gel will appear as floaters. While these floaters are annoying, they do not cause problems on their own. These floaters will be more noticeable when looking at a clear blue sky or a white wall. In some cases, the floaters are due to blood that was released when the retina tore. This blood eventually breaks down and disappears, but the rate of disappearance is unpredictable and may vary from days to months.

RETINAL VEIN OCCLUSION

The retina is fed by a system of blood vessels (arteries and veins) like a tree, with the trunk in the optic nerve and branches extending to the farthest edges of the retina. A branch retinal vein occlusion (BRVO) is vein blockage along a branch of the tree, usually at a point where an artery crosses over a vein and compresses it.  A central retinal vein occlusion (CRVO) is blockage of the large vein in the trunk. This results in poor blood flow to a section of the retina. Since the retina is like film in a camera, a patient experiences branch retinal vein occlusion as painless vision loss. If the vein occlusion is away from the center or the retina, central vision may be unaffected. If the vein occlusion affects the central retina, vision may be severely limited. Branch retinal vein occlusion occurs most often in patients with high blood pressure, diabetes, high cholesterol, atherosclerosis, or high intraocular pressure (glaucoma). Smoking is also a major risk factor for BRVO. In some cases, no clear cause is found for BRVO, and in some cases BRVO is caused by rare conditions such as blood disorders that cause spontaneous clotting. Your doctor will determine the appropriate workup for underlying causes of BRVO depending on your age and medical history.

EVALUATION. Your retinal surgeon may order diagnostic tests in the office to determine the degree of damage caused by the vein occlusion. Blood flow in the affected area may be permanently reduced. Swelling may occur in the central part of the retina (the macula) resulting in decreased vision. In some cases, the eye may grow abnormal blood vessels. These complications of BRVO can be detected by a combination of clinical examination and imaging tests. Optical coherence tomography (OCT) is a fast, non-invasive scan of the retina which measures and locates swelling in the retina. Fluorescein angiography (FA) evaluates blood flow in the retina with a series of photographs taken after intravenous injection of a dye (fluorescein).

TREATMENT. If swelling is present, your retinal surgeon may recommend one or more treatments including laser or injection of medicine into the eye. If the eye is growing abnormal blood vessels (neovascularization), your surgeon may recommend laser treatment. In all cases, treatment of underlying medical conditions such as high blood pressure is critical to preventing another retinal vein occlusion in the future.

RETINAL ARTERY OCCLUSION

A central retinal artery occlusion (CRAO) is blockage of blood flow to the retina in the main trunk with sudden, severe vision loss throughout the visual field of one eye. A branch retinal artery occlusion (BRAO) is blockage along a branch of the tree. This results in poor blood flow to a section of the retina. A patient experiences sudden, painless loss of a portion of vision. If the artery occlusion is away from the center of the retina, central vision may be unaffected. If the artery occlusion affects the central retina, reading vision may be severely limited. The blockage or occlusion may last only a few seconds, or it may be permanent. The common associations with retinal arterial occlusion are atherosclerosis, systemic hypertension, and diabetes. An embolus or “floating log jam” such as cholesterol or a detached blood clot may come from the heart or carotid arteries and block a retinal artery. Carotid artery disease occurs in 45% of patients with CRAO. If presenting before age 30, retinal artery occlusion is more often associated with migraine, trauma, and coagulation disorders (blood disorders that cause easy clotting). In elderly patients, a disease called giant cell arteritis can cause inflammation of the central retinal artery, resulting in occlusion.

EVALUATION. Your retinal surgeon may order diagnostic tests in the office to determine the degree of damage caused by the artery occlusion. Blood flow in the affected area may be permanently reduced. In some cases, the eye may grow abnormal blood vessels. These complications of BRAO or CRAO can be detected by a combination of clinical examination and imaging tests. Fluorescein angiography (FA) evaluates blood flow in the retina with a series of photographs taken after intravenous injection of a synthetic dye (fluorescein) which contains no iodine. Carotid studies, magnetic resonance angiogram, echocardiogram, and blood tests may be ordered to look for medical problems which may be life-threatening if untreated. While it is important to identify and treat the underlying cause of a retinal arterial occlusion, there are no well-established medical or surgical techniques for treating the actual occlusion. Massage of the eye may be attempted to increase blood flow, decrease eye pressure, and dislodge emboli. Fluid may be taken from the front of the eye to lower eye pressure quickly. If new vessels grow in the front of the eye, they may cause glaucoma, sometimes with pain and loss of vision. These abnormal new blood vessels can be treated with laser and injections of medicine into the eye, but these treatments do not restore vision. In all cases, treatment of underlying medical conditions (such as diabetes or high blood pressure) is critical to prevent stroke or blood vessel blockage elsewhere in the body.

Cryoretinopexy (cryotherapy) is a treatment of retinal tears, retinal detachment, and a few less common conditions such as Coats disease. Cryotherapy is delivered using a small probe to the outer surface of the eye by the surgeon while the patient reclines in an examination chair. Each treatment freezes a small amount of tissue from the outer surface of the eye through the eye wall to the retina. The freeze damages the retina just enough to form a scar. The scar serves as an adhesive between the retina and the eye wall, thereby sealing any breaks in the retina. In rare cases, cryotherapy is used to destroy abnormal blood vessels that cannot be safely treated using a laser. Most patients describe the discomfort of cryotherapy as an “ice cream headache.” This sensation usually lasts only a few seconds. Your surgeon will instill numbing eye drops to make you as comfortable as possible during treatment. Because cryotherapy is a non-invasive procedure, patients do not routinely require any eye drops after treatment and there is no significant risk of infection. If the eye feels irritated or dry after treatment, over-the-counter artificial tear drops may be used to sooth the eye. Some patients experience a headache, which may be treated using over-the-counter medications such as acetaminophen or ibuprofen as needed. The vision is often blurred for several hours after treatment, and vision in the treated eye may not return to pre-treatment levels for one or two days in some cases.

Laser photocoagulation is a controlled method of delivering focused laser power to the retina, creating limited burns. Laser photocoagulation has been used in retinal surgery for over 40 years.

Several different types of lasers are used in ophthalmology. The type of laser used in retinal treatment is different from the lasers used in glaucoma treatment or refractive surgery such as LASIK.

Laser photocoagulation is used in the office to treat a variety of conditions including: Diabetic macular edema, proliferative diabetic retinopathy, retinal vein occlusion, retinal tears or holes, retinal detachment, high risk lattice degeneration, and retinal arterial macroaneurysm. Depending on the condition being treated, laser may be delivered with the surgeon wearing a headset (indirect ophthalmoscope) while the patient lays in an examination chair, or with the surgeon and patient sitting on opposite sides of table-mounted equipment (slit lamp).

Some treatments, such as those for retinal edema or small tears, may require relatively few laser burns. Other treatments, such as those for proliferative retinopathies or large retinal tears, may require hundreds of pulses delivered in rapid succession. Your surgeon will work with you to minimize any discomfort during the procedure by modifying the laser settings, using eye drops, and occasionally using a numbing injection around the eye.

Because laser photocoagulation is a non-invasive procedure, patients do not routinely require any eye drops after treatment. If the eye feels irritated or dry after treatment, over-the-counter artificial tear drops may be used to sooth the eye. After extensive treatments, some patients experience a minor headache, which may be treated using over-the-counter medications such as acetaminophen or ibuprofen as needed. The vision is often blurred for several hours after laser treatment, and it is normal to experience colored hues in the vision during this time. Vision in the treated eye may not return to pre-treatment levels for one or two days in some cases.

Photodynamic therapy (PDT) is a type of laser treatment initially approved for use in the treatment of wet age-related macular degeneration (AMD). While the first line treatment for wet AMD now consists of medication injections directly into the eye, PDT is still sometimes used in combination with these therapies. PDT is also used in the treatment of central serous chorioretinopathy (CSCR), polypoidal choroidal vasculopathy (PCV), and choroidal hemangioma. PDT is a non-thermal or “cold” laser. Unlike the lasers used in retinal photocoagulation, which use thermal energy to create burns in the retina, PDT uses a laser to activate medication given intravenously. Verteporfin is a medication given through an IV. The medication travels throughout the blood stream into the choroid, which lies behind the retina. The choroid is where the abnormal blood vessels of wet AMD originate, and it is also the source of abnormal activity in other diseases such as CSCR, PCV and choroidal hemangioma. The PDT laser activates verteporfin in the region of abnormal blood vessels, thereby closing off the abnormal blood vessels and reducing the leakage of blood and fluid into the space between the retina and choroid.

Based on the characteristics of the IOL dislocation, there are several different approaches to repair. When the patient is experiencing symptoms, surgery becomes necessary. In the surgical procedure, the vitreous gel that fills the eye’s rear cavity is removed (vitrectomy) to prevent pulling on the retina while the IOL is being manipulated. There are 2 categories of repairing a dislocated IOL based on the individual IOL type and patient anatomy:

1. IOL rescue/reposition: The dislocated IOL is preserved and repositioned in a more stable location. The possibility of using the existing lens is based on many factors including the style and condition of the IOL.
2. IOL exchange: The IOL is removed and a new IOL is inserted. 

Potential complications of the procedure include retinal detachment, inflammation inside the eye, infection, increase eye pressure, bleeding and re-dislocation. Most patients have a good visual outcome following the corrective procedure.