Central serous chorioretinopathy, commonly referred to as CSC, is a condition in which fluid accumulates under the retina, causing changes in the perception of shapes and colors.
Central serous most often occurs in young and middle-aged adults. Vision loss can resolve on its own, but sometimes can recur or linger.
Retained Lens Fragments
As people age, the lens in the eye becomes opacified or cloudy, which produces a cataract. Cataract surgery aims to replace the cloudy lens to reverse vision loss caused by this process. Cataracts can also occur as a result of trauma and medical conditions, such as diabetes.
In most cases, cataract surgery is an uneventful procedure, leading to no complications. However, some individuals, sometimes due to an underlying propensity for a complication (i.e., previous trauma, advanced cataract), the cataract cannot be removed in its entirety, and fragments remain in the eye. Sometimes these fragments travel to the back of the eye, in the vitreous cavity, where they cannot be removed using routine cataract surgery instrumentation.
Diabetic retinopathy is a common condition that develops in patients with prolonged hyperglycemia, as can occur in diabetes mellitus. Screening exams are important to identify individuals at risk of vision loss from diabetic retinopathy.
What is diabetic retinopathy?
Elevated blood sugar leads to modification of proteins and other components inside of blood vessels. These modifications can be damaging to the eye’s circulation. When these tiny vessels are bathed in elevated blood sugar levels for many years, they become brittle, close off (capillary drop-out) or break (causing small hemorrhages). The leakage of blood, fluid and cholesterol from these fragile vessels can lead to blurry vision. When leakage occurs in the macula, this is called diabetic macular edema. When new blood vessels grow, this is called retinal neovascularization. Neovascularization can lead to bleeding in the vitreous cavity, which is called vitreous hemorrhage, and also lead to fibrotic tissue that contracts and detaches the retina (traction retinal detachment).
What causes diabetic retinopathy?
Hyperglycemia over the course of years as is encountered with diabetes mellitus. Hypertension can worsen diabetic retinopathy as well.
What are the symptoms of diabetic retinopathy?
This varies from no symptoms to severe loss of vision. Some will note blurry vision or central visual distortion (metamorphopsia). This can be due to macular edema, which describes swelling of the macula. Vitreous hemorrhage may present with floaters in one’s vision progressing to a near complete obscuration of vision. A retinal detachment caused by diabetes can present with poorly defined blurry vision with floaters, but symptoms vary depending on the age and severity of the detachment.
How is diabetic retinopathy diagnosed?
A dilated eye exam utilizing hand-held lenses, optical coherence tomography of the retina, fundus photography, and fluorescein angiography may be used in combination to identify and/or evaluate the condition. An ultrasound machine can be used to assess the positioning of the retina when a vitreous hemorrhage makes it impossible to directly visualize the retina.
What are the treatments for diabetic retinopathy?
Managing diabetes and hypertension is paramount to preventing retinopathy. Angiogenesis inhibitors are the first-line treatment for macular edema, but steroid injections and focal laser treatment are also utilized. Scatter laser treatment to retina with poor blood flow (ischemic retina) may be necessary to promote regression of neovascular tissue. Vitrectomy may be necessary to hasten recovery of vision after a vitreous hemorrhage, or to treat a retinal detachment.
Nerve impulses convey humans’ special senses. Without nerve impulses, humans are unable to feel, taste, smell, hear or see. These impulses depend on special proteins known as ion channels, that allow electrolytes like sodium, potassium, and chloride to pass across cell membranes. In single cell organisms, like algae, some of these ion channels are light-sensitive (light-gated ion channels); meaning, light can activate the ion channel, and subsequently affect a downstream cellular process (like cellular motility). These light-gated ion channels have been utilized extensively in the past two decades to study neural circuits. This technique is referred to as optogenetics. Earlier this week, researchers in Pittsburgh, Switzerland and France reported results of using optogenetics for the first time in humans. A microbial protein conferring light sensitivity onto retinal ganglion cells was expressed using viral-based gene therapy delivered with an intravitreal injection (an injection into the vitreous cavity of the eye). The protein expressed was a modified channelrhodopsin. Channelrhodopsins are what permit single cell organisms like algae to display phototaxis (i.e., their ability to move in response to light). This molecular trick bypassed degenerated light-sensing photoreceptor cells in a patient with retinitis pigmentosa, and allowed a patient to recover some limited sight with image-enhancing goggles.
With the exception of melanopsin-expressing retinal ganglion cells, retinal ganglion cells do not ordinarily detect light. Instead, retinal ganglion cells are normally conveying visual information coming from other cells in the retinal circuit–namely, the retinal bipolar cells. Bipolar cells convey electrical impulses from photoreceptor cells (the rods and cones). This circuit bypass means that with this technique, less well-defined information is being conveyed to the brain. Indeed, the researchers indicated that the patient spent several months learning to interpret what they were “seeing.” While more research and trials are needed, this adds to the growing list of strategies to recover lost vision in patients with acquired or inherited retinal degeneration.
Press release link:
https://www.nature.com/articles/d41586-021-01421-0
A patient who was initially doing well after a recent cataract surgery, experienced a sudden worsening of vision. Their eye became red, and they developed severe pain. The vision had worsened from 20/30 (two lines from 20/20) to counting fingers (only able to count fingers of the examiner presented one foot away from their face). I examined the patient, who had severe inflammation in the eye, and I performed an ultrasound of the eye, which showed dense inflammation in the vitreous cavity.
Fig. 1. Ultrasound image of the eye showing grainy white dense material consistent with infectious/inflammatory debris.
Normally, the vitreous cavity is clear, allowing light to pass through largely unimpeded to the retina. In this case, the vitreous inflammation was due to a severe infection following cataract surgery known as endophthalmitis. I discussed the diagnosis with the patient, and recommended treatment in the office, where I would first anesthetize the eye, then remove a sample of fluid from the vitreous cavity to send to a lab for bacterial cultures. Then, I would inject two broad spectrum antibiotics in the eye that would treat a wide range of potential bacteria. This was uneventful, and the patient did well with the procedure. The infection was controlled with this single treatment. One month later, however, the patient developed a retinal detachment. Cataract surgery, infection/inflammation, and removing vitreous for the culture can all cause the vitreous to move, potentially pulling on abnormal attachments between the vitreous gel and the retina. A tear in the retina can lead to a detachment. We scheduled surgery during which I placed a silicone band around the eye, flattened the retina, and performed laser to tack the retina down. I also placed silicone oil in the eye to help hold the retina in place, and explained the need to remove the oil after several months, after we confirmed that the retina was well positioned for a prolonged period.
Fig 2. Cross-sectional view of the macula showing silicone oil reflection on the retinal surface (white bright line), and a flattened retina without a detachment.
The vision is typically blurry with silicone oil in the eye, but still better than it would have been had the detachment worsened. Several months later during follow-up, while the retina looked in good position, the patient started to develop a macular pucker, a thin translucent membrane on the surface of the macula that can blur and distort vision.
Fig 3. Cross-sectional view of the macula showing a membrane on the retinal surface and cystic changes near the fovea related to the membrane.
Since we had planned on removing the oil around this time with an additional surgery, we discussed how this would be an appropriate time to remove the membrane at the same time the oil was being removed. The patient tolerated the surgery well, the oil and membrane were removed, and they recovered 20/25 vision in this eye that had a severe infection, then a retinal detachment, then a macular pucker.
Fig. 4. Cross sectional view of the macula after oil removal and after removing the macular pucker/membrane on the surface of the retina.
Some bacterial infections are more virulent. Even with the same persistence and expedient care, the same outcome cannot be replicated. Certain bacteria, for example, can spew bacterial toxins that destroy the retina, and other infections, such as those caused by viruses, can obliterate the blood flow to the retina, causing irreversible damage to it. As much as doctors try to provide a prognosis, sometimes both the provider and patient can be pleasantly surprised by the benefits of persistence.
Much like a cast immobilizes a limb and helps it heal, during retinal surgery, your surgeon may use an analogous immobilization/healing aid. Surgery on the retina that requires removal of the vitreous gel (called a vitrectomy) sometimes requires placing a vitreous substitute that exerts a force on the retina to flatten the retina. While the vitreous can be replaced with saline in cases where no such force is necessary, many retinal conditions such as retinal detachments and macular holes, require placing a gas mixture or oil in the eye. This gas or oil makes the vision blurry, because light does not pass through the gas and oil the same way it does through vitreous gel or saline. A retina specialist has special lenses that aid in focusing an image of their patient’s retina (on the specialist’s retina!) to assess the retina’s appearance and positioning. Much like a cast for a broken bone prevents one from using a limb, these vitreous substitutes also limit function of the eye. It does not hurt the eye to try to use it during this period. In fact, it is a good idea to keep the eye uncovered, to monitor the vision and ensure the vision is not worsening in any way. Worsening of vision during the post-operative period can suggest bleeding, recurrent detachment, or infection. So, it is important for patients to recognize their role in self-monitoring after a retina surgery, even with the limited vision they possess during this early phase after surgery. Positioning one’s head in different positions exerts a force on correspondingly different parts of the retina. Positioning one’s head with their face down, helps the gas mixture or oil in the eye press against the macula, the central part of the retina responsible for central vision. Sometimes, a detachment in the retina may involve a part of the retina that would be aided by positioning on one’s side, such that the vitreous substitute presses against the area that was detached prior to surgery. The substitute buys time for a laser or cryo scar to develop at the area that caused the detachment (often a tear or hole in the retina). Once a treatment scar develops, the chance of the retina detaching again decreases significantly. This usually takes about a week. If gas is placed in the eye, one should avoid going to high altitudes abruptly, such as in an airplane, or driving to high altitude without frequent enough stops. Gas mixtures placed in the eye expand under the lower atmospheric pressures, causing a sharp spike in eye pressure that can lead to blindness. Also, if a gas mixture is placed in the eye, one cannot undergo anesthesia that requires gas until the gas mixture dissolves from the eye. This usually happens 1-2 months after retinal surgery. If not, the gas anesthetic can travel to the eye, and cause an eye pressure spike, which can lead to blindness.
Central vision is critical for many daily activities ranging from reading to driving. Clear vision requires light be focused on a transparent tissue in the back of the eye called the retina. The retina has different regions, but the portion of the retina responsible for our central vision is known as the macula, and within the macula, the finest acuity is provided by a specialized portion known as the fovea. The fovea is where light is focused in our eyes to allow us to see fine details in the world around us. Diseases involving the fovea affect our ability to perform our day to day activities. One such condition is macular hole formation. Macular holes develop when the clear gel inside the eye (the vitreous) tugs abnormally on the retina. This tugging creates a hole. In rare cases, macular holes can develop after injury to the eye. Most of the time, it occurs because some people are born with abnormal attachments between the vitreous and the retina. As we age, the vitreous naturally liquefies and pulls away from the retina. In people born with abnormal attachments to the fovea, the gel does not peel away easily from the fovea, so when it pulls away it leaves a hole. Unfortunately, there is no way to predict who will develop a macular hole. When a hole develops, the central vision becomes blurry. If one does not check vision in each eye individually, the effects of a macular hole in one eye can go unnoticed for weeks or even months. Without intervention, the hole can enlarge, and more central vision can be affected. Most of the time, this occurs in only one eye, but 1 out of 5 patients can have this occur in both eyes.
Image showing a cross-section view of the macular hole.
Image showing a cross-sectional view of the other eye without the macular hole.
Fortunately, a treatment is available. Surgery is performed to remove the vitreous gel, peel a membrane from the surface of the retina, and replace the fluid in the eye with a gas mixture. This along with head positioning face down, for up to a week, helps press the edges of the macular hole closed. Face down positioning can be a challenging task. As the gas bubble dissolves and is replaced with fluid the eye produces, the vision improves. The improvement in vision can take weeks, even months. Surgery can improve vision, but a macular hole may have lasting effects on one’s sight. Some retina surgeons place more gas in the eye to reduce the need for having patients position face down, but placing more gas in the eye has its own risks, including cataract formation, and increasing the likelihood that the pressure in the eye becomes high.
Macular holes should not be confused with macular degeneration, a condition which affects the macula as well, but arises from deposits of proteins and other molecules under the retina as one ages. Blurry vision in one or both eyes that develops rapidly or slowly requires prompt evaluation by an optometrist or ophthalmologist. Putting this off can affect one’s vision permanently, and decrease your chance of attaining your best vision. If you are found to have a macular hole, you should be referred to a retina specialist to discuss treatment options.
Age-related macular degeneration (AMD) is a common cause of vision loss in people 50 years and older. The single-most important factor in this condition is age, and the longer we live, the more common this condition becomes. A lot of progress has been made in the last ten years in the treatment of AMD with more innovative alternatives in trial today that will decrease the burden of treatment and increase its effectiveness.
Many people with dry macular degeneration do well and have little to no visual symptoms. Such patients require observation alone, as they only possess early features of the condition known as drusen, which are a deposition of material (protein and lipids) under the retina. If these drusen are large enough or numerous enough, an over-the-counter vitamin containing zinc, copper, lutein, xeaxanthin, vitamin C and vitamin E has been found to reduce the risk of progression to more advanced stages of macular degeneration by 25%.
Image showing hallmark deposits of drusen in a patient with dry macular degeneration.
Patients can decrease the risk of progressing to advanced stages of macular degeneration by not smoking, eating a lot of vegetables, and monitoring vision at home with a grid or graph paper known as an Amsler grid. The Amsler grid is sensitive at picking up sudden changes that arise when patients develop the wet type of macular degeneration, where there is bleeding or leakage of fluid under the retina. Untreated, this bleeding and leakage can cause scarring under the retina that can lead to a permanent blind spot in the center of one’s vision. Treated with regular injections, patients visual outcome with wet macular degeneration is oftentimes preserved, if not, improved.
While sight saving, frequent injections of medicine to reduce leakage and bleeding from wet macular degeneration are needed. The three medicines (Avastin, Eylea, Lucentis) currently in use, only last in the eye 4-8 weeks.
Images showing an area of hemorrhage and scarring from wet macular degeneration in color photos and special fluorescein angiography images.
Macular degeneration can lead to a blind spot in one’s vision even in the absence of bleeding or leakage from abnormal blood vessels. This can result from a loss of the light sensing cells (photoreceptors) and their supporting tissue (retinal pigment epithelium). This tissue loss is referred to as geographic atrophy. Injections blocking a very specific component of one’s immune system, known as the complement system, are being evaluated to reduce this process from occurring. Several factors have been or are being tested along these lines, but nothing has shown success to date. However, it is still too soon to rule these avenues of research out.
Here are the most important things macular degeneration patients can do for themselves:
If recommended by your eye care provider, take the AREDs vitamin supplement which may also help reduce the rate of progression of macular degeneration.
Note: The above images were copied from my article on age-related related macular degeneration that can be found on eyewiki. https://eyewiki.aao.org/Age-related_macular_degeneration
Diabetes is a condition that can affect vision. This has become a health epidemic due to the increasing number of people with this disease. The result of diabetic changes in the eye do not always cause a noticeable change in vision. Diabetes can lead to anything from a mild blur in one’s vision to severe loss of vision. Remarkably, one cannot rely on their vision as an accurate predictor of one’s disease severity, as blindness can quickly develop in someone with previously normal vision. The fact that symptoms can be so unreliable in diabetic eye disease is the reason it is so important everyone with diabetes be evaluated by an eye doctor at regular intervals. Fortunately, many of the changes that occur in diabetes can be reversed, and as treatment options continue to expand and improve; the extent to which vision loss is permanent or is irreversible from diabetes is decreasing. The instances in which diabetes changes are not reversible can be due to interruption of blood flow to the retina or optic nerve. Since the retina and optic nerve are neural tissue, they do not tolerate lasting interruptions in blood flow.
We perceive our world when our brain processes and interprets images that are detected by the retina and transmitted to our brain via the optic nerve. Damage to any of these three components (retina, optic nerve, brain) leads to a blurred image of the world around us. The optical properties of the eye responsible for focusing light on the retina to form a clear image can also be affected by diabetes. So, even a deficiency of tears that bathe the front of the eye, can also blur vision. Unimpeded light transmission is absolutely essential to excellent vision. To permit light transmission, the eyes must be made of clear, transparent tissues. Light must pass through tears, cornea, aqueous fluid, lens, vitreous, and retina before it is detected. All of these components of the eye are transparent in their normal form. Loss of their transparency leads to vision loss, and is the underlying cause of many different diseases of the eye.
The main culprit of disease progression in diabetes is sustained elevation of blood sugar. Elevated blood sugar leads to modification of proteins and other components inside of blood vessels. These modifications can be damaging to the eye’s circulation. This occurs because when blood sugar levels are high, sugar molecules get tacked on to other components of blood and blood vessel lining. This process creates advanced glycation end-products, where glucose, or sugar, becomes attached to other molecules in the body. This is so important in diabetes that physicians exploit this to monitor one’s diabetes control, by measuring the percentage of a certain protein in the blood that has sugar attached to it (hemoglobin A1c). The higher the percentage, the higher the blood sugar levels have been, and vice versa. One can explain diabetic retinal disease by drawing an analogy to what happens when sugar, fat, and protein react together. The browning of food represents a chemical reaction known as the Maillard reaction, which describes the reaction of amino acids (which comprise proteins) to sugars. The Crème Brule phenomenon that creates a brittle sugar layer on top of dessert, and the browning process that results in a pie crust developing a golden appearance is similar to what happens within small vessels in the retina. When these tiny vessels are bathed in elevated blood sugar levels for many years, they become brittle, close off (capillary drop-out) or break (causing small hemorrhages). The leakage of blood, fluid and cholesterol from these fragile vessels can lead to blurry vision. The photo below depicts a view of some of the changes associated with severe retinopathy. The two photos were taken one week apart, before and after a treatment involving an injection of medicine in the eye that causes a prompt regression of abnormal vessels (arrowheads in the two photos).
Before treatment
One week after one injection of Bevacizumab
The effect of advanced glycation end-products in diabetes can be very detrimental. The importance of transparent tissues to vision cannot be stressed enough. Blood inside the eye abolishes the eye’s transparency, and if severe enough, may require a surgery called a vitrectomy surgery to remove the blood. Earlier treatments target the leakage that occurs from tiny blood vessels. In a retina that is extremely deprived of blood flow, laser surgery may be necessary to decrease the propensity of this retina to cause bleeding. Ultimately, like so many things in medicine, early detection and routine care can save a lot of grief and sight down the road.