*Please note that this information is for illustrative purposes only, providing a general overview on the topics listed. For any specific questions or concerns regarding your condition, please contact our office so that you can consult with the appropriate person or department to address your needs.
DIABETIC MACULAR EDEMA (DME)
Overview
Diabetes Mellitus is a group of diseases characterized by high blood glucose levels. Diabetes results from defects in the body's ability to produce and/or use insulin.
• Type 1 diabetes is usually diagnosed in children and young adults, and was previously known as juvenile diabetes. In type 1 diabetes, the body does not produce insulin. 5% of people with diabetes have this form of the disease.
• In Type 2 diabetes, either the body does not produce enough insulin or the cells ignore the insulin. This is the most common form of diabetes.
• A form of diabetes that occurs in pregnant women. Typically begins with high blood sugars in the second trimester and continues until delivery. Often resolves and the blood sugars normalize after pregnancy.
Pathogenesis (Origin or Development of a Disease)
Diabetic Macular Edema (DME) and Diabetic Retinopathy (DR) is caused by damage to blood vessels in the eye from elevated blood sugar. Prolonged hyperglycemia is the major etiologic agent in all of the microvascular complications of diabetes, including diabetic retinopathy. The cellular mechanisms through which hyperglycemia acts currently remain unclear.
Proposed mechanisms for the development of DME & DR include:
• Hyperglycemia (high blood sugars) may alter the expression of one or more genes, leading to increased (or decreased) amounts of certain gene products that can alter cellular functions.
• Glycosylated proteins (proteins altered by sugar) can undergo a series of reactions, leading to considerable alteration of proteins.
• Chronic hyperglycemia may produce oxidative stress in cells, leading to the formation of an excess of "toxic end products of oxidation" including peroxides, superoxides, nitric oxide, and oxygen free radicals.
• Chronic hypoxia (low oxygen levels in tissues) causes cells in the eye to produce elevated levels of Vascular Endothelial Growth Factor (VEGF)
• VEGF is released into the vitreous cavity (the center cavity of the eye) and promotes new blood vessel growth (NVD & NVE) on the surface of the retina and increases vascular permeability (leakage from retinal vessels) causing DME
• Hyperglycemia causes new blood vessels to grow on the surface the optic nerve & retina (NVD & NVE) which can bleed causing Vitreous Hemorrhage (VH) which is bleeding inside the eye
• Hyperglycemia also causes normal blood vessels to become deformed and develop microaneursyms (small blister-like out-pouchings from capillaries) in the macula (center of the retina where your fine vision comes from) and can leak causing Diabetic Macular Edema (DME). DME causes swelling of the macula which can cause decreased or blurry vision.
Many of the complications of diabetic retinopathy can be prevented or delayed by controlling blood glucose, blood pressure control, consistent medical monitoring by internists, endocrinologists and subspecialists.
Epidemiology
Diabetic retinopathy is a leading cause of new cases of blindness in people aged 20 to 74 years in the USA
The total number of people with diabetes is projected to rise from 285 million in 2010 to 439 million in 2030.
Diabetic retinopathy is responsible for 1.8 million of the 37 million cases of blindness throughout the world .
Diabetic Retinopathy is the 5th leading cause of blindness worldwide behind only cataracts, glaucoma, macular degeneration & corneal opacities.
Diabetic retinopathy (DR) is the leading cause of blindness in people of working age in industrialized countries.
The best predictor of diabetic retinopathy is the duration of the disease.
• After 10 years of diabetes, nearly 70% of patients with type 1 diabetes and 50% of patients with type 2 diabetes have diabetic retinopathy.
• After 20 years of diabetes, nearly 99% of patients with type 1 diabetes and 80% with type 2 have some degree of diabetic retinopathy.
• 33% of all patients with diabetes have signs of diabetic retinopathy.
Symptoms
Diabetic Macular Edema & Diabetic retinopathy can be asymptomatic in early stages but as the disease progresses symptoms may include:
• Sudden or gradual onset of blurred vision
• Decreased central vision
• Fluctuating vision
• Distorted vision
• Dark areas in the vision
• Poor night vision
• Impaired color vision
• Partial or total loss of vision
• Sudden onset of red or black floaters
Diagnostic Testing
Optical Coherence Tomography (OCT) is used to evaluate the macular anatomy and to rule out Diabetic Macular Edema in patients (see sample OCT).
Fundus Photography (FP) is used to document the level of maculopathy and retinopathy and for comparision to evaluate progression at future exams.
Fluorescein Angiography (FA) is used to evaluate the macular and peripheral circulation. Many patients with DME have a staining of microaneuryms, leakage of fluorescein from these microaneurysms and loss of normal capillary circulation (see Macular Ischemia) on the FA.
B-Scan Ultrasound (B-Scan) is used to evaluate the retina in patients with corneal opacities, cataracts, retinal hemorrhage or any other condition that makes visualization of the retina difficult with indirect ophthalmoscopy.
Classification
Diabetic Macular Edema is generally classified into three (3) stages:
• Cystic Diabetic Macular Edema (CME or DME)
• Clinically Significant Macular Edema (CSME)
• Ischemic Diabetic Maculopathy (IDM)
Findings
Cystic Diabetic Macular Edema (CME or DME) is defined by:
• the presence of any intraretinal cyst surrounding the fovea (center of the macula) on OCT
• moderate to severe CME or DME may be associated with subfoveal fluid (fluid accumulating in the space below the fovea)
Clinically Significant Macular Edema (CSME) is defined by:
• the presence of 500um of edema within 500um of the fovea
• the presence of hard exudates associated with edema within 500um of the fovea
• the presence of 1500um of edema within 1500um of the fovea
Ischemic Diabetic Maculopathy (IDM) is defined by:
• the loss or dropout of normal capillaries around the fovea (center of the macula)
• the loss of normal blood vessels in the center of the macula causes a deficiency or lack of oxygen at the fovea
• the lack of oxygen at the fovea leads to the death of the cone and rod cells (retinal cells that process and send formed images to the brain)
• the death of the cone cells in the fovea leads to a permanent loss of central vision
Medical Work-Up
A baseline eye exam with dilated fundoscopic exam (DFE) is recommended in Type 1 diabetics 5 years after onset, then annually thereafter. In Type 2 diabetics the first eye exam and DFE is recommended upon diagnosis and then annually.
The treatment of BDR includes a complete medical work-up to evaluate the adequacy of blood sugar control. This includes fasting blood glucose and a Hemoglobin A1C that should be repeated every three months by your primary care physician.
Your primary care physician and/or endocrinologist will prescribe a combination of diet, exercise, lifestyle changes and medication for the control of your blood sugar.
Ideally we would like to see your Hemoglobin A1C at a level of 6.5 or less to prevent worsening and progression of diabetic retinopathy.
Medical Treatment
Avastin, Lucentis & Eylea are all Anti-Vascular Endothelial Growth Factor (Anti-VEGF) medications approved for the treatment of Cystic Diabetic Macular Edema (DME/CME). This class of medication is typically the first line treatment for DME.
Focal Laser Photocoagulation (focal) is used to treat CSME. It may be used in combination with Anti-VEGF agents when DME & CSME are present together.
Ozurdex is a long acting steroid implant that is injected into the vitreous cavity to treat DME. Ozurdex therapy typically has a treatment effect for 3-4 months and may need to be repeated if DME returns. Ozurdex is typically used as a second line treatment for DME because of associated risks of cataract progression (65%), glaucoma (40%), and the need for glaucoma surgery (0.3%) to control intraocular pressure.
Iluven is a long acting steroid implant that is injected into the vitreous cavity to treat DME. Iluven therapy typically has a treatment effect for up to 3 years or more. Iluven is typically used as a second line treatment for DME because of associated risks of cataract progression (65%), glaucoma (40%), and the need for glaucoma surgery (5%) to control intraocular pressure.
Triessence (Triamcinolone) is a long acting steroid implant that is injected into the vitreous cavity to treat DME. Triessence therapy typically has a treatment effect for up to 3-6 months. Triessence is typically used as a second line treatment for DME because of associated risks of cataract progression (65%), glaucoma (40%), and the need for glaucoma surgery (5%) to control intraocular pressure. The generic version of Triamcinolone (with preservative) is associated with an additional risk of sterile endophthalmitis.
Surgical Treatment
Vitrectomy surgery with physical separation of the vitreomacular adehesions and removal of epiretinal membranes is the gold standard for treatment of DME that has not been responsive to medical treatment. The procedure is performed under local anesthesia, in either one of our outpatient surgical centers or local hospitals (see link to our surgical centers and hospitals).
The surgery is performed through three 25-gauge ports (about the width of a wire paper clip). The surgery is performed by placing an infusion canula, a light pipe & a vitrectomy cutter through each of the 3 ports. The infusion cannula keeps a constant pressure in the eye while the vitrectomy cutter removes the vitreous gel. As the gel is removed, balance salt solution replaces the gel in the vitreous cavity. The gel that is adherent to the retina is gently lifted off the optic nerve and macula to separate the vitreomacular adhesions and relieve any vitreomacular traction if present. Any membranes on the surface of the retina are then peeled off. The light pipe is used by the surgeon to see the vitreous and membranes as they are being removed inside the eye. After enough vitreous and membranes have been removed the surgeon removes the surgical instruments and trocars (3 ports) and the operation is complete. No sutures are typically needed in up to 95% of cases. Antibiotic ointment and a patch are placed over the eye for one night and removed the following day by the technician in our office.
Vision is usually blurry the first day after surgery but typically improves to at or better than your pre-operative vision about a week after surgery. Continued visual improvement often occurs over the first 6-8 weeks but some patients experience improvement even up to 6 months after surgery.
Patients typically experience little to no pain following surgery. Surface or external irritation (feeling of having something in your eye) is common. A deeper or more intense eye pain in not typical and may signal a more serious issue such as high intraocular pressure, serous or hemorrhagic choroidals or infection. A deeper or more intense eye pain needs to be reported to you physician immediately.
Post-operative restrictions are for 4 weeks after surgery and include:
- Bending at the waist putting your head below your waist (such as bending to tie your shoes). Bending at the knees with your head up is allowed.
- Heavy lifting greater than 15-20 lbs.
- Strenuous activity (including lifting weights, running, yoga, pilates, aerobics, yard work, snow shoveling, laundry, housecleaning, sexual intercourse) is not recommended as it will increase your risk of developing a retina tear or detachment. Walking, for exercise, after surgery is allowed (in patients who do not require post-operative head down position).
- Showering is allowed immediately after surgery but be sure to keep your eyes closed to prevent shower water from entering your eye.
- Swimming after surgery should be avoided for 4 weeks. You should not go under water for the first 4 weeks after surgery.
- Working restrictions is job dependent. Patients with desk jobs or who perform light stationary office work may sometimes resume work 2-3 days after surgery. Patients with jobs that require heavy lifting or strenuous activity may be required to be out of work for 2-4 weeks. Ask your physician about your individual work restrictions. We will be happy to provide you with a doctor’s note for your work and/or complete your temporary disability paperwork.
Risks and Benefits
The benefit of vitrectomy surgery is the potential for improved vision, reduced distortion of straight lines (when present pre-operatively), and reduction or elimination of floaters.
The risks of vitrectomy surgery include but are not limited to:
- More rapid cataract progression (in up to 20% of patients the lens may harden or become cloudy more rapidly after the vitreous gel is removed) that may require cataract surgery 1-2 years after the vitrectomy procedure.
- Vitreous (less than 5%) or choroidal (less than 1%) hemorrhage
- Retinal break or tear (less than 5%) or Retinal Detachment (less than 1%)
- Infection/Endophthalmitis (less than 1 in 500 patients)
- Permanent loss of vision/Blindness (approx. 1 in 10,000)
*Please note that this information is for illustrative purposes only, providing a general overview on the topics listed. For any specific questions or concerns regarding your condition, please contact our office so that you can consult with the appropriate person or department to address your needs.