Retinopathy PDF (2024-2025)

Block 2.1 (2024-2025) Retinopathy Done by : Aisha Alsalman Abdulhamid Alabbad Retinopathy DR. ABDULAZIZ AL TAISAN ASSISTANT PROFESSOR, KING FAISAL UNIVERSITY CONSULTANT, VITREORETINAL SURGERY Email: [email protected] topics retinopathy. Hyp...

Block 2.1 (2024-2025) Retinopathy Done by : Aisha Alsalman Abdulhamid Alabbad Retinopathy DR. ABDULAZIZ AL TAISAN ASSISTANT PROFESSOR, KING FAISAL UNIVERSITY CONSULTANT, VITREORETINAL SURGERY Email: [email protected] topics retinopathy. Hypertensive retinopathy. Retinal detachment. Age related macular degeneration.  Diabetic Retinopathy Diabetic retinopathy is an eye condition that affects people with diabetes. It occurs when high blood sugar levels damage the blood vessels in the retina, the light- One of the main causes of acquired blindness sensitive tissue at the back of the eye. In the retina clinic, almost 90% of patients have diabetic Risk Factors: retinopathy, whether for screening or due to complications. This highlights the significance of the Duration of DM The longer the duration of diabetes, the greater the possibility of developing the disease. disease. The rest 10% for retinal disease Poor DM control Pregnancy Other systemic diseases such as: dyslipidemia or HTN HTN (hypertension) Ischemia VEGF release neovascularization and edema. Pathophysiology in one line: - Ischemia can cause microangiopathy in the retina, When there is ischemia(lack of oxygen in retinal cells) the ischemic cells will release VEGF( vascular manifesting as diabetic retinopathy. endothelial growth factor) that’s leading to promote two things: 1- Growth of new blood vessels to supply more blood - In the kidneys, it results in diabetic nephropathy. 2-Increase permeability of pre- existing blood vessels leading to leakage blood due to this we have: - In the peripheral nervous system, it manifests as 1- neovascularization (abnormal progression of new blood vessels) diabetic neuropathy. 2- Edema (because of the leakage of blood vessels )  Pathogenesis of diabetic retinopathy Vascular microangiopathy Micro-aneurysms. 1) In the diabetic patient elevated blood sugar levels can lead to microvascular damage so at the level of capillary there will be leakage or closure of capillaries leading to ischemia and now the retinal cell will release VEGF 2) there will be formation of Micro-aneurysum How do we have microaneurysms? When we have weakneing in the capillary wall or arterial wall that will leads to outpouching and formation of microaneurysms  Consequences of chronic leakage Due to release VEGF we have two main consequences: 1-The first consequence is increased leakage from the blood vessels, which leads to the accumulation of fluids and exudatio  Consequences of retinal ischemia Venous beading Cotton-wool spots 2- The second consequence is the formation of new blood vessels or (neovascularization ) -So there will be neovascularization in the optic disc (NVDs) -Neovascularization in elswhere on retina (NVEs) -And neovascularization in iris we call it Rubeosis iridisor or (NVIs ) NVDs and NVEs  Two main categories: Obviously, the patient will initially develop non-proliferative diabetic retinopathy, which may then progress to Classification : proliferative diabetic retinopathy. 1 Non-proliferative (background): mild, moderate, severe. 2 Proliferative There is a separate entity called diabetic macular edema, which can Diabetic macular edema. present with or without non-proliferative diabetic retinopathy (NPDR) or proliferative diabetic retinopathy (PDR) or not happen at all Advanced: TRD, VH, NVG It’s possible to have a patient with proliferative diabetic retinopathy (PDR) who also has non-proliferative diabetic retinopathy (NPDR) in the following forms: - With macular edema - Without macular edema TRD: Tractional Retinal Detachment VH: Vitreous Hemorrhage Macular edema can occur in both NPDR and PDR. NVG: NeoVascular Glaucoma NDPR: non proliferative diabetic retinopathy PDR: proliferative diaper retinopathy  Non-proliferative: Micro-aneurysms. Bulging form It difficult to see it by a small image We need high magnification and a detailed examination to see this outpouching and small dilation of the arterioles Intraretinal hemorrhages Haemorrhage within the layer of retina hard exudates Venous beading Like this: Venous beading : constriction over all course of retinal vein (‫)مثل السبحة‬ Soft exudates (Cotton-wool spots ) There are two types of exudate (the doctor said it is not important to differentiate between them) -Hard exudates appear as small, bright , yellowish or white in color deposits in the retina They have a "hard" or well- defined margins -Soft exudates, also known as cotton-wool spots, have a fluffy, cotton-like appearance yelloish deposite in retina not very obvious in color, they large and diffuse margins  Proliferative: Affects 5-10% of diabetics There are signs of NPDR+ Neovascularization. How to Differentiate Between Neovascularization and Normal Blood Vessels: NVDs:neovascularization at the disc NVEs: - Normal Blood Vessels: These vessels are almost neovascularization elsewhere. VH, TRD. straight in their course, and each vessel branches into two distinct branches. If the patient is not treated, he will - Neovascularization:This appears web-like, making it progress to a more advanced stage. difficult to determine the origin of the vessels. The branching is irregular, and the vessels are very fragile and Normally: If you see a one normal blood vessel such as an arteriole, you will see that it divides into two prone to rupture, which can cause vitreous hemorrhage. main 1- branches. Also the new branches going to branch into two other main branches and so on. So the branching occurs in a predictable, symmetric, and ordered manner. 2- Normal retinal vessels have smooth and regular appearances. while in PDR: 1-You can see that the vessels can go anywhere and branch, they don't respect bifurcation. These new vessels often have a disorganized and irregular branching pattern. 2- They appear as fine, delicate networks of vessels. So a single vessel can give us a C fan shape. VH: Vitreous Hemorrhage TRD:Tractional retinal detachment  Advanced PDR: hemorrhage TRD: tractional retinal detachment. Vitreous hemorrhage. Vitreous hemorrhage: the new blood vessels has a week wall,therefor there will be bleeding causing collection of blood in vitreous region and you can’t see details NVG: neovascular glaucoma  Pulling the retina away Optic disc Rubeosis iridis =neovascularization There is neovascularization over the iris causing increasing the intraocular pressure (IOC) we call it neovascular glaucoma. Fibrous tissue There is abnormal fibrous tissue in the retina extending upward and downward, causing tractional retinal detachment. Abnormal large vessels are present over the iris and the angle of the eye. Non-Proliferative Diabetic Retinopathy (NPDR) and Proliferative Diabetic Retinopathy (PDR) are two stages of diabetic retinopathy, each with distinct signs: Signs of NPDR (Early Stage): 1. Microaneurysms: Tiny bulges in the blood vessels of the retina, which may leak fluid or blood. 2. Retinal Hemorrhages: Small spots of blood on the retina. 3. Hard Exudates: Deposits of cholesterol or other lipids leaking from blood vessels. 4. Macular Edema: Swelling in the macula (central part of the retina), leading to blurred vision. 5. Cotton Wool Spots: White, fluffy patches on the retina, indicating nerve fiber damage. 6. Mild Vision Changes: Blurring or difficulty with focus. Signs of PDR (Advanced Stage): 1. Neovascularization: Growth of abnormal new blood vessels on the retina or optic nerve. 2. Vitreous Hemorrhage: Bleeding into the gel-like substance (vitreous) inside the eye, which can cause dark spots or floaters. 3. Retinal Detachment: Scar tissue from neovascularization can pull the retina away from the back of the eye, leading to vision loss. 4. Severe Vision Loss: Due to retinal damage or complications like bleeding and detachment.  Macular edema Investigation of macular edema : Macular edema happens when fluid builds up in the macula, causing swelling. We can perform an Investigation with a device called optical This can distort vision, making things look blurry and colors look washed out. coherence tomography (OCT) to analyze retinal layer Macula Exudate Vitreous Fluid filled cyst Retinal pigmented epithelium Sclera  Treatment: If you have a patient with non-proliferative diabetic DM control. retinopathy and no macular edema, there is no need for Control other systemic diseases. treatment. Just focus on controlling diabetes mellitus (DM). PDR: panretinal photo coagulation If neovascularization is present in the retina, you need to perform laser treatment on the periphery of the retina to destroy the ischemic cells and reduce VEGF release, which will decrease edema. This is an aggressive treatment, as the patient may experience peripheral visual defects; If you have proliferative diabetic retinopathy, however, this is acceptable since the main goal is to preserve central vision and visual what do we do? acuity. Peripheral vision is not the primary concern. - First, ischemic retina leads to the release of VEGF, resulting in neovascularization. DME: antiVEGF. Can I eliminate neovascularization directly? No, so what do we do? In this picture, the We cannot perform laser treatment on patients with diabetic macular whitish spots in the periphery are laser scars created with a laser machine. By burning the edema (DME) because it can cause scarring in the macula, leading to central peripheral retina, which is ischemic, we reduce scotoma. Instead, the treatment is intraocular anti-VEGF injections. the ischemic areas. This will lower the level of VEGF, thereby decreasing the neovascularization. As an advantage, the patient will not have defects in the peripheral visual field. However, the disadvantage is that the effect of anti-VEGF is temporary, and after 2-3 months, complications may arise. This is why we administer anti-VEGF injections monthly until the edema resolves. Once the edema is gone, we can either stop the treatment or extend the interval to every 2-3 months, depending on the patient's response. VH: consider PPV “pars plana vitrectomy”. In Summary: Surgery - NPDR: No treatment needed. TRD: PPV - PDR:Treat with laser therapy. - Macular Edema:Treat with injections (anti-VEGF). VH: Vitreous Hemorrhage - Vitreous Hemorrhage (VH) or Tractional Retinal Detachment TRD:Tractional retinal detachment (TRD): Surgical intervention required.  Don’t panic Student's and doctor's questions : Q1)When should we start screening patients diagnosed with diabetes mellitus (DM)? - For Type 1 diabetes (DM1), screening should begin after 5 years of diagnosis. This is because Type 1 diabetes typically has an acute onset, and we don't expect the effects on the retina to manifest immediately. - For Type 2 diabetes (DM2), screening should occur at the time of diagnosis. This is important because patients might have had the disease for several years without being aware of it, which could already lead to retinal changes. Q2/Can we give anti-VEGF in PDR? Yes, we can. However, if you have a patient with proliferative diabetic retinopathy (PDR) and you treat them with laser therapy for one or two sessions, the vessels may continue to progress. This treatment often requires lifelong management. The challenge with laser treatment is that it burns the retina, destroying living cells. Since the treatment is typically done in the periphery, the patient may experience peripheral visual field defects. As a result, they might say: (‫ في الليل ما أشوف زين‬،‫)لما أشوف صرت أحس فيه ظالم حولي‬ Q3/ Can we give injections for PDR? Yes, but they must be administered frequently—every month or every two to three months. This means the patient might need ongoing injections. The problem arises if we consider a patient who is 65 years old, has a heart condition, mobility issues, and is already dealing with vision problems. You may not be sure if this patient will come in for their scheduled injections. This situation was particularly evident during the COVID-19 pandemic, when many clinics were closed for an extended period. After reopening, patients who had been controlled with injections for PDR began to experience tractional retinal detachment (TRD) and serious complications, which sometimes couldn't be resolved even with surgery.  Hypertensive retinopathy Arterial changes in hypertension are primarily caused by vasospasm. Pathogenesis: High BP leads to breakdown of capillaries; cotton-wool spots, retinal edema, papilledema. Asymptomatic in early stages Symptoms: only in advanced stages.  Staging: Asymptomatic Stage I: Arterioralconstriction. Stage II: Severe arteriolar constriction, arteriovenous nicking. Stage III: retinal hemorrhages, hard exudates, cotton-wool spots. Decrease vision Stage IV: Papilledema. However, in stage 4, the patient will not come to your clinic saying, "I have decreased vision." in this stage the patient could be in the ICU (Intensive care unit) Or OR( operating room )due to a stroke, or brain hemorrhage, or admitted to the ICU for complications related to hypertension.  If you see it, you might think the fundus of the retina appears normal. However, if you compare this picture to that of the patient before they developed hypertension, you may notice that the arterioles are larger. Stage I What do we see in Stage 1? In Stage 1, we observe arteriolar narrowing. Normally, the arteriole-to-venule size ratio is 2:3, meaning the arteriole is two-thirds the size of the venule.  obscuration of the vein at A/V crossing in 2nd stage the arteriol crossing the vein and compressing it. we call it AV nicking  Stage II As you know, the ‫فيبين كأنه مقطوع‬ arterioles experience high blood pressure, and when they cross the venules, this can lead to narrowing or constriction of the venules.  Stage III The patient will experience exudates and hemorrhages and have form of macular edema. However, the optic disc remains intact. You can see the vessels of the optic disc very clearly, and the edges of the optic disc are well-defined.  Stage IV you can’t see disk edge and there are exudates in the macula. patients in this stage mostly in the ICU  There is no ophthalmic treatment for hypertensive retinopathy also there is no screening for hypertensive retinopathy because if there is arteriolar constriction or AV nicking they can’t do anything Treatment: Treat HTN. Atreiolar changes are irreversible. If you treat the hypertension, the hemorrhages and exudates will resolve. However, the arteriolar changes may remain permanently. Do We need to screen? No, because there's no treatment so there is no benifete from screening Diabetic retinopathy we do screen to treat BUT! Here No let's supose that a patient came & found that he have stage ll So there's no benifite of screening Retinal Detachment The retina consists of 10 layers. These include 9 layers in the neurosensory retina and 1 pigmented layer Definition Retinal detachment refers to the separation of the neurosensory retina from the underlying retinal pigment epithelium, to which normally it is loosely attached. Types Rhegmatogenous. retinal detachment results from a tear—i.e., a break in the retina. Tractional. retinal detachment results from traction—i.e., from vitreous strands that exert tensile forces on the retina Exudative. retinal detachment is caused by fluid. Blood, lipids, or serous fluid accumulate between the neurosensory retina and the retinal pigment epithelium.  What complaint do you think this patient will come with? Inferior visual field defect. Does the visual acuity get affected and why? No, because the macula is intact. Therefore, if you check the patient's visual acuity, it might be 20/20 or 6/6. RRD Rhegmatogenous retinal detachment Retinal break. Subretinal fluid.subretinal space & detach the retina Fluid that goes from vitreous to But here the macula is involved Macular involvement ! so the patient will come with visual field defect & decrease in visual acuity retinal tear which can be named as horseshoe tear: Retinal detachment Normal attached retina  Why do patients develop flashes? Signs and symptoms: Patients develop flashes because any pulling of the retina activates photoreceptors, which translates to the brain as light. Continuous pulling of the retina can lead to the formation of a retinal tear or break, resulting in flashes. Flashes.. ‫المريض بيشوف زي البرق أو فالش الكاميرا في عينه‬ Floaters. Vitreous is moving so, if there is any opacity the patient will see it moving ‫المريض يشوف شيء يتحرك في عينه سواء خطوط أو نقاط‬ Visual field defect. VA ! As mentioned before, if the macula is involved, visual acuity may be affected  The concept of management is as follows: Reattach the retina Close the scar This is achieved by pushing the retina back into place and inducing a scar at the break to prevent it from reopening Management non surgical option: mean gas or air Pneumatic retinopexy. Scleral buckle. Most common Par plana vitrectomy.  Pneumatic Retinopexy: In this procedure, a special gas is injected into the eye. The gas bubble rises and pushes the retina back against the ocular wall. The retinal pigmented epithelium (RPE) will absorb the subretinal fluid over time, effectively sealing the break. After this, laser treatment is used to induce a scar around the break (360 degrees). This is important because the gas bubble remains in the eye for only 3 to 4 weeks before being absorbed. If the break is not sealed during this time, fluid may re-enter and cause the retina to detach again. This is a link to see how the procedure is done : https://youtu.be/X-b_P55PClg?si=0xf8GJnjC80sJHrv Scleral Buckle A silicone band is placed around the eye and tightened strongly to compress the ocular wall (‫) ينضغط‬. This compression pushes the retina against the ocular wall, facilitating attachment. Afterward, laser treatment or cryotherapy is performed to induce a scar and seal the break. This is a link to see how the procedure is done : https://youtu.be/QCf7MIxBtig?si=AAN0ilA0eYbYX0M9 ‫هذا الفيديو لعملية حقيقية‬ Par Plan Vitrectomy This is the most common procedure. It involves entering the eye to remove the vitreous gel that is causing the detachment or break. A special device is used to aspirate fluid from the subretinal space, allowing the retina to return to its proper position. After this, laser treatment is performed to secure the retina. This is a link to see how the procedure is done : https://youtu.be/FtrUZqtbvas?si=OH8HRucQEV5CspjE  Tractional retinal detachment TRD Proliferative diabetic region Most common cause: PDR Others: ROP, sickle cell retinopathy, etc The doctor said there are other causes, but they are not important Rx: PRP, PPV The treatment involves surgery to: - Remove the vitreous - Remove the fibrous membrane from the retina PRP:pan-retinal photo coagulation Intraoperatively, laser treatment (PRP) is performed. PPV:par plane vitrectomy Why?To prevent recurrence. 1 2 Can we perform PRP (laser) or not? 1- If the patient has aggressive fractional retinal detachment causing striations in the macula, PRP is performed surgically. 2- If there is small fibrous tissue that does not affect the macula, laser treatment may be appropriate. However, it’s important to note that the fibrous tissue will not disappear; it will only stabilize to prevent further progression. Exudate retinal detachment The exudative fluid does not originate from the vitreous ERD cavity because there is no access (no break). Instead, the fluid comes from the inferior choroid or sclera. Causes: tumors, inflammation, HTN, toxemia of pregnancy, others For example: Intraoculr tumor If a pregnancy occurs with ERT and the patient has preeclampsia or eclampsia, we recommend delivery as soon as possible to avoid complications. Rx: treat the underlying cause. Let’s suppose a woman comes to you after delivery. Three to five weeks later, the exudation will typically resolve, and the retina and vision should return to normal. As you can see in both photos, there is no break Chiroidal melanoma Inferior exudate retinal detachment Age related macular degeneration One of the leading causes of visual loss in patients above 60 years in the US. Do you think it is a common disease here in Saudi Arabia? No, as mentioned before, 90% of the cases are due to diabetic retinopathy. Additionally, risk factors such as race and light iris Risk factors: color are not prevalent in this region. Age. >65 years old Gender (female) Race (white). Smoking. Sunexposure. They are exposed to the sun more than we are. Light iris color. Such as blue or green iris. Symptoms: Decreased visual acuity. Central scotoma. :‫المريض يقول أنا أشوف بقعة سواء فهذا مقصده‬ Metamorphopsia. Irregular vision ‫المريض يقول أنا متعود أمشي بشارع أعرف إنه مستقيم‬ ‫بس الحين أحس أنه متعوج وأشوف مطبات‬ Normal Metamorphopsia Central scotoma  Types: 1- nonexudative (dry) The patient usually start having nonexudative and 2- exudative (wet, CNVM). than progress to exudative  Drusen -There is no hemorrhage, no fluid under the retina Dry ARMD: Drusen, pigmentary changes, RPE atrophy. Retinal pigmented epithelium The retinal pigmented epithelium (RPE) has many functions, one of which is to provide nutrients to photoreceptors and remove waste products from them. loss of pigmentation With aging, smoking, or sun exposure, there can be exudative damage to the RPE, impairing its ability to eliminate waste products. What happens to these waste products? They accumulate beneath the RPE. ‫تخيلوا سجادة ترفعونها‬ ‫ وش بيصير؟ بتنتفخ‬،‫وترمون تحتها‬. Exactly that happens with the RPE—it cannot metabolize the waste products, so they accumulate beneath it, forming what are known as drusen. Clinically, drusen appear as milky white or yellowish deposits under the retina. RPE with the time there will be proliferation but here it ( choroidal proliferation) Not retinal proliferation like in diabetic Wet ARDM: choroidal neovascular membrane Charactarized by CNVM (greyish subretinal lesion, maybe associated with blood or exudates). CNVM ( growing under the retina) fluid so it’s wet ( very poor vision at this stage) Absent RPE (retinal pigmented epithelium )  Management: Control risk factors: smoking, sun exposure. for Dry we can control the risk factors like stop smoking and decrease dirdct sun exposure to decrease the exudative damage Antioxidants (AREDS formula). The AREDS formula is a specific combination of vitamins and minerals (like vitamins C and E, zinc) that may help slow down the progression of ARMD. These nutrients act as antioxidants, protecting the eyes from damage. Amsler grid. Ask the patient to evaluate themselves: 1. Have them hold the Amsler grid paper and cover their left eye. 2. They should check if they can see the entire grid clearly. 3. Ask if all the lines are straight and if there are any scotomas. If everything appears normal, they should check the other eye. If they develop a scotoma at any time, it is an alarming sign that the patient may be converting from dry to wet age-related macular degeneration, and they should seek medical attention promptly. Wet ARMD: antiVEGF, laser Giving injection for life Quiz Q1/ Which of the following is a risk of Age Related Q2/ What is the hallmark of the proliferative diabetic Macular Edema? retinopathy? A. Male gender A. Hard exudate B.African race B.Soft exudate C.Light iris color C.Neovascularization D.Dyslipidemia Q3/ What is the drug of choice of tractional retinal detachment? A. Anti-VEGF B. Surgery (Pars Plana Vertictomy) C. Diabetes control D. Pan-retinal photo coagulation Answer; Q1/C Q2/C Q3/B Good Luck !