OPT 026: Ocular Disease 2 PDF

OPT 026: OCULAR DISEASE 2 Vitrectomy DIABETIC RETINOPATHY Introduction of microscopic instruments into the back of the eye through the white part of Retina the eye...

OPT 026: OCULAR DISEASE 2 Vitrectomy DIABETIC RETINOPATHY Introduction of microscopic instruments into the back of the eye through the white part of Retina the eye, termed the sclera, and It is the light-sensing tissue that resides in the back of the controlled removal of eye. hemorrhage from within the It is responsible for relaying images to the brain. eye. Contains millions of light-sensitive cells (rods and cones) Note: Application of retinal laser and other nerve cells that receive and organize visual treatment and intra ocular information. medications is also possible The retina sends this information to your brain through during this procedure your optic nerve, enabling good vision. Prognosis ○ The success of prognosis A Retinal Disorder or Disease dependent on the following Affects this very important tissue, which can affect vision 1. Specific cause to the point of blindness. 2. Severity Retinal diseases vary widely, but most of them cause 3. Duration visual symptoms. Early Management/Treatment ○ For patients suspected of Common Retinal Conditions retinal vascular disease, to obtain the best visual and 1. Age Related Macular Degeneration ocular health outcome, it is important to 2. Diabetic Retinopathy (Diabetic Eye Disease) 1. See their ophthalmologist ASAP 3. Hypertensive Retinopathy 2. Obtain an accurate diagnosis 4. Glaucoma (the optic nerves are affected) 3. Begin prompt treatment COMPLICATIONS OF TREATMENT 1. Retinal laser Blurring of vision Loss of visual field Trouble seeing at night (Nyctalopia) Eye pain 3 1 Photosensitivity 2. Intraocular anti-VEGF injections Infection Blurring of vision Subconjunctival hemorrhage Elevated intraocular pressure Eye pain 3. Intraocular steroid Infection 2 4 Blurring of vision Subconjunctival hemorrhage Elevated intraocular pressure Treatment Cataract Is available for some retinal diseases. Eye pain Depending on condition, in most case, if diagnosed early 4. Vitrectomy surgery at the primary level, the disease process may be to Infection stopped or slowed leading to: Cataract ○ Preservation of vision Elevated intraocular pressure ○ Improvement of vision Retinal detachment ○ Even restoration of vision Vitreous hemorrhage Subacute loss of vision due to air, gas or silicone oil Etiology within the eye Over time, too much sugar in your blood can lead to the blockage of the tiny blood vessels that nourish the retina cutting off its blood supply. As a result, the eye attempts to grow new blood vessels. But these new blood vessels don't develop properly and can leak easily 12 OPT 026: OCULAR DISEASE 2 Diabetic retinopathy is a major cause of blindness, Signs and Symptoms particularly among working-age adults. Non ophthalmoscopically The degree of retinopathy is highly correlated with: ○ Spots or dark strings floating in your vision (floaters) ○ Long Duration of diabetes ○ Blurred vision ○ High Blood Glucose Levels ○ Fluctuating vision ○ BP levels ○ Impaired color vision ○ Pregnancy: can impair blood glucose control and thus ○ Dark or empty areas in your vision worsen retinopathy ○ Vision loss Ophthalmoscopically ○ Non-proliferative retinopathy (Early stage) Vision symptoms are caused by macular edema or macular ischemia. However, patients may not Non-Proliferative Retinopathy have vision loss even with advanced retinopathy. Develops first and causes: Capillary microaneurysms ○ Increased capillary Dot and blot retinal hemorrhages permeability Cotton-wool spots (soft exudates) ○ Microaneurysms ○ are areas of microinfarction of the retinal ○ Hemorrhages nerve fiber layer that leads to retinal ○ Exudates opacification ○ Macular ischemia ○ fuzzy-edged and white and obscure ○ Macular edema underlying vessels. (thickening of the Hard exudates retina caused by fluid ○ are discrete, yellow particles within the retina leakage from capillaries) ○ they suggest chronic edema when present. Clinically significant macular edema may occur Subretinal / venous hemorrhages Intraretinal hemorrhages (dot blot hem, flame Proliferative Retinopathy shaped hem) Develops after non-proliferative ○ Proliferative retinopathy retinopathy and is more severe (Advance stage) May lead to vitreous Neovascularization hemorrhage and traction retinal Intraretinal detachment microvascular Characterized by abnormal abnormalities (IRMA) new vessel formation Venous abnormalities (neovascularization) (Tortuosity) Note: Neovascularization ○ is often accompanied by preretinal fibrous tissue, Signs in Later Stages: which, along with the vitreous, can contract, resulting Macular edema (seen on in traction retinal detachment. slit-lamp biomicroscopy as ○ may also occur in the anterior segment of the eye on elevation and blurring of retinal the iris; layers) ○ neovascular membrane growth in the anterior Venous dilation chamber angle of the eye at the peripheral margin of Intraretinal microvascular the iris can occur, and this growth leads to abnormalities “neovascular glaucoma” 13 OPT 026: OCULAR DISEASE 2 Hard Exudates Distinct yellow-white intra-retinal deposits which can vary from small specks to larger patches May evolve into rings known as circinates Ultimately large confluent plaques can form Largely made up of extracellular lipid which has leaked from abnormal retinal capillaries Often associated retinal oedema (which is not visible using direct ophthalmoscopy) FEATURES OF DIABETES The underlying problem is often apparent as the exudates will form a ring or ‘circinate’ pattern around the leaking Microaneurysm vessels (Black arrow) Found principally in the macular region and as the lipids Are the earliest clinically coalesce and extend into the central macula (fovea), visible changes of diabetic vision can be severely compromised retinopathy Are localized capillary dilatations which are usually saccular (round) Appear as small red dots which are often in clusters but may occur in isolation Do not affect vision Intraretinal Hemorrhages Intraretinal hemorrhages (depending upon the depth within the retina) The capillary network in the posterior retina is found in two layers ○ Nerve fiber layer (superficial layer) - tends to be “Flame shaped” Hemorrhage ○ Inner nuclear layer (deeper layer) - tends to be ‘dot’ or’ blot’ shaped (termed ‘dot/blot hemorrhages’) The clinical differentiation between dot hemorrhages and microaneurysms is difficult and of little consequence since Cotton Wool Spots both are changes of background retinopathy. Greyish-white patches of discoloration in the nerve fiber Fluorescein angiography will discriminate, layer which have indistinct (fluffy) edges microaneurysms lighting up with the dye. Result of local ischemia which leads to disruption of Vision is unaffected by these appearances axoplasmic flow Multiple blot hemorrhages imply significant retinal Appearances of one or two do not require intervention ischemia, characteristic of pre-proliferative retinopathy 14 OPT 026: OCULAR DISEASE 2 However, multiple cotton wool spots (more than 6 in one Vitreous Hemorrhage eye) indicate generalized retinal ischaemia and this is Give rise to profound loss of regarded as a pre-proliferative state vision if the macula is obscured Only a small amount of bleeding is required for blood to be dissolved in the vitreous produces a haze effect which impairs vision Risk factors: Duration of diabetes - the Venous Abnormalities longer the diabetes, the greater your risk of Venous dilatation, beading developing diabetic and duplication occur as retinopathy (usually 5 years retinal ischemia progresses. and above - long standing) Beading is a useful sign of Poor control of blood sugar diffuse retinal ischemia level Is seen early in diabetic High blood pressure retinopathy High cholesterol Pregnancy Intraretinal Microvascular Abnormalities (IRMAS) Tobacco use Are areas of capillary Being African-American, Hispanic or Native American dilatation and intraretinal new vessel formation COMPLICATIONS Arise within ischaemic retina Feature of pre-proliferative Vitreous Hemorrhage retinopathy The new blood vessels may bleed into the vitreous If the amount of bleeding is small, few dark spots (floaters) may be seen. Neovascularization In more-severe cases, blood can fill the vitreous cavity and As the retina becomes more completely block the vision. ischemic new blood vessels may Usually heals over time doesn't cause permanent vision arise from the optic disc or in the loss periphery of the retina. The blood often clears from the eye within a few weeks or The vessels usually originate from months large veins and are initially seen as Unless retina is damaged, the vision may return to its fine tufts on the surface of the disc previous clarity or from the vessels of the major arcades of vessels Retinal Detachment The new vessels are fragile and The abnormal blood vessels bleed easily, (proliferative diabetic associated with diabetic retinopathy) retinopathy stimulate the growth of scar tissue Which can pull the retina Retinal Detachment away from the back of the As the new vessels mature, connective tissue and fibrosis eye. (gliosis) occurs, allowing the vitreous to exert traction This may cause spots floating which may cause retinal detachment the vision, flashes of light or If the detachment extends across the fovea then vision will severe vision loss be lost Glaucoma New blood vessels may grow in the iris and interfere with the normal flow of fluid out of the eye Causing pressure in the eye to build up (glaucoma). This pressure can damage the nerve that carries images from the eye to the brain (optic nerve). 15 OPT 026: OCULAR DISEASE 2 Blindness Note: The burns cause the Eventually, diabetic retinopathy, abnormal new blood glaucoma or both can lead to vessels to shrink and scar complete vision loss. Done in an outpatient department for two or more sessions. Vision will be blurry for about a day after the TREATMENT procedure. Some loss of peripheral Early Diabetic Retinopathy vision or night vision after Mild or moderate the procedure is possible. nonproliferative diabetic retinopathy, patient may not Vitrectomy need treatment right away This procedure uses a tiny incision in Good blood sugar control can your eye to remove blood in the usually slow the progression vitreous as well as scar tissue that's Collaboration with an tugging on the retina that can cause endocrinologist to determine if there are ways to improve tractional retinal detachment diabetes management It's done in a surgery center or hospital using local or general anesthesia Proliferative Diabetic Retinopathy Proliferative diabetic retinopathy with macular edema, Pharmacologic Therapy prompt surgical treatment is required Anti-VEGF Photocoagulation / Focal laser Vascular endothelial growth factor Laser treatment, also known as (VEGF) inhibitors (injection) focal laser treatment, can stop Help stop growth of new blood or slow the leakage of blood vessels by blocking the effects of and fluid in the eye. growth signals the body sends to During the procedure, leaks generate new blood vessels. from abnormal blood vessels Ranibizumab (Lucentis) are treated with laser burns. Bevacizumab (Avastin) Usually done in an outpatient department or in a eye single Triamcinolone session clinic Administered intravitreally; corticosteroid used in the If vision is worst from macular treatment of diabetic macular edema edema before surgery, prognosis might not be restored by Intraocular steroid injection the procedure, however, it might prevent worsening of the condition Glucose Control The Diabetes Control and Complications Trial found that Grid Laser Photocoagulation intensive glucose control in patients with type 1 diabetes Grid laser photocoagulation for (previously called insulin-dependent diabetes mellitus diffuse clinically significant diabetic [IDDM]) decreased the incidence and progression of macular edema diabetic retinopathy. Treatment of choice for cases not It may be logical to assume that the same principles apply responding to anti-VEGF and in type 2 diabetes (previously called steroids non-insulin-dependent diabetes mellitus [NIDDM]) For “recalcitrant” (Stubborn) cases DM Ret OPTOMETRIC MANAGEMENT Panretinal Photocoagulation (PRP) Comprehensive Eye Examination Laser treatment, also known as Close monitoring for patient suspected and risk for DM Ret scatter laser treatment, can Dilated retinal examination shrink the abnormal blood Promptly refer patients with any level of: vessels. 1. Macular edema The areas of the retina away from 2. Severe nonproliferative diabetic retinopathy (a the macula are treated with precursor of proliferative diabetic retinopathy) scattered laser burns. 3. Proliferative diabetic retinopathy 16 OPT 026: OCULAR DISEASE 2 PREVENTION STAGES 1. Regular eye exams, good control of blood sugar and blood “Keith Wagener Barker (KWB) grading system” pressure, and early intervention for vision problems can help prevent severe vision loss Grade 1 2. Reduce the risk of getting diabetic retinopathy by doing ○ High blood pressure the following: ○ Narrowing of the arteries is mild Manage diabetes ○ Generally, no symptoms are present Healthy diet Physical activity is part of daily routine Grade 2 Moderate aerobic activity, such as walking, each ○ High blood pressure week. ○ AV Nicking Take oral diabetes medications or insulin as directed. ○ Narrowing of the arteries is more Monitor blood sugar level pronounced. Keep blood pressure and cholesterol under control ○ Generally no symptoms are present. Avoid smoking Pay attention to vision changes (frequent changes in Grade 3 prescription, sudden vision loss) ○ Signs of damage such as retinal Lifestyle modification hemorrhage (bleeding) ○ Cotton wool spots (white patches on the retina, are present upon inspection) HYPERTENSIVE RETINOPATHY ○ Symptoms may be present Complication of high blood pressure (hypertension) Grade 4 Due to persistent, untreated high blood pressure can ○ Severe Grade 3 plus swelling of the cause damage to the retina optic disc (papilledema) Occurs when the force of blood against the artery walls is ○ Symptoms are present too high, causing: ○ This system simply combines the first ○ Arteries to stretch two categories into one ○ Narrow ○ Damaged over time PATHOPHYSIOLOGY Damage to the retina increases with: ○ Severity of high blood pressure ○ Length of time Retinal blood vessels have distinct features, which Who are at risk: Older people differentiate them from other blood vessels Arteriosclerotic changes of hypertensive retinopathy ○ The absence of sympathetic nerve supply ○ caused by chronically elevated blood pressure ○ Autoregulation of blood flow ○ Presence of blood-retinal barrier Atherosclerosis An increase in blood pressure (BP) is transferred directly to the vessels which initially constrict. A further increase in BP overcomes this compensatory tone and damage to the muscle layer and endothelium PHASES Vasoconstrictive Phase In this phase, the local autoregulatory mechanisms come into play. This causes vasospasm and retinal arteriolar narrowing, which is evident by the decrease in the arteriole to venule ratio (Normal = 2:3) American College of Cardiology/American Heart Association (ACC/AHA) - definitions for high blood Sclerotic Phase pressure in 2017 Persistent increase in BP causes certain changes in vessel wall: ○ Intima layer: Thickening ○ Media layer: Hyperplasia ○ Arteriolar wall: Hyaline degeneration This leads to: a. Severe form of arteriolar narrowing 17 OPT 026: OCULAR DISEASE 2 b. Arteriovenous (AV) crossing changes SIGNS AND SYMPTOMS c. Widening and accentuation of light reflex (silver and copper wiring). Permanent arterial narrowing Arteriovenous crossing abnormalities (arteriovenous nicking) Arteriosclerosis with moderate vascular wall changes (copper wiring) to more severe vascular wall hyperplasia and thickening (silver wiring) ○ Retinal arterioles appear orange or yellow instead of red ("copper wiring") ○ Retinal arterioles look white if they have become occluded ("silver wiring) ○ Retinal arterioles look dull white if with severe occlusion (“Ghost vessel”) AV nicking - artery is crossing a vein Exudative Phase Seen in patients with severely increased BP Characterized by: ○ Disruption of the blood-brain barrier ○ Leakage of blood and plasma into the vessel wall - disrupting the autoregulatory mechanisms Retinal signs: ○ Retinal hemorrhage (flame-shaped and dot blot) ○ Hard exudate formation ○ Necrosis of smooth muscle cells ○ Retinal ischemia (cotton-wool spots) During total vascular occlusion: ○ Arteriovenous nicking is a major predisposing factor to the development of a branch retinal vein occlusion ○ for SEVERE CASES, these are the following clinical findings: Superficial flame-shaped hemorrhages Small, white, superficial foci of retinal ischemia (cotton-wool spots) Yellow hard exudates Malignant Hypertension Optic disk edema Severe intracranial hypertension leads to optic nerve ischemia and edema (papilledema) TREATMENT Other factors that may contribute to the likelihood of developing high blood pressure include: ○ Obesity Managed primarily by controlling hypertension. ○ Sedentary Other vision-threatening conditions should also be lifestyle aggressively controlled. ○ A diet high in salt If vision loss occurs, treatment of the retinal edema with ○ Stress laser or with intravitreal injection of corticosteroids or anti ○ A family history of vascular endothelial growth factor drugs (ranibizumab, high blood pegaptanib, bevacizumab) may be useful. pressure ○ Diabetes Treatment ○ Moderate to high Giving up smoking alcohol intake Losing weight Taking regular exercise Dietary changes Reducing alcohol intake 18 OPT 026: OCULAR DISEASE 2 Medication WARNING SIGNS OF RETINA PROBLEMS a. Angiotensin-converting enzyme (ACE) inhibitors b. Angiotensin-2 receptor blockers (ARBs) Flashing of Lights c. Thiazide diuretics d. Calcium channel-blockers A symptom of a number of conditions: e. Beta-blockers ○ Migraines ○ Eye injury Prevention ○ Retina problems If a person doesn’t often suffer from headaches or have Careful management of high blood pressure and related never experienced random flashing lights before: conditions, such as diabetes ○ a sign of a retinal disease or problem. Lifestyle changes, such as losing weight or giving up The retina is responsible for sending light signals to the smoking brain. Regular monitoring of blood pressure When the retina is damaged or diseased, it can send Regular eye screening (Annual eye Check up) incorrect and/or abnormal signals to the brain, which could cause it to experience the “flashing light” phenomenon. Complications 1. Retinal vein occlusion - vein retina becomes blocked Dimmer Vision due to clots Characterized as things looking darker than usual, being 2. Retinal artery occlusion - artery in the retina becomes “muddied”, and seeing less contrast. blocked due to clots, resulting in possible loss of vision 3. Ischemic optic neuropathy - normal blood flow to the Double Vision eye being blocked, resulting in damage to the optic nerve 4. Malignant hypertension - rapid increase of blood The doubled version is often blurry and less sharp pressure compared to what is actually seen. 5. Stroke and heart attack The two images are often overlapping, layered, and/or blurry, which can be disorienting and uncomfortable for Prognosis people with this symptom. Double vision can be a symptom of various disorders, it Mild hypertensive retinopathy (grade 1 or 2) often points to a retinal issue ○ is relatively positive, so long as blood pressure levels are controlled Distorted Vision Severe hypertensive retinopathy ○ If not properly managed, the condition can enter a Retinal problems experience a few types of distorted “malignant” stage vision, including: ○ Relatively poor prognosis ○ Double vision ○ Wavy lines ○ Things appearing crooked OPTOMETRIST’S ROLE ○ Blurred vision Severity of these vision problems can vary, and many Optometrist plays a critical role people mistake their blurry vision as simply worsening 1. Early detection and diagnosis of ocular manifestations vision related to age. associated with HTN Role of Optometrist: “Always evaluated the eye to rule out 2. Lead to timely referral and more appropriate management serious issues like a retinal disease” Challenge to all new and old optometrist Specks and Lines in Vision “We can affirm the role of the optometrist as a primary Lines/specks don’t go away, that could be a sign of retinal health-care provider, by performing a comprehensive eye damage or degeneration. examination, which includes blood pressure evaluation” Blind Spots / Scotoma MACULAR HOLE Developing larger or an increased number of blind spots is cause for concern and a definite warning sign of retinal Function of the Retina issues. These could be in the form of The light-sensitive tissue in ○ Complete blind spots, the back of the eye ○ Large shadows, or Contains specialized cells ○ Something “blocking” the vision in a certain area called photoreceptors Photoreceptors cells are Noticeable Vision Issues That Worsen Over Time responsible for covering converting light rays to Drastic changes in a short period of time, that’s cause for electrical impulses to the brain concern. 19 OPT 026: OCULAR DISEASE 2 MACULAR HOLE STAGES A defect of the Stage 1 foveal retina Is known as foveal detachments, the first indication of a involving its full small macular hole. thickness from the About half of all stage 1 macular holes will progress into a internal limiting worsened state without treatment. membrane (ILM) Occasionally referred to as the yellow dot stage to the outer Expected vision 20/40 segment of the photoreceptor Stage 2 layer. Is called partial-thickness holes. Early Stages The vitreous gel continues to pull on the edges of the hole; it's more likely to continue and require medical Blurred intervention. Distorted vision Straight lines look wavy or distorted Stage 3 Trouble reading small print Is when a full-thickness hole exists. Advance Stages At this stage, the central and detailed vision has become severely affected. See a small black patch It’s likely to have little to no central vision left. "missing patch" in the center of the vision It is still attached with partial vitreomacular A painless total loss of central vision adhesion/traction. Expected vision 20/160 Full-Thickness Macular Hole Stage 4 Showing a grayish macular rim (surrounding cuff of fluid) Is when a full-thickness macular hole exists - suggestive of subretinal fluid With presence of a complete separation of the vitreous from the macula and the optic disc. It is when the posterior vitreous detaches. Expected vision 20/200. TYPES OF MACULAR HOLE AND ETIOLOGY Trauma-Related Macular Hole Thought to be linked to a concussive blow delivered from the opposite site of the head. As a result, the macula ruptures at its thinnest point Idiopathic Related Macular Hole Stage 1 The retina is connected tightly to the vitreous, a layer surrounding the interior of the eye that is Stage 2 filled with vitreous gel. The vitreous is constructed of millions of very fine intertwined fibers. As we age, the vitreous Stage 3 gel begins to liquefy and/or clump and shrink. Causing to the pulling of the vitreous to the side as the gel and vitreous sac contracts. The retina is attached to the vitreous, and when the Stage 4 vitreous shrinks, it pulls the retina and creates a hole at the thinnest part of the macula. 20 OPT 026: OCULAR DISEASE 2 Note Best's disease (inherited condition causing macular Determine how much it will affect vision: damage) ○ The size of the hole Eye injury ○ Location on the retina Central and detailed vision is often lost when a stage 3 DIAGNOSTIC TESTING macular hole develops. If left untreated, a macular hole can lead to a detached retina Optical Coherence Tomography ○ a sight-threatening condition that requires immediate The current gold standard in the diagnosis, staging, and medical attention management of macular holes. Assist in the determination: Clinical Manifestations ○ If there is an associated epiretinal membrane The severity of the symptoms is dependent on ○ If the posterior hyaloid is still attached or not ○ Partial Thickness ○ Critical in deciding on the surgical approach ○ Full-Thickness ○ It can also be used to aid in gauging the prognosis of Metamorphopsia (distorted, wavy vision) the fellow eye Blurred central vision Difficulty in detail tasks such as reading TREATMENT: SURGICAL APPROACH Central blind spot or gray area Amsler Grid Vitrectomy (Pars Plana Vitrectomy - PPV) Amsler Grid with straight lines as seen by a Is a surgical technique involving the removal of the normal-sighted person. vitreous body A person with macular problems may notice distortion of The surgeon inserts thin tubes called cannulas into the the grid pattern such as bent lines and irregular box eyes through scleral incisions or incision of the eye wall to shapes or a gray shaded area. relieve traction exerted by the vitreous to the central retina and close the hole Ophthalmoscopic/Fundus Photo Finding Macular hole surgery consists of two parts: ○ The operation itself (which involves a vitrectomy with Well-defined round or oval lesion in the macula the peeling of the inner limiting membrane and a gas Yellow-white deposits at the base (drusen-like deposits) injection) Cuff of subretinal fluid, intraretinal edema ○ “Posturing” after the surgery These yellow dots represent: Three small holes (ports) in the sclera ○ Lipofuscin-laden macrophages (Lipid, proteins, ○ The first of these will have a constant flow of fluid carbohydrates) passing through it for infusion. ○ Nodular proliferations (Plaques) ○ The second is used to insert a fiber-optic ‘light pipe’ ○ Associated eosinophilic material (protein) into the eye for adequate illumination. Long-standing cases may have retinal pigment epithelial ○ The third port is used for all other instruments that are changes at the margin of the subretinal fluid. required during the macular hole repair, including the ‘cutter’ for removal of the vitreous and forceps for removal of the membrane on the retina’s surface Importance of “posturing” ○ Air in eye is replaced with gas ○ At the end of the macular hole repair operation ○ Forms a bubble in the eye and floats upwards to press the press against the macular hole ○ Let the patient look vertically down towards the floor to get the gas bubble to press against the macula “Face-down posturing” Full-thickness macular hole Full-thickness macular hole ○ Tilt the head forwards and point the face down with typical yellowish granular showing a surrounding ○ For 50 minutes out of every hour for five days deposits on the RPE cuff of subretinal fluid ○ But not during sleep During sleep time Risk Factors ○ It is recommended to sleep on either side or even Vitreomacular traction (vitreous shrinkage / separation) front, Diabetic eye disease ○ But not sleep on their back as that would make the Severe myopia bubble move away from the macular hole Macular pucker Walking during post surgery period ○ formation of scar tissue over the macula that can ○ Is allowed and encouraged for its health benefits warp and contract, causing wrinkling of the retina ○ Done by looking vertically downward when walking Retinal detachment ○ Trying to keep the head up as upright as possible 21 OPT 026: OCULAR DISEASE 2 Risk Factors RETINAL DETACHMENT Aging - retinal detachment is more common in people over age 50 An emergency situation in which a thin layer of tissue (the Previous retinal detachment in one eye retina) at the back of the eye pulls away from its normal Family history of retinal detachment position Severe myopia Separates the retinal cells from the layer of blood vessels Previous eye surgery, such as cataract removal that provides oxygen and nourishment Previous severe eye injury The longer retinal detachment goes untreated, the greater Previous other eye disease or disorder, including the risk of permanent vision loss in the affected eye retinoschisis, uveitis or thinning of the peripheral retina The longer retinal detachment goes untreated, the greater (lattice degeneration) the risk of permanent vision loss in the affected eye Diabetic retinopathy The areas where the retina detaches lose their blood supply and stop working, causing to lose vision TREATMENT: SURGICAL APPROACH Laser Surgery (Photocoagulation) The laser beam creates laser burns around the retinal tear, resulting in scarring tissue that then fuses the tissue back together The laser beam creates laser burns around the retinal tear, resulting in scarring tissue that then fuses the tissue back together Cryotherapy cryosurgery, cryopexy, or freezing, involves applying extreme cold to destroy abnormal or diseased tissue. Retinal Tear produces a delicate scar that helps connect the retina to the wall of the eye The retina could tear before it detaches Scleral Buckling A torn retina usually has the same symptoms as a In the area where the retina has detached, very thin bands detached one of silicone rubber or sponge are sewn onto the sclera, the outside white of the eye. Clinical Manifestations The tissue around the area may be frozen or lasers may Sudden appearance, increase or change in floaters be used to scar the tissue. Photopsias (flashes of light) Curtain or veil across the visual field Vitrectomy Any sudden, unexplained loss of vision The vitreous gel is removed from the eye Vitreous hemorrhage that obscures the retina A gas bubble or silicone oil bubble is used to hold the retina in place. TYPES OF RETINAL DETACHMENT AND ETIOLOGY The wound is stitched Silicon oil needs to be removed 2 to 8 months after the procedure Rhegmatogenous Retinal Detachment The most common type Pneumatic Retinopexy Caused by a hole or tear in the retina that allows fluid to used if the detachment is uncomplicated. pass through and collect underneath the retina, pulling the freezes the tear area, using cryopexy retina away from underlying tissues injecting a bubble into the vitreous cavity of the eye The most common cause of rhegmatogenous detachment is aging Possible Complications of Surgery For Retinal The same pathophysiology in macular hole Detachment Cataract formation Tractional Retinal Detachment Glaucoma Occur when scar tissue grows on the retina's surface, Infection causing the retina to pull away from the back of the eye Hemorrhage into the vitreous cavity Typically seen in people who have poorly controlled Vision loss diabetes or other conditions 22 OPT 026: OCULAR DISEASE 2 Diagnostic Testing RETINITIS PIGMENTOSA Ophthalmoscopy/fundus photography Genetic testing rare, genetic disorders that Electroretinography involve a breakdown and loss ○ measures the function of the retina of cells in the retina ○ people with RP have reduced electrical activity in the photoreceptors progressively retina, which indicates that the photoreceptors are not lose function functioning properly Peripheral vision, slowly Visual field testing - RP affect peripheral (side) vision worsens over time Optical coherence tomography (OCT) - help diagnose RP Central vision typically and find out how it is affecting your retina declines in the advanced stages of the disease Treatment and Management Night vision is also affected No known effective treatment for retinitis pigmentosa (RP) Focus of management: Note ○ Slow vision loss Signs of RP can usually be detected during a routine eye ○ Restore some sight exam when the patient is around 10 years old. 1. Vitamin A palmitate (about 15,000 international units) - symptoms usually do not develop until adolescence may help slow the progression of the disease in some Currently no known cure or effective treatment for retinitis patients. pigmentosa 2. Omega 3 fatty acid, lutein plus zeaxanthin diet supplementation may also slow the rate of vision loss Pathophysiology 3. Special glasses - light amber filter can be added to Inherited disorder that results from harmful changes in any general eyeglasses to help improve tolerance of bright one of more than 50 genes. lights Genes carry instructions → Produce proteins that are 4. Gene therapy currently being studied, experimental needed to create photoreceptors → Genes mutation → therapy involves: Cannot make the required protein, limiting the cell's ○ Replacing or deactivating mutated genes that are function → Produce a protein that is toxic to the cell → causing disorder Abnormal protein that doesn't function properly → ○ Inserting a new gene to help the body fight a specific Damage to the photoreceptors → Retinitis pigmentosa disease 5. Retinal implant Presenting Signs and Symptoms ○ For patients with total or near total vision loss Nyctalopia (most commonly the earliest symptom) (late-stage RP) Tunnel vision (peripheral visual field constriction) ○ Epiretinal and subretinal computer chip implants can Central visual loss (advanced cases) restore some visual sensations Photopsia (seeing flashes of light) ○ Images are converted to electrical pulses that are Ring shape scotoma sent to the retina Ophthalmoscopic Findings CENTRAL SEROUS CHORIORETINOPATHY (CSCR) Classic triad of fundus findings in RP ○ Bone spicule pigment deposits (HALLMARK sign) ○ Vessel attenuation A disease in which a ○ Waxy pallor of the optic disc (in advanced cases) serous detachment of the Other findings associated with RP: neurosensory retina ○ Diffuse RPE atrophy with relative macular sparing occurs over an area of ○ Cystoid macular edema leakage from the ○ Epiretinal membrane choriocapillaris through ○ Optic disc drusen the retinal pigment ○ Anterior-segment abnormalities (such as posterior epithelium (RPE). subcapsular cataract) It is a self-limited macular disease of about 3 months Common ocular disease characterized by decompensation of the retinal pigment epithelium (RPE) Which results in: ○ Neurosensory retinal detachment ○ Serous pigment epithelium detachment (PED) ○ RPE atrophy. It is a self-limited macular disease marked by: a) Distortion 23 OPT 026: OCULAR DISEASE 2 b) Blurry vision Diagnostic Testing c) Metamorphopsia Ophthalmoscopy/Fundus Photo Optical coherence tomography (OCT) TYPES OF CSCR Fluorescein angiography Classic CSCR TREATMENT & MANAGEMENT is caused by isolated leaks in the RPE CSCR is usually a self-limiting disease Diffuse RPE dysfunction 3–4 months: resolution with overall good visual outcome 50% of patients within the first year occurs when the leakage and changes to the RPE are ○ recurrences are seen widespread Photodynamic Therapy Chronic CSCR photosensitizing drug is injected into the bloodstream CSCR that endures for 6 months or more, compared to low-level laser light is applied to activate the drug without the normal duration of about 3 months damaging surrounding tissue Decompensated RPE Anti-VEGF Medications is described as retinal detachment, combined with: used to successfully treat the complication of choroidal ○ RPE atrophy neovascularization following CSCR ○ Pigment mottling - fundal pigment granularity ○ Degenerate with time Fundus color photograph of a patient with Central Serous Retinopathy SIGNS & SYMPTOMS The arrows point to a blister of fluid under the retina 1. Blurred vision/visual loss (usually unilateral) 2. Dark spot or scotoma in the central visual field 3. Metamorphopsia (image distortion) Fluorescein angiogram of a patient 4. Micropsia (reduction of the apparent size of objects) with central serous retinopathy 5. Mild dyschromatopsia (abnormal color perception) 6. Reduced contrast sensitivity. The arrow points to an area of fluorescein dye leaking under the Note: CSC may also be asymptomatic retina causing the blister of fluid seen when fluid accumulation is away from macula on the color retinal photograph Clinical Presentation The white arrow points to the Serous retinal detachment but no subretinal blood blister of fluid under the Pigment epithelial detachments retina due to leakage of fluid Choroidal neovascularization may develop after multiple that has lifted up the retina episodes of CSCR Risk Factor a. Predominantly affects young or middle-aged (25 to 50 AGE-RELATED MACULAR DEGENERATION years) adults b. Men being affected more frequently than women c. Type A personality (people who are stressed and find it an acquired macular disorder hard to relax) which is characterized by any of d. Stress the following fundus changes: e. Steroid use ○ Pigmentary atrophy and f. Helicobacter pylori infection degeneration g. Autoimmune disease ○ Drusen and lipofuscin deposits h. Sleep disturbances like insomnia ○ Elevation of the outer retinal i. Hypertension complex in the macular area Usually occurs in patients over age 55 Stress and CSR Results in: ○ Progressive, irreversible loss of central visual function from either fibrous scarring or diffuse, geographic atrophy of the macula. 24 OPT 026: OCULAR DISEASE 2 CLASSIFICATION SYMPTOMS Dry AMD (non-vascular/non-exudative type) 1. Distorted (fuzzy) vision in the form of metamorphopsia Deterioration of the retina a grid of straight lines appears wavy and parts of the associated with the formation of small yellow grid may appear blank deposits, known as drusen (under the macula) Patients often first notice this when looking at things leads to a thinning and drying out of the macula, like miniblinds in their home, or telephone poles while causing the macula to lose its function. driving The amount of central vision loss is directly related to 2. Extreme glare the location and amount of retinal thinning caused by 3. Photophobia the drusen. 4. Visual acuity drastically decreasing (two levels or more), Dry AMD is called non-neovascular AMD and 20/20 to 20/80 non-exudative AMD 5. Blurred vision because it does not involve the exuding (exudation) Nonexudative macular degeneration that is leakage of fluids from blood vessels. ○ may be asymptomatic Drusen are accumulations of acellular, amorphous debris ○ notice a gradual loss of central vision subjacent to the basement membrane of the retinal Exudative macular pigment epithelium (Bruch's membrane) ○ rapid onset of vision loss (often caused by “late dry” AMD are called geographic atrophy (GA) leakage and bleeding of abnormal blood vessels) large - advanced cases 6. Trouble discerning colors, specifically dark ones from dark sections of the retina that are well demarcated ones and light ones from light ones (geographies) stop functioning. 7. A loss in contrast sensitivity 8. Flashing lights have also been associated with severe visual loss secondary to wet AMD Risk Factors Aging: over 50 Family history Smoking Hypertension (high blood pressure) Atherosclerosis High cholesterol Obesity Fat intake Exposure to UV light from sunlight Wet AMD (neovascular type) TREATMENT Abnormal blood vessels under the retina begin to grow toward the macula. Dietary supplements This can result in a rapid and severe loss of central vision. Intravitreal anti-vascular endothelial growth factor drugs Occurs when new abnormal blood vessels develop under Laser treatments for wet AMD the retina in a process called “choroidal Supportive measures neovascularization” (abnormal new vessel formation) “Choroidal NeoVascularization” (CNV) Clinical Findings ○ they tend to break, bleed, and leak fluid, damaging the macula and causing it to lift up and pull away from its base (detachment) Retinal pigment epithelial detachment ○ is caused by localized macular edema or hemorrhage that elevates an area of the macula ○ Causes a disciform scar under the macula (if left untreated) 25 OPT 026: OCULAR DISEASE 2 GLAUCOMA is a group of eye disorders that lead to progressive damage to the optic nerve. characterized by loss of nerve tissue that results in vision loss the most common form of optic nerve damage leading to vision loss Fluid builds up in the front part of the eye. This extra fluid puts pressure on the eye, gradually damaging the optic nerve TYPES Primary Glaucoma Low-Tension Glaucoma Congenital Glaucoma GLAUCOMA Secondary Glaucoma Pigmentary Glaucoma Intraocular pressure (IOP) Traumatic Glaucoma ○ is the fluid pressure of the eye Exfoliative Glaucoma ○ Carefully regulated, and disturbances are often Neovascular Glaucoma implicated in the development of pathologies such as Uveitic Glaucoma glaucoma ○ IOP exists as a fine-tuned equilibrium between the Primary Glaucoma production and drainage of aqueous humor Open-Angle Glaucoma Aqueous humor most common form of glaucoma, ○ produced by the ciliary epithelium of the iris ciliary accounting for at least 90% of all glaucoma cases body caused by the slow clogging of the drainage canals, ○ accumulates in the posterior chamber resulting in increased eye pressure ○ flows through the pupil into the anterior chamber Has a wide and open angle between the iris and cornea Develops slowly and is a lifelong condition Aqueous humor then exits the anterior chamber via one of Has symptoms and damage that are not noticed. three routes: “Open-angle” means that the angle where the iris meets ○ 1st Route (vast majority) the cornea is as wide and open Trabecular meshwork at the angle of the anterior chamber and into the Schlemm canal where it Strong Risk Factors enters episcleral veins ➔ High eye pressure ○ 2nd Route (small amount) ➔ Family history of glaucoma Passes into the suprachoroidal space and enters ➔ Age 40 and older for African Americans venous circulation in the ciliary body, choroid, and sclera Potential Risk factors ○ 3rd Route (even smaller amount) ➔ High myopia (very severe nearsightedness) transits through the iris and back into the ➔ Diabetes posterior chamber ➔ Eye surgery or injury ➔ High blood pressure Homeostatic mechanism which maintains intraocular ➔ Use of corticosteroids pressure Symptoms “Sympathetic nervous system” ➔ Gradual loss of peripheral vision ○ influences the secretion of aqueous ➔ Tunnel vision in the advanced stages beta-2 receptors Angle-Closure Glaucoma ○ increased secretion a less common form of glaucoma Caused by blocked drainage canals alpha-2 receptors Has a closed or narrow angle between the iris and cornea ○ decreased secretion occurs when the drainage angle in the eye (formed by the cornea and the iris) closes or becomes blocked 26 OPT 026: OCULAR DISEASE 2 With age, the lens in the eye becomes larger, pushing the Pigmentary Glaucoma iris forward and narrowing the space between the iris and This is a type of open-angle glaucoma that typically the cornea develops during early or middle adulthood Fluid in the eye is blocked from the drainage system It involves changes in the pigment cells that give color to the iris Medical Emergency Cells build up in the channels that drain fluid from the eye, ➔ Demands immediate medical attention: they can affect the normal flow of fluids in the eye ◆ Intense pain in your eye ◆ Nausea Traumatic Glaucoma ◆ Red eyes ◆ Blurred vision Caused by injuries that “bruise” the eye (called blunt trauma) and injuries that penetrate the eye Risk Factors causes bleeding inside the eye ➔ Age 40 and older an excess amount of blood, plasma and debris can ➔ Family history of glaucoma accumulate and clog the drainage system. ➔ Farsightedness ➔ Eye injury or eye surgery Exfoliative Glaucoma ➔ East Asian Also called pseudoexfoliative glaucoma Occurs when a flaky, dandruff-like material peels off the Symptoms outer layer of the crystalline lens ➔ Severe eye pain The material collects in the angle between the cornea and ➔ Nausea and vomiting iris and can clog the drainage system of the eye ➔ Sudden onset of visual disturbance (often in low light) ➔ Blurred vision Neovascular Glaucoma ➔ Halos around lights caused by the abnormal formation of new blood vessels ➔ Reddening of the eye on the iris and over the eye's drainage channels. always associated with other abnormalities, most often Low-Tension Glaucoma diabetes Also known as normal tension glaucoma new blood vessels block the eye’s fluid from exiting Rare form of glaucoma in which eye pressure is not higher through the trabecular meshwork but still causes damage to the optic nerve Low-tension glaucoma may have the following: Uveitic Glaucoma ○ abnormally sensitive optic nerve Infections of the uvea (uveitis) may follow an injury, ○ reduced blood supply to the optic nerve caused by a result from bacteria or a virus condition such as atherosclerosis occur in association with autoimmune or inflammatory conditions Risk Factors infection can produce enough swelling that slow the eye’s ➔ Cardiovascular disease natural drainage and elevate IOP ➔ Family history of glaucoma If steroids are used in treatment, they can also increase ➔ Low eye pressure IOP Congenital Glaucoma CLINICAL SIGNS Occurs in babies when there is incorrect or incomplete development of the eye's drainage canals during the prenatal period IOP Greater than 22mm Hg rare condition that may be inherited ○ patients developing visual field loss increases rapidly, The child may have: most notably at pressures higher than 26-30 mmHg ○ Buphthalmos Cupping ○ Haab striae (breaks in Descemet's membrane) ○ because of increased pressure in the eye and/or loss ○ Epiphora (tearing) of blood flow to the optic nerve, these nerve fibers ○ Cloudiness in the cornea begin to die. ○ Photosensitivity ○ A cup to disc ratio greater than 0.6 (six tenths) is generally considered to be suspicious for glaucoma Secondary Glaucoma Disc hemorrhage (Drance / splinter hemorrhages) ○ a disc hemorrhage is a sign of trouble, indicating that Eye injury/trauma the disease is active and progression is likely Inflammation ○ Sometimes called splinter hemorrhages because they Steroid use look like splinters running parallel to the nerve fibers Advanced cases of cataract or diabetes in the nerve fiber layer Eye surgery 27