Vision loss Flashcards

Question

What is the treatment for neovascularisation?

Answer 1

**_Pan-retinal photocoagulation_** (note that this is not just for treating neovascularisation from proliferative diabetic retinopathy, it's for treating neovascularisation of any cause)

Answer 2

Severely affected patients are usually left with only a small island of temporal vision that can detect counting fingers at best without intervention. Those with branch occlusion usually recover normal vision completely (~80%)

Answer 3

Each quadrant of the retina (ST, SN, IT, IN) is drained by multiple minor retinal veins which coalesce to form a main retinal vein. **_The confluence of the superotemporal and superonasal main retinal veins forms the superior papillary vein, while the confluence of the two inferior main retinal veins forms the inferior papillary vein_**. **_The superior and inferior papillary veins converge creating the central retinal vein, which drains the retina and the optic nerve_** The central retinal vein exits the eye globe via the lamina cribrosa, and courses in the centre of the optic nerve alongside the central retinal artery

Answer 4

Pathophysiology: The central retinal artery and vein share a common adventitial sheath as they exit the optic nerve head and pass through a narrow opening in the lamina cribrosa. Because of this narrow entry in the lamina cribrosa, the vessels are in a tight compartment with limited space for displacement. **_Atherosclerotic changes in the central retinal artery transform the artery into a rigid structure and impinge on the pliable central retinal vein, causing haemodynamic disturbances (slowing of venous blood flow), endothelial damage, and thrombus formation (Virchow's triad) in the central retinal vein_**! This mechanism explains the fact that there maybe an associated arterial disease with CRVO. However, this association has not be proven consistently Thrombotic occlusion in the central retinal vein not only can be caused by atherosclerosis in the central retinal artery, it can also be caused by compression of the vein (mechanical pressure due to structural changes in lamina cribrosa e.g. glaucomatous cupping, inflammatory swelling in optic nerve, orbital disorders); haemodynamic disturbances (associated with hyperdynamic or sluggish circulation); vessel wall changes (e.g. vasculitis); and changes in the blood (e.g. deficiency of thrombolytic factors, increase in clotting factors) * Think about the **_Virchow's triad_** - **_hypercoagulability_**, **_venous stasis_**, **_endothelial damage_** Thrombotic occlusion of the central retinal vein leads to the backup of blood in the retinal venous system and increased resistance to venous blood flow. This increased resistance causes stagnation of the arterial blood and ischaemic damage to the retina. **_Ischaemic damage to the retina stimulates increased production of VEGF in the vitreous cavity_**. VEGF stimulates neovascularisation of the anterior and posterior segment, increasing the risk of secondary complications e.g. recurrent vitreous haemorrhage and neovascular glaucoma in CRVO. In addition, **_VEGF causes increased capillary permeability (more leaky), which together with increased capillary hydrostatic pressure (from thrombotic occlusion of the central retinal vein)_**, leading to **_cystoid macula oedema_** which is the **_leading cause of visual loss in both ischaemic CRVO and non-ischaemic CRVO_** **_Retinal ischaemia also causes direct endothelial damage to retinal blood vessels, causing extravasation of blood --\> haemorrhages_** (\*\*Central retinal vein occlusion occurs secondary to **_atherosclerotic thickening of the central retinal artery_** **_compressing the central retinal vein at a common crossing point_**)

Answer 5

Pathophysiology of BRVO: * Common adventitia binds the branch retinal artery and the branch retinal vein together at the arteriovenous crossing. The artery lies anterior to the affected vein in 99% of eyes with BRVO * Thickening of the arterial wall compresses the vein underneath resulting in turbulence of flow, endothelial damage and thrombotic occlusion * **_\> 50% of BRVO cases occurs in the superotemporal quadrant_**

Answer 6

**_Non-ischaemic CRVO_** (**_more common_**; 75% of cases) - a milder type characterised by leaky retinal vessels with macular oedema **_Ischaemic CRVO_** (25% of cases) - a more severe type with closed-off small retinal blood vessels

Answer 7

Risk factors of CRVO: * **_Old age_** - \> 50% of cases occur in patients \> 65 yrs old * **_Cardiovascular disease_** - diabetes mellitus, HTN, hyperlipidaemia, smoking, alcohol - **_more common in elderly_** * **_Hypercoagulable state_** - thrombophilia, malignancy (myeloma, leukaemia), antiphospholipid syndrome, previous DVT, polycythaemia * **_Autoimmune disease_** e.g. SLE, sarcoidosis - **_more common in those \< 50 yrs old_** * **_Ophthalmic disease e.g. glaucoma_** * **_Infections e.g. syphilis_** * **_Drugs - COCP_**

Answer 8

Presentations: * **_Sudden unilateral painless visual loss or reduced visual acuity (a lot worse in ischaemic type)_** * **_RAPD_** * Fundoscopy shows: * **_Retinal haemorrhage - dot/blot and flame-shaped haemorrhages_** * **_Central retinal vein occlusion has a haemorrhage in all 4 quadrants (widespread)_** while in **_branch retinal vein occlusion it's more localised (e.g. affects one particular quadrant)_** * The retinal veins are less expandable compared to arteries, so they can rupture easily * **_Dilated tortuous retinal veins_** * **_Papilloedema (optic disc swelling)_** * **_Cystoid macula oedema_** - usually seen at late presentation * Often observed in Optical Coherence Tomography (OCT) * In addition to the above, findings suggestive of **_ischaemic CRVO_** include: * **_Cotton wool spots_** * **_Neovascularisation of the optic disc, fundus and iris_** as a result of chronic ischaemia --\> **_recurrent vitreous haemorrhage_** + **_neovascular glaucoma_**

Answer 9

The image on the left is a normal OCT The one of the right shows **_macula oedema_**

Answer 10

Ix: * CRVO is usually a **_clinical diagnosis_** - based on **_clinical features_**, **_fundoscopy findings_** and **_the presence of cardiovascular risk factors_** * If needed, the diagnosis can be confirmed using **_fluorescein angiography_**. A fluorescent dye is injected intravenously, the retinal vessels are then assessed through imaging to look for **_evidence of slowed flow or a filling defect_** * Bedside Ix: * Visual acuity * Colour vision * Test RAPD * Ocular tonometry to determine IOP - as glucoma is a risk factor * BP - as HTN is a risk factor * ECG - to rule out AF, ACS * AF can cause central retinal artery occlusion which in turn causes central retinal vein occlusion * Laboratory Ix: * FBC, ESR, CRP * Random blood glucose - as diabetes is a risk factor * Lipid profile - as hyperlipidaemia is a risk factor * Coagulation screen - as thrombophilia, polycythaemia, malignancy, antiphospholipid syndrome * Serum protein electrophoresis to rule out myeloma * Laboratory Ix for those \< 50 yrs old (where atherosclerosis is less likely) include: * Serum ACE to rule out sarcoidosis * Anticardiolipin, Lupus anticoagulant (LAC) - both are to rule out antiphospholipid syndrome * Autoantibodies: RF, ANA, ANCA, dsDNA * Thrombophilia screen: protein C and S, and factor V Laiden * Syphilis serology * Imaging * Not usually needed unless the patient has an atypical presentation or is \< 50 yrs old * CXR to look for sarcoidosis

Answer 11

Mx: * Treat underlying cause + optimise risk factors * Anti-VEGF injections to treat macular oedema * Laser therapy to treat neovascularisation of the fundus or iris

Answer 12

Permanent visual loss Cystoid macula oedema Recurrent vitreous haemorrhage Neovascular glaucoma

Answer 13

Retinal layers: There are **_10 distinct layers_** of the retina! **_From closest to farthest from the vitreous body_** * **_Inner limiting membrane_** * Basement membrane spanned by Muller cells (retinal glial cells) * **_Nerve fibre layer_** * Contains **_axons of ganglion cell bodies (= optic nerve fibres)_** * **_Ganglion cell layer_** * Contains **_cell bodies of ganglion cells_**, the axons of which become the optic nerve fibres , and some **_amacrine cells (inhibitory interneurons)_** * **_Inner plexiform layer_** * Contains the synapse between the bipolar cell axons and the dendrites of the ganglion and amacrine cells * **_Inner nuclear layer_** * Contains the **_cell bodies of the bipolar cells, amacrine cells and horizontal cells_** * **_Outer plexiform layer_** * Contains **_projections of rods and cones_**. They form synapses with the dendrites of the bipolar cells and horizontal cells * In the macular region, this layer of the retina is known as the Fibre layer of Henle * **_Outer nuclear layer_** * Contains **_cell bodies of rods and cones_** * **_External limiting membrane_** * A layer that separates the inner segment portions of the photoreceptors from their cell bodies * **_Inner segment/ outer segment layer_** * Inner segments and outer segments (contains light-sensing apparatus) of rods and cones * **_Retinal pigment epithelium_** * A single layer of cuboidal epithelial cells * This layer is **_closest to the choroid_**, and **_provides nourishment and supportive funvtions to the neural retina_** * Contains **_melanin_** (hence it's a "pigmented" layer) which is a black pigment that **_prevents light reflection throughout the eyeball_** - very **_important for clear vision_** In pre-clinical years, we were taught that the retina only has 2 layers - the inner neural layer and the outer pigmented layer. The outer pigmented layer is essentially the retinal pigment epithelium, and **_the inner neural layer includes all other layers except for the retinal pigment epithelium_**!

Answer 14

Remember, the retina is part of the CNS (part of the brain), and whenever information is delivered, it has to go through 3 neurons: Light hits: **_Photoreceptors (rods + cones)_** --\> **_bipolar cells_** --\> **_ganglion cells_** The axons of the ganglion cells converge to form the optic nerve. **_The axons coming from the nasal side of the retina (nasal fibres) decussate in the optic chiasm_**

Answer 15

See image!

Answer 16

Retinal detachment is an **_ophthalmic emergency_** caused by **_separation of the inner neurosensory retina from the underlying retinal pigment epithelium_**, which **_allows vitreous fluid to accumulate in the subretinal space_**. If left untreated, the fluid accumulation will cause **_further progressive retinal detachment_**, resulting in **_progressive loss of vision_** in the affected eye. If the retina in the macula starts detaching, you will start to lose central vision as well The retina is constantly supplied with blood by the choroid layer, so if it's not reattached ASAP, ischaemia of the retina occurs and subsequently infarction --\> **_permanent visual loss in the affected eye_**

Answer 17

There are 3 main types of retinal detachment: * **_Rhegmatogenous (most common)_** - your vitreous shrinks (becomes liquidifed) as part of the normal aging process. When it does that, it can pull the retina along with it, causing a retinal tear or break. Continued traction by the vitreous on the retina allows fluid to enter the subretinal space, causing retinal detachment * Most gradual **_posterior vitreous detachment (PVD)_** does not result in retinal detachment. However, in acute form the vitreous can suddenly come away from the retina causing retinal detachment! * **_Tractional_** * Most commonly seen in people with **_proliferative diabetic retinopathy_** * Diabetic retinopathy can result in fibrous scar tissue forming inside the vitreous and on the retinal surface. This scar tissue can then pull on the retina (traction) causing a retinal detachment! * Unlike the rhegmatogenous form, there is no retinal break! * Other causes include: * CRVO * Proliferative sickle cell retinopathy * Exudative (rare) * This is caused by leakage of fluid from the choroid vessels lying behind the retina into the subretinal space * Often due to inflammation of the choroid (**_posterior uveitis_**), malignancy (e.g. **_choroidal melanoma_** or **_ocular metastases_**), **_hypertensive choroidopathy_**, or **_iatrogenic (e.g. vitrectomy or laser treatment)_** * There are no hole or tear present

Answer 18

a) . Rhegmatogenous - due to posterior vitreous detachment (PVD) b) . Tractional - due to diabetic retinopathy c) . Exudative - due to posterior uveitis or choroidal melanoma

Answer 19

**_True_** - **_the incidence of retinal detachment increases with advancing age_** (**_60-70 yrs old_**) Rare in young people (tend to be the exudative type)

Answer 20

**_Myopia (short-sightedness)_** - increases the risk of PVD, and the peripheral retina maybe thinned making it more likely to tear! **_Trauma_** (e.g. a blow) directly to the eye Those who have **_already had a detachment in one eye_** - increases the risk of detachment in the other eye **_FHx_** of retinal detachment **_Previous cataract surgery_** - accelerates posterior vitreous detachment. It increases the risk of retinal detachment 9 fold! **_Poorly controlled diabetes (proliferative diabetic retinopathy)_** **_Inflammatory conditions e.g. uveitis, scleritis_** and those with spondyloarthropathies (e.g. ankylosing spondylitis) **_Malignancy e.g. choroidal melanoma or ocular metastasis_**

Answer 21

Presentations: 4 cardinal symptoms * **_Sudden unilateral painless progressive loss of vision_** - often described as a **_dark shadow_** which usually starts in the periphery and progresses towards the centre over hrs, days, or weeks as the detachment extends * If macula detaches --\> central visual loss * **_Blurring_** of the vision * **_Floaters (black dots)_** * Caused by bits of debris in the vitreous gel casting a shadow on your retina * Take many shapes e.g. black dots, rings, spiders' legs or cobwebs * Not a problem if the patient has had them for months or years. However, if the patient experiences a dramatic increase in the number of floaters or notice showers of dust-like floaters, this is bad! * **_Flashing lights_** in the periphery * They happen when the retina is stimulated by something within the eye rather than by light entering the eye. Often caused by the vitreous gel inside the eye moving across and pulling on the retina Signs * **_Reduced visual acuity (VA)_** * VA is normal if the macula is still attached (as you see things with the centre of your vision) * VA is severely impaired if the macula is detached * **_Peripheral visual field loss_** * If loss of central vision = macular detachment * If loss of peripheral vision = peripheral retinal detachment * **_RAPD_** * Fundoscopy findings show: * **_Asymmetric red reflex_** * In infants - white papillary reflex (leukocoria) or squint (strabismus) * **_Opaque translucent layer - detached retinal folds_** * **_Weiss ring_** (a large, ring-shaped floater that is sometimes seen if the vitreous body releases from the back of the eye) --\> **_posterior vitreous detachment_** * **_Vitreous haemorrhage_** * **_Retinal tears_** - actually appears as tears in a detached retina * **_Tobacco dust_** - caused by the retinal pigment epithelial cells releasing pigmented cells into the vitreous

Answer 22

Detached retinal fold --\> large retinal detachment (macula is spared)

Answer 23

Retinal tear!

Answer 24

**_Weiss ring_**--\> posterior vitreous detachment!

Answer 25

Tobacco dust --\> retinal detachment

Answer 26

Ix: * **_Clinical diagnosis_** based on clinical features and fundoscopy findings * Bedside Ix: * Visual acuity using Snellen chart * Ocular tonometry to measure IOP * Fundoscopy * If fundal view is very hazy --\> do a **_B-scan (USS of the eye)_** to visualise the fundus and rule out any retinal tears or detachments * B-scan ultrasonography is used to diagnose lesions of the posterior segment of the eyeball

Answer 27

Mx: * Primary care * **_Immediate same-day referral to an ophthalmologist if there are signs of sight-threatening disease e.g. visual field loss/ reduced VA, or fundoscopic signs of retinal detachment or vitreous haemorrhage_** * Urgent referral to an ophthalmologist to be seen within 24 hrs, if there is: * No visual field loss * No change in VA * No fundoscopic sign of retinal detachment or vitreous haemorrhage * Advise the person to contact the DVLA if they have a visual field defect and/or have had retinal treatment in both eyes * Advise on early warning signs of possible future retinal tear/ detachment and explain the need for immediate ophthalmology assessment * Surgery * **_Vitrectomy_** * A 'key-hole' procedure where the entry points are through the pars plana. The vitreous humour is then removed and replaced with either a gas bubble or clear silicone oil to hold the retina in place against the inside of the eye * **_Scleral buckle_** * Involves attaching a tiny piece of silicone sponge around the exterior aspect of the globe beneath the extraocular rectus muscles, causing the inside of the eye to slightly move inwards. This pushes the inside of the eye against the detached retina into a position that helps the retina to reattach. Cryotherapy or laser will then be used to seal the area around the globe * **_Tractional detachments require relief of the tractional elements through peeling off the epiretinal or subretinal membranes that give rise to the tractional forces_** * **_Exudative retinal detachments are managed non-surgically by treating the underlying cause_**

Answer 28

Vitreous haemorrhage is bleeding into the vitreous humor. It's one of the most common causes of **_sudden painless visual loss_**. Often the blood vessels affected are those formed due to \*\***_neovascularisation_**. These vessels are **_new brittle vessels_** prone to **_leaking_** or **_breaking_** in the event of a **_retinal tear_** or **_retinal detachment_**. Therefore, **_vitreous haemorrhage is often suggestive of other underlying pathology_**! Vitreous haemorrhage - think causes of neovascularisation!

Answer 29

Causes of vitreous haemorrhage (= causes of neovascularisation) Common causes: * **_Proliferative diabetic retinopathy (most common, \> 50%)_** * Posterior vitreous detachment/ retinal breaks/ retinal detachment * Trauma (most common in children and young adults) Less common causes: *

Answer 30

Presentations: Symptoms * **_Large bleeds --\> sudden unilateral painless visual loss or haze (most common)_** * **_Moderate bleeds --\> dark spots_** * **_Small bleeds --\> floats_** - often described as a "gush" of floaters * **_Blurred vision_** * If the vitreous humour is clouded or filled with blood, the vision will be impared * **_Red hue in the vision_** Signs * **_Decreased visual acuity_** * **_Visual field defect_** if severe haemorrhage * Fundoscopy findings: * Severe vitreous haemorrhage --\> **_hazy fundal view_**, **_absent red reflex_** * Moderate vitreous haemorrhage --\> **_partially obscured fundal view due to a localised vitreous haemorrhage_** * Chronic vitreous haemorrhage --\> **_yellow lesion_** - due to Hb breakdown forming bilirubin * Look for signs of underlying pathology: * Retinal tear/ detachment - opaque translucent layer, tobacco dust in the vitreous * Posterior vitreous detachment - Weiss ring * CRAO - cherry red spot

Answer 31

Ix: * **_Dilated fundoscopy_** - may show haemorrhage in vitreous cavity * **_Slit-lamp examination_** - shows RBCs in anterior vitreous * **_B-scan ultrasonography_** - to rule out retinal tear/ detachment and if haemorrhage obscures the retina * **_Fluorescein angiography_** - to identify neovascularisation * **_CT of the orbit_** if open globe injury/ laceration (penetrating/ perforating eye injury)

Answer 32

Mx: * **_Observation_** * **_A vitreous haemorrhage without a retinal tear or detachment often resolves within a couple of weeks_** * During this time - **_regular follow up_** to detect any retinal tears or detachment + **_give warning signs for retinal detachment_** e.g. flashing lights, floaters, changes in vision * **_Advise to avoid any heavy lifting_** - as an increase in BP may disrupt the clot and cause new active haemorrhage * **_Laser therapy (pan-retinal photocoagulation)_** - for **_proliferative diabetic retinopathy_** * It reduces the production of VEGF by reducing the oxygen demand from the retina * **_Surgery_** * For those with **_posterior vitreous detachment_** and a **_non-clearing vitreous haemorrhage lasting months_** or a retinal detachment

Answer 33

Age-related macular degeneration (AMD) is a **_progressive loss of central vision (i.e. affects the macula)_** associated with **_drusen formation_** and **_changes in the retinal pigment epithelium (hypo/hyperpigmentation)_**. It has \*\***_no obvious precipitating cause_** and it affects primarily in people **_aged 50 yrs and over_** (There is \*\***_no clear, defined cause of AMD_**. Instead, there is a multitude of lifestyle and environmental factors that contribute to the development of the disease in susceptible individuals)

Answer 34

2 types: * **_Dry macular degeneration (most common but better prognosis, 80% cases)_** * **_Non-exudative + Geographic atrophy_** * Geographic atrophy refers to **_regions of the retina where cells waste away and die_**. Sometimes these regions of atrophy look like a map to the doctor who is examining the retina with a fundoscope, hence the term geographic atrophy)**__** * Characterised by the presence of **_drusen (hard/ soft)_**, which are **_yellow round spots found between the RPE and the Bruch's membrane_** * **_Wet macular degeneration (less common but worst prognosis, 20% cases)_** * **_Exudative + neovascularisation_** * Characterised by **_choroidal neovascularisation_** * These new blood vessels extend through the Bruch's membrane and invade the space between the RPE and the Bruch's membrane, and also through the RPE into the subretinal space * These vessels are **_leaky and brittle_** --\> **_leakage of serous fluid and blood into the potential spaces_** --\> further separation between the RPE and Bruch's membrane, and further separation between the neural layer of the retina and the RPE --\> rapid vision loss (\*\***_Wet AMD almost always arise from dry AMD, so patients usually get dry AMD first before progressing to wet AMD_**)

Answer 35

a) . It's the **_leading cause of severe, irreversible vision loss in people over 55 yrs old in the developed world_** and the **_leading cause of blindness in the UK_**. Incidence and prevalence of AMD increase with age (average age of presentation is **_70 yrs old_**) b) . **_YES! AMD causes more cases of blindness than diabetic retinopathy_**! c) . **_AMD affects women slightly more_** and is more commonly seen in **_European_** people d) . **_Dry AMD is a lot more common (80% of cases). However, wet AMD is responsible for 90% of severe visual acuity loss_**!

Answer 36

Risk factors: _**\*Old age**_ _**\*FHx/ genetics**_ _**\*Northern European ancestry**_ _**\*Smoking (2-3 fold increased risk)**_ Co-morbidities e.g. cardiovascular disease, HTN, obesity, presence of AMD in the other eye Diet low in omega 3 and vitamins A, C, and E, high in saturated fats and cholesterol, and with a high glycaemic index Ocular characteristics - light iris (blue eyes), hyperopia (long-sighted)

Answer 37

**_Smoking_**!

Answer 38

In summary, the **_imbalance between the production of damaged cellular components and degradation leads to the accumulation of harmful products_**, for example, **_intracellular lipofuscin_** and **_extracellular drusen_** The retina is the most oxygen-consuming tissue in the body with a consumption level of 50% higher than the brain or kidneys. Most of this oxygen consumption occurs in photoreceptors (rods + cones) which are most abundant in the macula and fovea. This results in the accumulation of oxidative and photo-oxidative damage in the photoreceptors (esp in the macula) To get rid of the damaged parts, photoreceptors continuously renew their outer segment by shedding membranous disks (the portion that captures light in cone cells) in RPE. This daily cycle of renewal and shedding places a heavy metabolic burden on the underlying RPE cells, so over time, the phagolysosomes of RPE cells become overwhelmed and are unable to fully degrade these molecular debris, resulting in accumulation of sacs of molecular debris inside the RPE cells. These debris form lipid-protein aggregates called **_lipofuscin_**. As the person ages, more and more of these functionless lipofuscin residues accumulate, causing progressive engorgement of the RPE cells. This causes the RPE cells to excrete these aberrant materials into a potential space located between the Bruch's membrane and the RPE layer in the form of **_drusen_** (hard/ soft yellow deposits) * **_Hard drusen - small, hard, solid deposits_** * **_Soft drusen - larger soft deposits_** (Lipofuscin is intracellular while drusen is extracellular, both are made of the same materials) Dry AMD: As **_drusen_** builds up, they 'lift' the RPE away from the Bruch's membrane, causing hypoxia of the RPE and inflammation. Hypoxia of the RPE results in **_atrophy of choriocapillaries, RPE and photoreceptors_**, and also **_hypo/ hyper-pigmentation of the RPE_** * In advanced dry AMD, you get advanced map-like area of atrophy extends to foveal centre - this is called "**_geographic atrophy_**" Wet AMD: Inflammation attracts monocytes/ macrophages which releases VEGF-A. The VEGF-A, in turn, causes **_choroidal neovascularisation_**, which is the growth of new blood vessels that originate from the choroid through a break in the Bruch membrane into the sub-retinal pigment epithelium (sub-RPE). **_The presence of choroidal neovascularisation = wet AMD_** These new vessels are **_leaky and brittle_**, this causes fluid and blood to leak beneath and into the retina --\> **_exudation and haemorrhage_** --\> ischaemia and infarction of the macula --\> **_disciform scar formation_** over the macula --\> **_central vision loss (a scotoma)_**

Answer 39

Mainly 4 changes: * **_Drusen_** - collections of lipid material that accumulate in the space between the RPE and the bruch's membrane * **_RPE hypo-/ hyperpigmentation_** * **_Geographic atrophy_** * The areas of atrophy can enlarge over time and may or may not involve the fovea * **_Choroidal neovascularisation (= Wet AMD)_** * These blood vessels easily bleed or leak blood constituents, resulting in distortion and scarring (disciform scar) of the retina

Answer 40

AREDS classification: * **_No AMD_** * A few small drusen \< 63 micrometers in diameter, or none * **_Early AMD_** * Several small drusen, or * At least one medium drusen (63-124 microns), or * Mild pigmentary abnormalities * **_Intermediate AMD_** * Many medium drusen, or * At least one large drusen (\>/= 125 microns), or * Geographic atrophy not involving the fovea * **_Advanced AMD_** * Geographic atrophy at the fovea, or * Neovascular AMD

Answer 41

Presentations: * Patients typically present with a subacute onset of visual loss with: a reduction in visual acuity, particularly for near field objects difficulties in dark adaptation with an overall deterioration in vision at night fluctuations in visual disturbance which may vary significantly from day to day they may also suffer from photopsia, (a perception of flickering or flashing lights), and glare around objects

Answer 42

Diabetes can affect your eyes in a number of ways, thus it can manifest itself through several eye conditions, grouped under the term **_diabetic eye disease_**: * **_Swelling of the lens_** - the high sugar levels found in the fluid around the lens causes the lens to swell with more water than usual. The lens then focuses light differently on the retina at the back of the eye, this may cause your spectable prescription to be unstable * **_Cataracts_** - diabetes predisposes an individual with cataract at an early age * **_Glaucoma_** * **_Diabetic retinopathy_** * The **_most prevalent_** of these * Caused by **_damage to the microvasculature supplying the retina_**, leading to a progressive deterioration in vision and eventually blindness * **_Retinal artery/ vein occlusions_**, **_corneal problems_**, **_eye muscle problems_**, **_cranial nerve palsies_**

Answer 43

* It's the **_most common cause of blindness_** in the **_working-age_** demographic of the UK * **_Almost all patients with T1DM will have some degree of retinopathy within 20 yrs of diagnosis_** * Many patients with T2DM may already have some signs of retinopathy at diagnosis, after going through an asymptomatic period of hyperglycaemia

Answer 44

Chronic hyperglycaemia --\> weaken blood vessels that supply the retina --\> dilatation of the vessel walls --\> **_microaneurysms_** --\> rupture --\> **_small haemorrhages_** Damaged pericytes and erythrocytes increase vascular permeability, causing lipoproteins, lipids and other products that are carried by blood to leak out and cluster onto the retina as **_hard exudates_** As blood flow becomes increasingly compromised , regions of the retina become ischaemic. This hypoxia stimulates the release of inflammatory mediators such as **_vascular endothelial growth factors (VEGF)_** which promotes **_neovascularisation_** (the body's attempt to generate new blood vessels to supply blood to the ischaemic retina). However, these new vessels are **_poorly formed and brittle_** so they easily rupture causing **_bleeding_** --\> **_vi_****_treous haemorrhage_** --\> sudden painless visual loss or haze. In addition, these new blood vessels can form in areas that do not have them, for example the iris, causing **_rubeosis iridis_**. These new blood vessels can also grow into the angle of the eye and they have a surrounding contractile fibrovascular membrane that can cause the angle to be pulled closed by peripheral anterior synechiae --\> **_neovascular glaucoma (acute angle closure glaucoma secondary to neovascularisation)_** Along with the secondary angle closure, new leaky blood vessels promote **_secondary open-angle glaucoma_** and may cause blockage of the trabecular meshwork When the retina remains ischaemic for a long time, retinal tissues start to die and fibrosis takes place. **_The fibrous scar tissue that forms inside the vitreous and on the retinal surface can pull on the retina_**, causing a **_tractional type of retinal detachment_**!. It's most commonly seen in people with **_proliferative diabetic retinopathy_**

Answer 45

Risk factors: * **_Duration of poor diabetic control (i.e. length of exposure to hyperglycaemia)_** * The more time a patient's eye has been exposed to high blood sugars, the greater is the severity of diabetic retinopathy * **_Duration of diabetes_** * Patients who have had diabetes for a greater length of time are more likely to develop diabetic retinopathy * **_HTN_** * **_Hyperlipidaemia/ hypercholesterolaemia_** * **_Smoking_** * Ethnicity * Individuals with T2DM belonging to ethnic minority groups are more susceptible to developing diabetic retinopathy compared to those of Caucasian background * **_Diabetic nephropathy_** * Characterised by proteinuria * If present, it's a strong indicator that the patient will also have diabetic retinopathy * **_Pregnancy_** * **_Rapid improvement of blood sugar levels_** * Rapidly lowering blood sugar levels (a decrease of HbA1c \> 30 mmol/mol or 3 %) can increase the progression of diabetic retinopathy

Answer 46

Presentations: * **_Most are asymptomatic_**, even in the presence of proliferative disease. Most patients will only present after developing a clinically significant macular oedema (CSMO) or having a large vitreous haemorrhage * In those that are symptomatic: * **_Floaters_** - due to small haemorrhages obscuring areas of vision, usually self-resolving * **_Blurred vision and distortion_** - central vision maybe blurred if the macula is affected * **_Gradual painless reduction in visual acuity_** * **_Sudden unilateral painless visual loss_** if large haemorrhage * **_Permanent blindness_** as a result of tractional retinal detachment if left untreated

Answer 47

* **_Non-proliferative diabetic retinopathy (NPDR)_**, which is further subdivided into: * **_Background diabetic retinopathy_** * **_Pre-proliferative diabetic retinopathy_** * **_Proliferative diabetic retinopathy_** * **_Diabetic maculopathy/ diabetic macular oedema_**

Answer 48

The presence of 1 or more microaneurysm

Answer 49

**_Multiple microaneurysms_** **_Dot and blot haemorrhages_** **_Hard exudates_** Evidence of retinal ischaemia such as **_cotton wool spots_**, **_venous beading/ looping_**, **_arteriolar narrowing_**, and **_intraretinal microvascular abnormalities (IRMAs)_**

Answer 50

Remember the **_4-2-1 rule_**: **_Dot and blot haemorrhages and microaneurysms_** in **_4 quadrants_** **_Venous beading_** in at least **_2 quadrants_** **_IRMA_** in at least **_1 quadrant_**

Answer 51

**_Neovascularisation_** - new vessels on the disc (NVD) and/or new vessels elsewhere (NVE) **_Vitreous haemorrhage_** **_Tractional retinal detachment_** (due to fibrous tissues forming in the vitreous and on the retinal surface) \*Proliferative diabetic retinopathy is more common in **_T1DM_**, with 50% of patients going blind in 5 yrs

Answer 52

If the blood vessels near the macula are leaky, fluid can build up at the macula and cause macular swelling --\> **_macular oedema_**. As the macula is responsible for central vision, patient often complains of **_blurred vision_** when **_reading and writing_** or **_difficulty recognising faces in front of them_**. **_The colors will also appear washed out_**. In time, it may give you **_a blank patch in the middle of the vision_** DMO can be subcategorised into: * **_Focal/ diffuse macular oedema_** * The fluid that escapes from damaged vessels can be well-circumscribed (focal) or more widespread and poorly demarcated in nature (diffuse) * **_Ischaemic maculopathy_** * Patients will be **_symptomatic with defects in visual acuity_** due to ischaemia at the site of the macula * Best visualised with fluorescein angiography * **_Clinically significant macular oedema (CSMO)_** * _**\*Hard exudates**_, **_retinal thickening_** and **_microaneurysms_** found within a certain distance to the fovea or greater than a certain size \*DMO is more common in **_T2DM_** \*You are unlikely to be asked to identify DMO as it's hard to visualise using a direct ophthalmoscope!

Answer 53

a) . **_Proliferative diabetic retinopathy_** is more common in **_T1DM_** b) . **_Diabetic macular oedema (DMO)_** is more common in **_T2DM_**

Answer 54

Check **_HbA1c_** to assess how well or poorly a patient's diabetes is being controlled **_Optical Coherence Tomography (OCT)_** - more typically used when examining **_diabetic macular oedema_** to help quantify the levels of oedema and retinal thickness in the macula **_Fluorescein angiography (FA)_** - gold standard for **_visualising the vasculature_** of the retina

Answer 55

Mx: * Medical management * **_Glycaemic control_** - ensure blood sugar levels are well controlled will delay the progression of diabetic retinopathy. Aim for a HbA1c between 48-58 mmol/mol * **_BP control_** - aim to stabilise BP to \< 140/80 mmHg to help prevent progression of diabetic retinopathy * **_Diet, exercise and smoking cessation_** * **_Advise that they may not be able to drive or play sports_** * **_Photocoagulation_** to manage **_proliferative diabetic retinopathy_** and in some cases, severe non-proliferative diabetic retinopathy * **_Involves the use of a laser to create burns in the retina, thus destroying the photoreceptors_**. With fewer photoreceptors, oxygen demand in the retina decreases so endothelial cells release less VEGF, delaying the progression of diabetic retinopathy * 2 different methods of photocoagulation (see image) * **_Focal/ grid photocoagulation_** * **_Focal photocoagulation targets a specific point of leakage around the macula with laser_**, while **_grid photocoagulation targets more diffuse retinal thickening_** **_and oedema with no obvious point of leakage around the macula_**. * Complications - **_decreased acuity of central vision_**, paracentral scotoma, DMO may worsen * **_Pan-retinal photocoagulation (PRP) - more commonly used_** * **_The periphery of the retina is targeted_** with the aim of achieving a global reduction in oxygen demand. The macula (centre) is not treated * Complications - **_restricted peripheral vision_**, reduced night vision, eye pain, DMO may worsen * **_Intravitreal anti-VEGF/ corticosteroid injections_** * Aim at **_minimising neovascularisation_** and thus are used in **_proliferative diabetic retinopathy_** * Complications - cataract, raised IOP * **_Anti-VEGF injections are contraindicated in patients who have had a stroke or MI in the last 3 months_** * **_Vitrectomy_** if persistent vitreous haemorrhage or in central, sight-threatening tractional retinal detachment * Proliferative diabetic retinopathy can cause bleeding into the vitreous humour (vitreous haemorrhage), which further increases the risk of retinal detachment. I**_n most cases, waiting for the haemorrhage to settle can allow sufficient view to perform laser therapy_**. **_However, in persistent haemorrhage, a vitrectomy maybe performed_**. This allows the vitreous to be removed and repairing of any scarring/ retinal detachment

Answer 56

YESSSSSS! **_The NHS provides an annual eye screening programme for any individual \> 12 yrs old with diabetes_**

Answer 57

**_Neovascular glaucoma_** (a type of secondary angle closure glaucoma) --\> acutely painful red eye with visual loss **_Vitreous haemorrhage_** **_Tractional retinal detachment_**

Answer 58

If left untreated, half of patients with proliferative diabetic retinopathy will lose their vision within 2 years Around 90% of patients will have lost most of their vision within 10 yrs

Answer 59

Cotton wool spots, seen in pre-proliferative diabetic retinopathy

Answer 60

**_Diabetic macular oedema_** - you see **_hard exudates_** (waxy yellow lesions with relatively distinct margins arranged in clumps or rings, often surrounding leaking microaneurysms)

Answer 61

Diabetic macular oedema (DMO)

Answer 62

Pan-retinal photocoagulation (PRP)

Answer 63

A cataract is the opacification of the crystalline lens that affects vision and the leading cause of curable blindness worldwide

Answer 64

The lens is made of the capsule, epithelium, cortex and nucleus (see image). It has 2 functions primarily: refraction and accommodation reflex

Answer 65

The types of cataract depends on the location of the lens being affected: * **_Nuclear_** * The nucleus of the lens is affected * **_Common in old people_** * Slow progression * **_Cortical_** * The cortex of the lens is affected * Slow progression * **_Polar_** * **_Commonly inherited_** * **_Posterior subcapsular_** * Involves the subscapular cortex * Common in patients with **_diabetes_** and **_steroids use_** * **_Quicker progression_** compared to the others * **_Dot opacities_** * Common in normal lenses * Also seen in patients with **_diabetes_** and **_myotonic dystrophy_**

Answer 66

Causes/ risk factors: * Aging * Aging is the most common cause of cataract in adults \> 60 yrs old * Eye disease e.g. chronic uveitis, acute angle-closure glaucoma, high myopia, retinitis pigmentosa, scleritis, intraocular tumours * Trauma e.g. blunt/ penetrating injury to the eye, electric shock, exposure to radiation, a complication of eye surgery * Trauma is the most common cause of unilateral cataract in young people * Systemic disease e.g. diabetes mellitus, myotonic dystrophy, Neurofibromatosis type 2 (NF2), atopic dermatitis * Congenital and developmental cataract in children * Unilateral --\> usually idiopathic. Most cases are non-hereditary and children are otherwise well * Bilateral --\> mostly idiopathic but a cause can be identified in 40% of affected children. Causes include: * Hereditary cataracts (usually autosomal dominant) * Genetic syndromes e.g. Down syndrome, Edward syndrome, Marfan syndrome * Intrauterine infections (TORCH) * Metabolic disorders e.g. galactossaemia, hypocalcaemia, Wilson's disease, Lowe syndrome (AKA oculocerebrorenal syndrome) * Other risk factors: * Long-term steroid use * Cumulative lifetime exposure to UVB light * Asian * FHx * Female * HTN * Smoking

Answer 67

a) . More common as we age. \> 50% of people over 60 yrs old develop cataracts worldwide b) . Affects women more c) . YES! Cataract is the leading cause of curable blindness worldwide d) . YES! Cataract surgery is the most common elective surgical procedure in the UK

Answer 68

Prognosis: Adults * Without treatment --\> steady decline in visual acuity without any chance of recovery * With surgery --\> 95% people will have 6/12 best-corrected vision Children * Without treatment --\> deprivation amblyopia (lazy eye), which leads to serious lifelong visual impairment, even if the cataracts are removed when older * With surgery --\> prognosis can be unpredictable and varied * For congenital cataracts, a critical period for visual development occurs in the first 6 weeks of life, but performing congenital cataract surgery during infancy is associated with 30% risk of developing glaucoma

Answer 69

Presentations: Symptoms * Gradual and painless reduction in visual acuity * 'Myopic shift' - where there is an improvement in nearsightedness but deterioration in longsightedness, due to the effect of the opacity on refractive power of the lens * Blurred vision * Poor night vision (difficulty seeing at night) * Difficulty reading texts * Sensitivity to lights and glare i.e. lights appear brighter than normal * Haloes around lights and double vision in a single eye * Polyopia (seeing multiple images) * Gradual reduction in colour intensity, esp blue light * Difficulty recognising faces * Problems watching TV * Frequent changes of glasses prescription as a result of cataracts developing Signs * Reduced VA (tested by Snellen chart) * Loss of red reflex or a white pupil (leukocoria) * Nystagmus * Squint (stabismus)

Answer 70

Refractive error Corneal disease e.g. Fuch's endothelial dystrophy (where there is gradual loss of corneal endothelial cells and increasing oedema of the cornea) Presbyopia Age-related macular degeneration Primary open angle glaucoma Chronic uveitis Diabetic maculopathy Diabetic retinopathy Drugs e.g. chloroquine, hydroxychloroquine, isoniazid, tetracycline, ethambutol, methanol Retinoblastoma Optic neuritis

Answer 71

Ix: * Clinical diagnosis with a direct ophthalmoscope or slit lamp * Refer the patient to an optometrist/ ophthalmologist for further assessment using a slit-lamp. This is to confirm the diagnosis of cataract, the type and exclude other causes of visual loss! * Non-urgent referral if adult * URGENT referral if children * Findings: * Opacity of the lens indicating cataract * Loss of red reflex * Obscuration of eye details * IOP measurement to rule out glaucoma * A glare vision test * Examine for squint (stabismus) in children

Answer 72

Mx: * **_Non-surgical_** * In early stages, age-related cataracts can be managed conservatively by prescribing stronger glasses/ contact lenses, or by encouraging the use of birghter lighting. This will help optimise vision but do not actually slow down the progression of cataracts * **_Surgery (definitive management)_** * Involves removing the diseased lens and replacing it with an artificial one * NICE suggests that referral for surgery should be based on whether a visual impairment is present, impact on quality of life (or activities of daily living), and patient choices (NEVER RATIONED ON THE BASIS OF VISUAL ACUITY ALONE!). Also, whether both eyes are affected and the possible risks and benefits of the surgery should be taken into account as well * 2 main techniques: * Phacoemulsification * Standard extracapsular cataract extraction surgery * Advice * Advise all drivers that they must meet the following standards of visual acuity: * In good daylight be able to read a modern vehicle number plate at a distance of 20 m * Visual acuity must be at least Snellen 6/12 with both eyes open or in the only eye if monocular * Advise that Group 2 bus and lorry drivers require a higher standard of VA: * A visual acuity of at least: * Snellen 6/7.5 in the better eye * Snellen 6/60 in the poorer eye

Answer 73

Complications: * Immediate * Posterior capsule rupture (most common intraoperative complication) * Endophthalmitis * Corneal oedema * Cystoid macular oedema * Malposition/ dislocation of the lens * Raised IOP * Toxic anterior segment syndrome * Haemorrhagic occlusive retinal vasculitis (HORV) * Delayed * Posterior capsular opacification (most common post-operative complication) * Due to proliferation of remnants of lens epithelial cells, forming a opague membrane on the back of the artifical lens. This membrane causes decreased VA, blurred vision or glare * Occurs gradually over months or years after surgery * **_Treated with laser_**! * Retinal detachment * Macular degeneration

Vision loss Flashcards

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