Retina And Its Pathology PDF

Retina and its Very important to know: OSCE: OCT ⭐ ⭐ pathology DMR , stages ,presentation and management *New notes added on BLUE Dr. ABDULAZIZ M. AL- HADLAQ...

Retina and its Very important to know: OSCE: OCT ⭐ ⭐ pathology DMR , stages ,presentation and management *New notes added on BLUE Dr. ABDULAZIZ M. AL- HADLAQ Good luck ASSISTANT PROFESSOR QUMED 38 – Batch A Lecture Notes Team QASSIUM UNIVERSITY Notes by Ferial Ali The Retina:  It is neural transparent multilayered highly specialized sensory tissue.  Absorbs the light and transforms it into electrical impulses that are transmitted throughout the optic nerve toward the brain.  Originating embryologically from the neuro-ectoderm.  Extends from the optic nerve until the ora serrata anteriorly.  Formed mainly by two layers (neural layer & retinal pigment epithelium layer).  Visual and non-visual neural cells. Horizontal & Amacrine cells The photoreceptors “ rods and cones” , bipolar & ganglion cells  The globe of the eye has 3 main layers, from outermost to innermost: Tunica Fibrosa: Sclera & Cornea. Fibrous layer for protection & refraction. Anatomy Tunica Vasculosa: Uvea. Choroid + Ciliary body + Iris. Vascular pigmented layer for nutrition & reduction of retinal damage by absorbing light. Tunica Nervosa: Retina. Neurosensory layer for visual perception. From neuroectoderm. Cannot regenerate. Regarding refraction; anything in the path of the visual axis must be crystal clear. e.g. Ptosis can cover the cornea & modify its shape; this can lead to amblyopia or astigmatism. Remember that amblyopia has 3 main causes: Strabismic (misaligned eyes) Refractive (anisometropia) Deprivational (e.g. due to ptosis, cataracts etc.) (These couple of points outside the green box aren’t directly related to the retina but the doc mentioned them anyway.) ! The sharpest area that sense absorbs the lights ? The fovea centralis at the macula because it’s the thinnest area. -So the retina is divided into two parts: 1)Macula 6mm in diameter, Extends from the optic nerve temporally, in the macula there’s the fovea 1.5mm & inside it the foveola. 2)Extra-macular Histology Light enters Light enters the eye and reaches the retina. Photoreceptors at the back of the retina convert light into action potential signals.  h Retina ganglion cells receive the signals from photoreceptors, then transmit the visual information via axons through the optic nerve to the lateral geniculate nucleus of the thalamus. Contains bipolar, horizontal and amacrine cells. Photoreceptor layer; rods and cones. Between the pigmented epithelium and the neural layer is a potential space; there are no tight junctions between these two layers. Associated with retinal detachment. Histology  Differences b/w ROD & CONES Rods Cones Responsible for night vision (B&W). Responsible for sharp vision (good visual acuity) and color vision (RGB). Cannot detect color. Poor sensitivity in the dark (hence why Affected in retinitis pigmentosa → colors are perceived to be dimmer in night blindness. the dark). Less concentrated around the macula Affected in color blindness. and more around the periphery. More concentrated around the macula.  Retinal Disorders;  1-Vascular disease. DM is the commonest cause  2-Degenerative disease.  3-Congenital disease.  4-Neoplastic disease. Diabetic retinopathy Is it necessary that every diabetic will have retinopathy? No only around 15%-20% of them have the risk.  Progressive dysfunction of the retinal blood vessels caused by chronic hyperglycemia.  DR can be a complication of type 1 or type 2 diabetes.  Initially, DR is asymptomatic. If not treated, it can cause low vision and blindness. That’s why screening is important Risk factors for severity: Most important risk factor  Duration of diabetes May be asymptomatic in the first 5-10 years.  Poor blood sugar control  HTN  Hyperlipidemia Especially hypertriglyceridemia.  Barriers to care Poor screening protocols, lack of follow-up etc. Pathophysiology:  Diabetic Retinopathy is a microvasculopathy that causes:  a) Retinal capillary occlusion  b) Retinal capillary leakage  Stages: The difference between the two stages is the growth of new vessels May be mild, moderate, severe or very severe non-proliferative DR.  Non-proliferative diabetic retinopathy: (diabetic macular edema) Can lead to May be early, high-risk or advanced proliferative DR.  Proliferative diabetic retinopathy: (vitreous hemorrhage, tractional retinal detatchment) Where the Neovascularization occur? On the surface of the retina: -neovascularization of disc (NVD) -neovascularization elsewhere (NVE) Or in more worse complication, the neovascularization can be seen in the iris (NVI or rubeosis iridis) this is bad because it can lead to neovascular glaucoma.  Golden reflection in the retina > Retinal exudate Dot blot hemorrhage & Macular edema Neovascularization on the disc (NVD) Non-proliferative diabetic retinopathy (Left eye) Neovascularization elsewhere (NVE) Fundus appearance  Normal The fovea is located temporal and inferior to the optic nerve. Diabetic retinopathy  Dot blot hemorrhage. Dot plot hge= Retinal (non-proliverative) Large obscuring hge= Pre-retinal (proliferative)  Hard exudates.  Microaneurysm. Hard exudate Earliest sign of DR. If alone: mild non-proliferative DR.  Macular edema. Dot blot hemorrhage Detected via optical coherence tomography. Main complaint in non-proliferation DR OSCE Identify? Optical coherence tomography What’s the abnormality? Macular edema Causes? Diabetic retinopathy. (a): Disappearance of edema after anti-VEGF treatment. Optical coherence tomography  Picture showing OCT of the macula (c) cystoid macular edema with sub retinal fluid.  (b) Less sub retinal fluid after receiving intravitreal anti VEGF injection.  (a) Improved cystoid macular edema with disappearance of subretinal fluid. Macular edema occurs due to increased permeability of retinal capillaries. (Diabetic retinopathy → retinal ischemia → increased vascular endothelial growth factor → neovascularization & increased capillary permeability → leakage → edema) Anti-VEGF inhibits this process. (c) & (b): Cystic fluid-filled spaces within the retina.  Proliferative DR The macula is obscured by large hemorrhage (pre-retinal) Fibrosis This is early PDR (no fibrosis/membranes), all the white dots are laser “Pan-retinal photocoagulation” Advanced stage. *Both photos show fibrosis all over the retina, Is it proliferative or non? It’s sever form of proliferative DR, the whitish membranes are proliferation.  Vitreous hemorrhage.  Tractional retinal detachment. Traction membrane OCT - skipped  Treatment options: For NPDR: Surgical treatment 1. Control the diabetes 2. If there’s macular edema➡ intravitreal anti-VEGF injection. For PDR: 1. Early stages: Pan-retinal photocoagulation laser (PRP laser). 2. Advanced stages: Surgery -no need to know its name- For tractional retinal detachment, combined detachment, vitreous hemorrhage:  Pars plana vitrectomy + membrane peeling + endolaser.  RECOMMENDED EYE EXAMINATION SCHEDULE Diabetic Eye Disease Patient type 2 DM without DR what you will do for him ? Follow up annually Key Points Recommended Time of Diabetes Type Recommended Follow-up* First Examination Type 1 3-5 years after diagnosis. Yearly. Type 2 At time of diagnosis. Yearly. Treatments exist butNowork retinopathy to mild moderate NPDR: every 3-12 months. Prior to pregnancy best Prior before to conception vision and early in is lost (type 1 or type 2) the first trimester. Severe NPDR or worse: every 1-3 months. Treatment  Prevention. Especially controlling blood glucose.  Laser photocoagulation. PDR cases  Intravitreal injections of anti vascular endothelial growth factors. e.g. Avastin (bevacizumab), Lucentis (ranibizumab), Eylea (aflibercept). Intravitreal steroid injections may also be used.  Surgical intervention. For traction detachment brosis and vitreous hemorrhage Hypertensive retinopathy;  Clinical term that refers to the funduscopic signs that is presents with the patient who has hypertension.  Microvascular process that leads to the following vascular changes:  1- Vasoconstrictive phase.  2- Exudative phase.  3- Sclerotic phase.  Hypertensive changes without arteriosclerotic changes in case of secondery hypertension (e.g. pregancy induced). e.g. preeclampsia & eclampsia  Hypertensive retinopathy; Ocular findings: May be associated with:  Arteriolar narrowing & A-V nicking  Branch retinal artery occlusion (BRAO)  Cotton wool spots  Branch retinal vein occlusion (BRVO)  Retinal hemorrhages  Central retinal vein occlusion (CRVO), results in neovascular glaucoma  Optic nerve swelling (edema) Main presentation of hypertensive emergencies (acute HTN).  Retinal artery macro aneurysm (RAMA) Seen in chronic HTN.  Retinal ischemia & neovascularization  PT present with: 1-sudden painless loss of vision Hypertensive retinopathy; 2-clear red re ex If HT not control >>> blindness Q: Old PT with hypertension present to your clinic with painless loss of vision , the red re ex is bright re ex the fundus ( as you see in pictures below) CRVO BRVO RUPTURED macro aneurysm Sectoral hemorrhage 8 Central retinal vein occlusion; entire retina is Branch retinal vein occlusion; wedge-shaped Nerve ber infarction Pathognomic for hypertensive retinopathy. affected, hemorrhaging all over. hemorrhaging area. (Not in DMR) Treatment ;  Multidisciplinary action.  Retinal Vein occlusion; Hemorrhage Sectoral hemorrhage ( hypertension Patient) Retinal hemorrhage  Retinal artery occlusion; Whitish area Sectoral Whitish area Sectoral Whitish area secondary o To thrombosis ,embolised retinal artery Could be with : 1-HT patient 2- brillation patient  RheuGMATOGENOUS retinal Only de nition detachment RRD  BY DEFINITION : RETINAL BREAK + SUBRETINAL FLUID..  CLINICAL PRESENTATION : FLAOTERS  TTT: SURGERY Retinal tear Detachment between neurosensory retina and retinal pigment epithelium There is no tight junction between them>>> easy detachment RETINAL BREAKS Read it quickly  PERIPHEARL RETINAL BREAKS  PRESENTED WITH FLOATERS AND NO SUBRETINAL FLUID FTMH What is the image technique? OCT Upright re ex  TRAUMATIC VS AGE RELATED.. Management : surgical intervention O VITREOUS HGE  DIABETIC , TRAUMATIC, PVD RELATED Large hemorrhage obscuring the retinal detalis > pre-retinal hemorrhage Macular Degeneration: No details  Group of disease involving the photoreceptor layer resulting in progressive loss of their function without abnormal subretinal vascularization Fundus fluorescein angiography to visualize blood vessels.  As diagnostic tool OCT, FFA were crucial in that Optical coherence tomography for macular imaging.  Treatment: amsler grid, multivitamins, intravitreal injections of Anti-VEGF, PDT. Photodynamic therapy Retinal detachment : Know it in details  Detachment of the neurosensory retina from the underlying retinal pigmented epithelium.  Divided into: Rhegmatogenoius, Tractional, Exudative. (A) Rhegmatogenous: Most common type. Break or tear in retina → vitreous humor gets behind retina → retinal detachment. (B) Tractional: Scar tissue pulls retina away → retinal detachment. (C) Exudative: Fluid builds up behind retina → retinal detachment.  Risk factors: high myopia, trauma, PVD, ocular surgery. Post-vitreous detachment  Treatment depends on the type and the cause. (pars plana vitrectomy, scleral buckle, pneumatic retinopexy) Rhegmatogenous retinal detachment. (look at the tear) Scleral buckle for rhegmatogenous retinal detachment. The buckle is secured around the eyeball, moving the wall of the eye closer to the detached retina. This allows the fluid under the retina to be pumped out, and the retina to reattach. Cryotherapy is also used to form a permanent adhesion around the tear and prevent reaccumulation of fluid and re-detachment. Retinitis Pigmentosa  Defined as a progressive bilateral retinal dystrophy. Affecting rod cells.  Inherited vs sporadic.  The cardinal features are: night blindness, nyctalopia  Clinically presented with bilateral diffuse retinal pigmentation along the blood vessels with retinal vascular atrophy with pale optic disc.  Treated with refraction, low vision aid, retinal implants, genetic counseling.  Advance stage  Pigmented bone spicules.  Attenuated blood vessels.  Pale disc Thank you