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Peripheral fundus & its disorders
Peripheral fundus & its disorders Presented by Dr Rohit Rao This document summarizes the key anatomical structures and pathologies of the peripheral retina. It describes the ora serrata, pars plana, vitreous base, dentate processes, meridional folds, and other peripheral features. It then discusses various degenerative conditions like lattice degeneration, retinoschisis, and pavingstone degeneration. Treatment options for retinal breaks including cryopexy and laser photocoagulation are also summarized.
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Peripheral fundus & its disorders
- 1. Peripheral fundus &its disorders Presented by Dr Rohit Rao
- 2. References • Peripheral OcularFundus 3rd edition by William L. Jones • Ophthalmology 3rd edition.by Yanoff, Duker • Clinical ophthalmology 7th Edition - Jack Kanski • Wolff's Anatomy of the Eye and Orbit 8th by Bron, Tripathi. • Retina by Stephen.J .Ryan
- 3. Retina Optic Disc Peripheral Retina OraSerrata Area Centralis Perifoveal Parafoveal Fovea Foveola
- 4. Near Periphery: 1.5mm AroundArea Centralis Periphera Retina Mid Periphery: 3mm Wide Zone Around Near Periphery Far Periphery: Extendes From Optic Dics, 9-10mm Temoprally & 16mm Nasally
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- 6. Pars plana • Ciliarybody starts 1 mm from the limbus and extends posteriorly for about 6 mm. • First 2 mm pars plicata and 4 mm pars plana. • Width is about 4.0-4.5 mm.
- 7. Vitreous base • Vitreousbase is a 3–4 mm wide zone straddling the ora serrata. • Vitreous is strongly attached at base, so that following PVD, posterior hyaloids face remains intact. • Pre-existing retinal holes within the vitreous base do not lead to RD. • Severe blunt trauma may cause tearing of nonpigmented epithelium of pars plana & of retina.
- 9. Ora Serrata • Retinabecomes opalescent and often is marked by small rows of cystoid cavities. • Extensive cystoid changes do not represent pathology. • Neural retina stops abruptly at ora serrata and is continued by nonpigmented ciliary epithelium • Pars plana is more deeply pigmented, so choroidal pattern not seen.
- 11. 0.7-0.8 mm N 2.1 mm 7.0 mm T N 6.0mm 7.0 mm 7.0 mm T
- 12. • Dentate processesare teeth-like extensions of retina onto the pars plana. • Oral bays are the scalloped edges of the pars plana epithelium in between the dentate processes. • Enclosed oral bay is a small island of pars plana surrounded by retina as a result of meeting of two adjacent dentate processes. ▫ Not be mistaken for a retinal hole • Granular tissue characterized by multiple white opacities within the vitreous base ▫ Can be mistaken for small peripheral opercula.
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- 14. Meridional fold • Smallradial fold of thickened retinal tissue in line with a dentate process, • It bigns at ora serrata and runs posteriorly & perpendicularly to it in a meridional fashion • Superonasal quadrant . • Small retinal hole at its apex • Found in approximately 20% of all eyes • Meridional complex is composed of an enlarged dentate and ciliary process associated with a meridional fold
- 15. • Vitreous tractionon meridional folds and complexes may result in the formation of retinal breaks. • Meridional folds are not a common cause of RD, may be because these are found at vitreous base. • Because of anterior location , cryopexy is
- 17. Pars plana cyst •Pars plana cysts are clear cystoid spaces between the pigmented and nonpigmented epithelia. • Scleral depression • Fluid contains hyaluronic acid. • Mostly acquired; few are congenital. • idiopathic or secondary to ocular disease. ▫ Retinal detachment, may be the result of traction by the shrinking vitreous base. ▫ Posterior uveitis. ▫ Multiple myeloma
- 19. Congenital Hypertrophy ofthe Retinal Pigment Epithelium • Common benign lesion. • Congenital and not a degenerative condition. • Flat round or oval lesion, well defined, dark grey or black in colour and up to three disc diameters in size. • Outer retina change and does not affect the vitreo-retinal interface; so does not predispose to RD. • Can lose pigment over time
- 20. • When occurin groups, known as bear track, Familial Adenomatous Polyposis.
- 23. Pavingstone(Cobblestone degeneration or ChorioretinalAtrophy) • 25% of the population • Well defined yellow white patches between the equator and the ora serrata. • Absence of the outer layers of the retina, in particular the choroid, which permits an uninterrupted view of the sclera. • Congenital and not be considered a degeneration. • No predisposition to break formation
- 26. Microcystoid degeneration • Tinyvesicles with indistinct boundaries. • Always starts adjacent to ora serrata and extends circumferentially and posteriorly with a smooth undulating posterior border. • Present in all adult eyes, • Increasing in severity with age • Although it may give rise to retinoschisis. • Do not give rise to RD
- 28. Honeycomb (reticular) degeneration •Age-related change • Fine network of perivascular pigmentation which may extend posterior to equator. • Caused by RPE degeneration • More prominent in nasal quadrant
- 29. Snowflake Vitreoretinal Degeneration •Snowflake vitreoretinal degeneration appears as tiny yellow-white spots in the far peripheral retina • Superior temporal quadrant • Lattice degeneration • Vitreous shows fibrillar degeneration & liquefaction.
- 31. Lattice degeneration • • • • • • • • • • An Areawith Absence of ILM Overlying Area of Liquefied Vitreous Condensation & Adherence of Vit Gel Inner Retinal Layer Atrophy More common superiorly Arranged parallel to the ora serrata. Incidence- 8% to 10% RRD :: Lattice account for 20% Symmetric and bilateral, Horse shoe Tears &Atrophic holes
- 34. Complications (A) Atypical radial lattice without breaks; (B)U-tears (C) Linear tear along posterior margin. (D) multiple small holes within islands of lattice
- 35. Management of LatticeDegeneration • • • • Lattice without Retinal Breaks - No Rx Lattice with Atrophic Holes - No Rx Lattice + Holes+ Sub clinical RD – Treat Lattice+ Traction Tear - Treat : If Fellow eye has RD,Strong Family History of RD,Aphakic Eyes • Asymptomatic Traction Tear - No Rx • Acute Symptomatic Tears - Treat in Phakics & Aphakics
- 36. Vitreoretinal Tufts • SmallPeripheral Retinal Elevation • Focal Vitreous Traction • Operculated or flap tears when strong vitreous traction is applied • Rarely cause retinal detachments. • Treatment is rarely indicated • Cryopexy or photocoagulation.
- 38. Snailtrack degeneration • Snailtrackdegeneration is characterized by sharply demarcated bands of tightly packed ‘snowflakes’ which give the peripheral retina a white frost-like appearance. • Longer than in lattice degeneration • Overlying vitreous liquefaction.
- 40. Degenerative retinoschisis • 5%of the population over the age of 20 years and is particularly prevalent in hypermetropes. • Bilateral • Coalescence of cystic lesions • Results in separation or splitting of the NSR into an inner (vitreous) layer and an outer (choroidal).
- 41. • Typical retinoschisissplit is in outer plexiform layer, • Reticular retinoschisis, less common, splitting occurs at level of NFL. • Early retinoschisis seen in inferotemporal with a smooth immobile elevation of retina. • Progress circumferentially • Snowflakes , sheathing or ‘silver-wiring’ of blood vessels. • Microaneurysms and small telangiectases , • Complications are very rare, • Breaks, RD in the presence of PVD, Vitreous haemorrhage
- 44. White with pressure •Translucent grey appearance of the retina, induced by indention. • It does not move when indenter is moved. • Normal eyes and may have abnormally strong vitreous attachment. • It is also observed along the posterior border of islands of lattice degeneration, snailtrack degeneration and the outer layer of acquired retinoschisis.
- 46. White without pressure •Has the same appearance but is present without scleral indentation. • May be mistaken for a flat retinal hole. • Giant tears occasionally develop along the posterior border of ‘white without pressure’. • For this reason, if ‘white without pressure’ is found in the fellow eye of a patient with a spontaneous giant retinal tear, prophylactic therapy should be performed. • It is advisable to treat all fellow eyes of non-traumatic giant retinal tears prophylactically by 360° cryotherapy or indirect argon laser photocoagulation, irrespective of the presence of ‘white without pressure’, if they have not developed a PVD.
- 48. TREATMENT • Upon thediscovery of a retinal break, the initial decision is whether the benefits of treatment (to prevent retinal detachment) outweigh the risks and cost of treatment • The factors under consideration in each case include ▫ ▫ ▫ ▫ ▫ ▫ Presence or absence of symptoms; Age and systemic health of the patient; Refractive error of the eye; Location, age, type, and size of the break; Status of the fellow eye; Whether the patient is aphakic, pseudophakic, or will soon undergo cataract surgery
- 49. • Retinopexy • Cryopexyand laser photocoagulation. • Cryotherapy ▫ Delivered transconjunctivally. ▫ It destroys the choriocapillaris, RPE, and outer retina to provide a chorioretinal adhesion ▫ It is not immediate; 1 week for partial adhesion and up to 3 weeks for the complete. • Laser photocoagulation ▫ Argon green, argon blue-green, krypton red, or diode laser. ▫ Slit lamp and the indirect ophthalmoscope. ▫ Instant, but maximal adhesion occurs 7–10 days later.
- 50. • Cryopexy hasthe advantage of not requiring clear media • In general, retinal cryopexy and indirect ophthalmoscopic laser photocoagulation are preferred for anterior retinal breaks • Similarly, posterior breaks managed with the slit lamp or an indirect laser delivery system. • Retinal tear with persistent traction and recurrent vitreous Hemorrhage requires scleral buckling or vitrectomy
- 51. Cryopexy • Indirect ophthalmoscopicvisualization, • Cryoprobe is placed on the conjunctiva that overlies the break until the retina adjacent to the tear becomes gray-white. • Approximately 2 mm of retinal whitening around the entire break • Multiple applications are placed until the break is surrounded completely with confluent treatment. • Do not to treat the choroid and RPE directly beneath the break, can lead to macular pucker and proliferative vitreoretinopathy.
- 52. Photocoagulation • Goldmann three-mirrorlens or panfundoscope lens with the slit-lamp delivery system. • Tear should be surrounded completely by three to four rows of laser burns. • Settings are 200–500 mm spot size and 0.1–0.2 seconds • Indirect laser delivery system can also be used • Advantage is simultaneous scleral depression allows treatment of anterior tears and even dialysis.
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