RETINAL DETACHMENT.pptxRetinal detachment is the separation of the neurosensory retina from the underlying retinal pigment epithelium.

Retinal detachment is the separation of the neurosensory retina from the underlying retinal pigment epithelium. It causes sudden, painless vision loss, flashes of light, or floaters. Common causes include trauma, high myopia, or retinal tears, requiring urgent surgical treatment.

1. RETINAL DETACHMENT

2. REFERRENCES Ryan’s Retina - Seventh Edition Kanski’s Clinical Ophthalmology - A Systematic Approach - Ninth Edition Ophthalmology - Sixth Edition, 2023, by Myron Yanoff and Jay S. Duker

3. SCOPE ANATOMY INTRODUCTION TYPES LOCATION RHEGMATOGENOUS TRACTIONAL EXUDATIVE

4. MICROSCOPIC STRUCTURE OF RETINA Retinal pigment epithelium Layer of rods and cones External limiting membrane Outer nuclear layer Outer plexiform layer Inner nuclear layer Inner plexiform layer Ganglion cell layer Nerve fibre layer Internal limiting membrane

5. ANATOMY OF PERIPHERAL RETINA PARS PLANA Ciliary body starts 1mm from limbus – extends posteriorly for 6mm 2mm – pars plicata 4mm – pars plana Pars plana surgical incision/ intravitreal injection – 4mm from limbus in phakic eyes 3.5mm from limbus in pseudophakic eyes 3mm from limbus in aphakia

6. ORA SERRATA Junction between retina and ciliary body Dentate process – teeth like extensions of retina onto pars plana – more marked nasally Oral bays – scalloped edges of pars plana epithelium in between dentate processes Meridonial fold – small radial fold of thickened retinal tissue in line with dentate process – superonasal quadrant, may exhibit a small retinal hole at its apex Enclosed oral bays – small islands of pars plana surrounded by retina as a result of meeting of two adjacent dentate processes

7. VITREOUS BASE Strongest adhesion of vitreous 3-4 mm wide zone straddling ora serrata Cortical vitreous is strongly attached Severe blunt trauma – avulsion of vitreous base

8. SITES OF VITREOUS ADHESION Physiological Vitreous base(very strong) Optic disc margins (fairly strong) Perifoveal (fairly weak) Peripheral blood vessels (weak)

9. ABNORMAL VITREOUS ADHESIONS Associated with retinal tear formation – dynamic vitreoretinal traction associated with acute PVD Posterior border of islands of lattice degeneration Retinal pigment clumps Peripheral paravascular condensations Vitreous base anomalies White with pressure and white without pressure

10. VITREORETINAL TRACTION Force exerted on retina by structures originating in vitreous Dynamic traction – induced by eye movements – centripetal force towards vitreous cavity – pathogenesis of retinal tears and rhegmatogenous RD Static traction – independent of ocular movements – pathogenesis of tractional RD and proliferative vitreoretinopathy

11. WHAT KEEPS RETINA ATTACHED? Active mechanisms Retinal pigment epithelial sheaths Retinal pigment epithelial pumps Passive mechanisms Inter photoreceptor matrix Mechanical interdigitation between RPE microvilli and tips of OS of photoreceptors Hydrostatic pressure Osmotic pressure of choroid Vitreous support

12. RETINAL DETACHMENT Separation of inner neurosensory retina from retinal pigment epithelium (RPE)

13. Based on tractional component

14. TYPES Rhegmatogenous RD – spontaneous retinal break, full-thickness defect in sensory retina, which allows fluid to enter subretinal space Tractional RD – NSR is pulled away from RPE by contracting vitreoretinal membrane in absence of retinal break Exudative RD – retinal or choroidal conditions that disturbs RPE outer retinal barrier  accumulation of fluid in the subretinal space without traction or full thickness retinal breaks Combined tractional-rhegmatogenous RD – retinal break is caused by traction from an adjacent area of fibrovascular proliferation Subclinical RD - an asymptomatic break surrounded by a relatively small amount of SRF, extending further than one-disc diameter away from the edge of the break but less than two disc diameters posterior to the equator

15. LOCATION Oral breaks – within vitreous base Post oral breaks – between posterior border of vitreous base and equator Equatorial breaks – at or near equator Post-equatorial breaks – behind equator Macular breaks – fovea

16. FUNDUS DIAGRAM Detached retina – blue , flat retina – red Retinal breaks – drawn in red with blue outlines Flat part of retinal tear – blue Thin retina – red hatching outlined in blue Lattice degeneration – blue hatching outlined in blue Retinal pigment – black Retinal exudates – yellow , vitreous opacities – green

17. FINDING THE PRIMARY BREAK Primary break – responsible for RD Distribution of breaks in eyes with RD 60% in upper temporal quadrant 15% in upper nasal quadrant 15% in lower temporal quadrant 10% in lower nasal quadrant Upper temporal quadrant – most common site for retinal break formation 50% RD – more than one break – located within 90° of each other

18. Configuration of SRF SRF spread is governed by (a) gravity (b) by anatomical limits ( ora serrata and optic nerve) (c) the location of the primary retinal break Primary break located superiorly – SRF first spreads inferiorly on same side as break and then spreads superiorly on opposite side

19. MODIFIED LINCOFF’S RULES Shallow inferior RD – SRF will be slightly higher on the same side as that of the break Primary break at 6 o clock position – inferior RD with equal fluid levels

20. MODIFIED LINCOFF’S RULES Bullous inferior RD – primary break lies above horizontal meridian Primary break in upper nasal quadrant – SRF revolve around optic disc – rise on temporal side until it is level with primary break

21. MODIFIED LINCOFF’S RULES Subtotal RD with superior wedge of attached retina – primary break in periphery near its highest border SRF crosses vertical midline above – primary break near 12 o clock – lower edge of RD corresponding to side of break

22. RHEGMATOGENOUS RETINAL DETACHMENT Most common type A rising from one or more full-thickness retinal breaks in combination with vitreous traction Retinal break – tear or a hole Full thickness retinal defect in sensory retina Tear – break caused by vitreous traction at sites of strong vitreous attachment Location - superior fundus – temporal > nasal most common is horseshoe tear Hole – atrophic round break , in areas of lattice degeneration round to oval in shape temporal fundus – upper>lower usually smaller than tears less risk of RD

23. Primary Break – when responsible for production of detachment Secondary – when they are present postoperatively but are not responsible for detachment Subsequently lifted up by SRF Also includes the breaks which develop after retinal detachment At sites of old chorioretinal scar At time of photocoagulation

24. MORPHOLOGY Retinal breaks may be flat or associated with a surrounding cuff of SRF. If fluid extends more than one-disc diameter from the edge of a break  RD U-tears – horse shoe / flap / arrow head – consist of a flap – apex of which is pulled anteriorly by vitreous – base attached to retina – 2 anterior extensions – horns – running forward from apex Incomplete U-tears – linear, L shaped or J shaped – paravascular

25. Operculated tears – flap completely torn away from retina by detached vitreous gel Atrophic Retinal holes - round or oval Dialysis - circumferential tear along the ora serrata and is usually a consequence of blunt ocular trauma. vitreous gel remains attached to the posterior margin. Appears as a large very peripheral break with a regular rolled edge

26. Giant Retinal Tears Circumferential retinal breaks ≥90 degrees arise from circumferential vitreous traction in the region of the posterior vitreous base, in the presence of a PVD most commonly develop just posterior to the ora but also may be found at the equator (15%) and sometimes posterior to the equator Idiopathic

27. RHEGMATOGENOUS RETINAL DETACHMENT Characteristics of RRD Existence of abnormal mobility of partially liquefied vitreous gel Tractional forces that can precipitate a retinal break Presence of a retinal break that will allow the passage of liquefied vitreous into the subretinal space All these factors needs to be present to cause a rhegmatogenous RD

28. PATHOGENESIS Changes in vitreous Peripheral retinal degeneration predisposed to retinal detachment. Developmental variations predisposed to retinal detachment High risk factors of retinal detachment

29. Vitreous Liquefaction Vitreous – homogenous gel, consisting of a network of collagen fibrils separated from one another by macromolecules of hyaluronic acid With aging, fragmentation of collagen fibers and an aggregation of proteoglycans around these fragments  destabilizing the vitreous gel and leading to liquefaction ( synchisis ) and collapse of fibrillar frame work of vitreous gel (syneresis) The liquefied vitreous gel may coalesce into large lacuna within gel With extensive liquefaction within vitreous cavity  reduction in shock-absorbing capabilities and stability of gel

30. Vitreous Liquefaction When the denser posterior vitreous cortex ruptures, the liquefied vitreous can pass into the subhyaloid space and separate the posterior vitreous surface from the internal limiting membrane of the retina producing a true PVD In presence of PVD, condensed vitreous moves about within the vitreous cavity and rotational movements of eye exert traction  retinal breaks

31. Ocular trauma  traumatic complete or partial PVD Result in retinal breaks and subsequent rhegmatogenous retinal detachment Blunt trauma can also cause acceleration vitreous liquafaction In young patients, trauma may lead to retinal dialysis which represents a disinsertion of the retina at the ora serrata Dialyses - more common in the inferotemporal quadrant although most of the dialyses in the superonasal quadrant are associated with a definite history of preceding trauma

32. Posterior Vitreous Detachment Acute event, following signification liquefaction of vitreous gel

33. Acute PVD – 45-65 years – fellow eye affected within 6months to 2 years Acute PVD with no complications – vitreous cortex detaches completely without sequelae Retinal tears – symptomatic , U shaped , upper fundus , vitreous hemorrhage – retrohyaloid fluid has direct access to subretinal space Avulsion of peripheral blood vessel – vitreous hemorrhage in absence of retinal tear RD without PVD – retinal dialysis – round holes in young female myopes

34. PERIPHERAL RETINAL DEGENERATION Predisposing to RD Lattice degeneration Snail tract degeneration Retinoschisis White without pressure and white with pressure Not predisposing to RD Peripheral cystoid degeneration Paving stone degeneration Pigmentary degeneration of retina

35. LATTICE DEGENERATION Peak incidence – 2 nd and 3 rd decades Most common in moderate myopes Most important degeneration related to RD Bilateral (42-45%) – temporal>nasal – superior>inferior Discontinuity of ILM – atrophy of NSR Spindle shaped areas of retinal thinning – between equator and posterior border of vitreous base Arborizing network of white lines within islands Hyperplasia of RPE

36. SNAILTRACK DEGENERATION Sharply demarcated bands of tightly packed snow flakes – white frost like appearance Islands are longer – associated with vitreous liquefaction Round holes within snailtracks present

37. DEGENERATIVE RETINOSCHISIS Coalescence of cystic lesions – degeneration of neuroretinal and glial supporting elements within areas of peripheral cystoid degeneration Splitting of NSR into inner vitreous layer and outer choroidal layer – severing of neurones – complete loss of visual function – typical – split in outer plexiform layer Reticular retinoschisis – splitting at level of nerve fibre layer

38. WHITE WITH PRESSURE , WWOP White with pressure – translucent grey appearance of retina – induced by indenting sclera – normal eyes – associated with abnormally strong attachment of vitreous gel – posterior border of islands of lattice degeneration , snail-track degeneration and outer layer of acquired retinoschisis White without pressure – without scleral indentation – giant tears develop along posterior border of WWOP

39. PERIPHERAL RETINAL DEGENERATIONS Microcystoid degeneration – tiny vesicles with indistinct boundaries on greyish white background – adjacent to ora serrata – extends circumferentially and posteriorly – smooth undulating posterior border – may give rise to retinoschisis Paving stone degeneration – discrete yellow-white patches of focal chorioretinal atrophy – 25% normal eyes

40. Honey comb (reticular) degeneration – age related – fine network of perivascular pigmentation – extend posterior to equator Peripheral drusen – clusters of small pale lesions – hyperpigmented borders – elderly individuals

41. DEVELOPMENTAL VARIATIONS Enclosed oral bays - coalescence of adjacent dentate processes to form a ring. Brownish in color with granular appearance Meridional folds and complexes - oblong radially oriented areas of thickened retinal tissue, usually located in superonasal quadrant When a prominent dentate process (meridional fold) align with a ciliary process afront in the same meridian  meridional complex, located superonasally Cystic retinal tufts - noduar projections of retinal tissue that are typically surrounded by cystic retinal degeneration, appear as discrete, sharply circumscribed opaque white lesions Zonular traction tufts - anterior projections of the retina attached to one or more thickened zonular fibers , single and unilateral, located within vitreous base in nasal quadrant

42. HIGH RISK FACTORS Myopia Cataract extraction - risk 2-8% after ICCE, 0-3.6% after ECCE, 0.8-2% after Phacoemulsification Trauma Family history of retinal detachment Retinoschisis Retinal detachment in the other eye

43. SYMPTOMS Photopsia – sensation of flash of light Floaters – moving vitreous opacities - Weiss ring - detached attachment of the cortical vitreous on the optic nerve head seen as single annular floater - Cobwebs – condensation of collagen fibrillar network of vitreous - Sudden shower of dark spots Visual field defect – black curtain Rapid painless loss of vision

44. SIGNS Gray reflex on DDO Marcus Gunn pupil – if extensive RD Low IOP by 5mmHg Mild iritis Evaluation of any cataract which may obstruct the posterior view Tobacco dust – pigment cells in anterior vitreous Retinal breaks – discontinuities in retinal surface

45. FRESH RETINAL DETACHMENT Convex configuration, greyish white Opaque, corrugated appearance – retinal oedema SRF – extends upto ora serrata B-scan – good mobility of retina and vitreous

46. LONG-STANDING RD More fixed Proliferative Vitreoretinopathy changes sets in, the margins of breaks become everted, the star folds appear in the inferior quadrants followed by superior quadrants Retinal thinning secondary to atrophy Secondary intraretinal cysts – RD for 1 year – disappear after retinal reattachment Subretinal demarcation lines – high water marks – proliferation of RPE cells – junction of flat and detached retina – 3 months – convex wrt ora serrata

47. PROLIFERATIVE VITREORETINOPATHY Epiretinal and subretinal membrane formation Cell-mediated contraction of membranes – tangential retinal traction – fixed retinal folds Occurs following surgery for rhegmatogenous RD or penetrating injury Retinal folds and rigidity – retinal mobility induced by eye movements or scleral indentation decreased

48. Grade A – minimal PVR – diffuse vitreous haze and tobacco dust – pigmented clumps on inferior surface of retina Grade B – moderate PVR - wrinkling of inner retinal surface, tortuosity of blood vessels, retinal stiffness , decreased mobility of vitreous gel, rolled edges of retinal breaks – epiretinal membrane not identified clinically

49. Grade C – marked PVR – rigid full thickness retinal folds – heavy vitreous condensation and strands – A anterior – P posterior – severity in each area – no. of clock hours of retina involved

50. TRACTIONAL RETINAL DETACHMENT Due to vitreoretinal traction bands developing as a result of the underlying ocular/systemic disease Causes: Proliferative Diabetic retinopathy Retinopathy of prematurity (ROP) Penetrating trauma Retinal venous occlusion and PVR Concave surface, more localized and not extending to ora serrata

51. VITREORETINAL TRACTION - TYPES Tangential traction – contraction of epiretinal fibrovascular membranes – puckering of retina – distortion of retinal blood vessels Anteroposterior traction – contraction of fibrovascular membranes from posterior retina – association with major arcades – vitreous base anteriorly Bridging – trampoline traction – contraction of fibrovascular membrane – stretch from one part of posterior retina to another – between vascular arcades

52. Proliferative Diabetic Retinopathy With contraction of an extensive sheet of fibrovascular proliferation, distortion or displacement (“dragging”) of the macula may occur Contraction of vitreous or areas of fibrovascular proliferation may also lead to retinal detachment Limited to avulsion of a retinal vessel, usually a vein, sometimes accompanied by vitreous hemorrhage Relatively thin fold of retina may become elevated, with only a narrow zone of retinal detachment adjacent to its base, sometimes outlined by a pigmented demarcation line Extensive concave RD may be also seen

53. Proliferative Diabetic Retinopathy Occurrence and severity of retinal detachment are influenced by the timing and degree of shrinkage of the vitreous and fibrovascular proliferations and by the type, extent, and location of the new vessels responsible for vitreoretinal adhesions Extensive nets of large-caliber new vessels accompanied by heavy fibrous tissue produce broad, tight vitreoretinal adhesions Contraction of such proliferations is often followed by extensive retinal detachment New vessels with little accompanying fibrous tissue tend to produce less extensive vitreoretinal adhesions and less risk of retinal detachment, particularly when posterior vitreous detachment begins soon after the onset of NV

54. Retinopathy of Prematurity ROP has both exudative and traction retinal detachments At least three factors are involved Existence of permeable, leaky blood vessels  are capable of supplying large amounts of proteinaceous fluid to both the vitreous cavity and subretinal space Neovascularization growing into the subretinal space Blood vessels can bleed into both the vitreous cavity and subretinal space

55. Penetrating trauma

56. TRD – CLINICAL FEATURES Photopsia , floaters absent Visual field defect – progress slowly – stationary for months or years RD – concave – breaks absent Retinal mobility – reduced – shifting fluid absent SRF – shallower Highest elevation of retina – vitreoretinal traction Develops break – combined tractional-rhegmatogenous RD B-scan – PVD , immobile retina

57. TRACTIONAL RETINAL DETACHMENT Concave surface More localized, often not extending to ora serrata As the vitreous gel contracts with the fibrovascular tissue, these vessels and the underlying retina are drawn anteriorly toward the vitreous base Because of relatively strong vitreoretinal adhesions along the temporal arcades these areas are most prone to detach and the detachment can spread both peripherally and centrally toward the macula

58. COMBINED TRACTIONAL AND RHEGMATOGENOUS RETINAL DETACHMENT Characterized by a full-thickness retinal break and a significant tractional component Combined tractional–RRDs  seen in proliferative diabetic retinopathy, PVR, proliferative sickle-cell retinopathy, and penetrating intraocular injuries Not bullous Concave appearance

59. EXUDATIVE RETINAL DETACHMENT Lesions which lead to RPE pump failure (outer retinal barrier) Accumulation of SRF – absence of retinal breaks or traction Vascular, inflammatory and neoplastic disease involving NSR, RPE and choroid Fluid leaks outside vessels – accumulates in subretinal space Characteristic feature - presence of shifting subretinal fluid Surface - smooth

60. PATHOPHYSIOLOGY Three potential sources for fluid accumulation Vitreous fluid, Retinal vessels, Choroidal vessels main mechanisms for keeping the retina in a dehydrated state are the presence of inner and outer blood–retinal barriers and the fluid movement across the retinal pigment epithelium (RPE) Inner barrier - made of an endothelial tight junction of the retinal vessels Outer barrier - produced by the tight junction of retinal pigment epithelial cells

61. PATHOPHYSIOLOGY Three mechanisms guarantee the one-way movement of fluid across the RPE: Active transport of the RPE Plasma oncotic force, which is higher in the choroidal side Hydrostatic pressure When the RPE is injured  tight junction may be damaged  breakdown of the outer retinal barrier  active transport of fluid may be affected, compromising the unilateral mode of fluid movement Alternatively, diseases affecting the retinal vascular causing significant breakdown of the inner barrier may lead to fluid first gathering in the intraretinal space and then gaining access into the subretinal space

62. PATHOPHYSIOLOGY Adequate fluid outflow is required for the retina to maintain a state of dehydration Outflow pathways Vitreoretinal–choroidal outflow - carries the vitreous fluid to the RPE and to the choroid through the pumping action of RPE Uveoscleral outflow - carries the fluid from the choroid to leave the eye through choroidal vortex outflow Transscleral outflow - allows protein and fluid draining out through the emissary channels

63. ETIOLOGY

64. Clinical Features Photopsia absent Floaters present – associated vitritis Visual field defect – develop suddenly, progress rapidly RD – convex configuration – smooth surface Shifting fluid – detaches area of retina underneath Leopard spots – scattered areas of subretinal clumping – detachment has flattened

65. Central Serous Chorioretinopathy Characterized by a circular area of serous detachment of the posterior retina Caused by increased permeability of the choroidal vessel Atypical manifestations: Bullous Retinal Detachment Acute onset with simultaneous or sequential involvement of the two eye Fundus examinations reveal multiple areas of serous RD in the posterior retina with lower bullous RD Chronic Central Serous Chorioretinopathy Multiple poorly defined areas of chronic persistent or recurrent RD in the posterior pole Subtle or obvious areas of RPE changes are noted in the posterior pole and in the juxtapapillary regions; a gravity tract forming vertical band or reverse funnel-shaped depigmentation, along with pigment migration or bone-spicule pattern of pigmentary changes within the tract and in the inferior part of the retina Shallow or bullous detachment in the inferior retina is a frequent finding

66. Uveal Effusion Syndrome Idiopathic, seen in middle-aged men with normal ocular size, presenting with unilateral or bilateral serous choroidal, ciliary and retinal detachment Central vision decrease or distortion secondary to macular serous detachment or upper visual field defect from lower serous RD Severity ranges from macular serous detachment with insignificant ciliary and choroidal detachment to obvious ciliochoroidal detachment and bullous RD Protein concentration of the SRF - 2.5–3 times that of the normal plasma Fellow eye - affected within a few weeks or a few months after lesions developed in the first eye Protracted course of disease, with wax and wane of the SRF, eventually leaving areas of mixed RPE atrophy and pigment clumps in a leopard-spot pattern Pathogenesis - decreased drainage of extravasated protein through scleral emissary channels of the transscleral outflow pathway

67. Coats Disease Nonfamilial developmental retinal vasculopathy More common in males, unilateral, may occur in infants All vessels - affected, showing telangiectasis combined with a large amount of hard exudates Mild form - focal telangiectasia and microaneurysms, temporal to macula, with or without mild hard exudates Moderate form - cystoid macular edema with significant hard exudates surrounding the area containing telangiectatic vessels or microaneurysms Severe form - wide and scattered vascular lesions, with hard exudates accumulating around the disc and in the posterior pole, causing exudative detachment Advanced form - bullous detachment with the retina coming in direct contact with the crystalline lens; cholesterol crystals accumulate in the subretinal space

68. Accelerated Hypertension and Pregnancy-Induced Hypertension Prolonged or severe hypertension - damages retinal vascular system, choroidal circulation, and disc circulation The difference in vascular structures, autoregulation, and tissue resistance determines the different susceptibility of these three systems to increased blood pressure Leakage from retinal vessels and the optic disc - source of SRF Hypertension-induced choroidopathy - causes exudative RD Choroidopathy Acute ischemic phase Dhronic occlusive phase Chronic reparative phase First two phases - white or reddish patches in the outer retina, possibly caused by RPE necrosis; exudative detachment is often present Reparative phase – large areas of irregular REP atrophy Elschnig spots (a central hyperpigmented lesion surrounded by a hypopigmented ring of RPE changes) Siegrist spots (spots of pigmentary changes similar to Elschnig spots arranged linearly along choroidal vessels in the equatorial region) Exudative detachment disappears

69. Pregnancy-Induced Hypertension Exudative detachment may be limited to the macular area or appear as bullous detachment After delivery, with control of hypertension, exudative detachment rapidly subsides Good visual recovery Posterior pole - RPE changes forming hyperpigmented lines or patches mixed with yellow spots of RPE atrophy

70. Diabetic Retinopathy Fluid leaking out from the vessels first accumulates within the retina;  fluid may gain access into the subretinal space, causing sensory detachment Severe macular edema leads to detachment Exudative detachment combined with macular edema - severe breakdown of the inner retinal barrier

71. Vascular Occlusive Diseases Exudative detachment - in branch, hemispherical, and central retinal vein occlusion (CRVO) Vascular leakage from congested retinal veins outside the macular area - major source of SRF at the fovea Increased intravascular pressure and vascular permeability cause leakage of fluid and blood components into the subretinal space SRD is typically located beneath the fovea, and the height of the RD was greatest in the fovea

72. Vogt–Koyanagi–Harada Syndrome Multisystem inflammatory disease - neurologic, ocular, and cutaneous symptoms Ocular involvement includes anterior and posterior uveitis Multiple SRDs with congested disc - typical finding Bullous RD - in severe cases VKH - human leukocyte antigen (HLA)-DR4 and HLA-DRw53, with strongest associated risk for HLA-DRB1*0405 haplotype

73. Degenerative AMD with CNV, serous and hemorrhagic detachment of the retina occurs frequently Neovascular membrane causes leakage of serous exudates and red blood cells into the sub-RPE space  into the subsensory retinal space Fundus examination - light-grayish elevated mass corresponding to a serous and hemorrhagic detachment of the RPE and sensory retina

74. Choroidal Melanoma Commonly associated with exudative RD The tumor lesion - found during a routine eye examination Flashing lights – complaint during tumor growth or tumor invading into the retina Presents as a wide-based or dome-shaped pigmented mass under the retina Exudative detachment may develop above and surrounding the tumor or in the lower dependent part away from the tumor location

75. Intraretinal macrocysts Focal secondary retinoschisis Occur only in areas of long-standing retinal detachment 2-3 DD in size, found in periphery Choroidal Detachment Bullous, with a smooth contour Nasal/Temporal bullae – larger than superior/inferior bullae Brown choroid can be seen beneath retina Hour glass configuration – choroid is tethered to sclera by vortex veins or along the course of long posterior ciliary artery Choroidal tumours Elevated choroidal lesions can be confused with RD Appears more solid, lacking translucent appearance of RD, smooth in contours, lacking undulations