RETINAL DETACHMENT AND PREDISPOSING LESIONS lecture by Iddi.pptx

Retinal Detachment and predisposing lesions

1. RETINAL DETACHMENT AND PREDISPOSING LESIONS PRESENTER: DR. IDDI NDYABAWE MODULATOR: DR. LUSOBYA REBECCA DATE: FRIDAY 11/03/2022 MAKERERE UNIVERSITY COLLEGE OF HEALTH SCIENCES DEPARTMENT OF OPHTHALMOLOGY

2. Outline Retinal Breaks Posterior Vitreous Detachment Lesions Predisposing Eyes to Retinal Detachment Lesions not predisposing eyes to Retinal Detachment Prophylactic treatment of Retinal breaks Retinal Detachment Differential Diagnosis of Retinal Detachment Macular Lesions Associated with Retinal Detachment

3. RETINAL BREAKS Definition: any full-thickness defect in the neurosensory retina. Clinical significance: allow fluid from vitreous to collect in the epithelioretinal interspace, hence causing a RRD. Classification of Retinal Breaks: -flap , or horseshoe, tears -giant retinal tears - operculated holes -dialyses -atrophic retinal holes

4. Definitions A flap tear: strip of retina is pulled anteriorly by vitreoretinal traction, following PVD or trauma. c/o: photopsias , floaters, or both. A giant retinal tear extends 90deg (3 clock-hours) or more circumferentially. Along the posterior edge of the vitreous base . An operculated hole occurs when traction tears a piece of retina completely free from the adjacent retinal surface . A retinal dialysis is a circumferential, linear break at the ora serrata , with vitreous base attached to the retina posterior to the tear's edge. Commonly after blunt trauma. An atrophic hole: not associated with vitreoretinal traction. Not linked to increased risk of retinal detachment.

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6. Traumatic breaks Blunt or penetrating eye trauma can cause retinal breaks by: - direct retinal perforation - contusion , or - vitreous traction. Late occurance : vitreoretinal traction and subsequent detachment ;caused by fibrocellular proliferation Traumatic breaks are often multiple. Commonly found in the inferotemporal and superonasal quadrants.

7. Mechanisms of traumatic retinal breaks Blunt trauma can cause retinal breaks by direct contusive injury to the globe through 2 mechanisms: ( 1) coup (2 ) contrecoup . Blunt trauma compresses the eye along its anteroposterior axis and expands it in the equatorial plane. Slow compression of the eye has no deleterious effect on the retina because the vitreous body is viscoelastic. But rapid compression of the eye results in severe traction on the vitreous base that may tear the retina .

8. . Contusion injury may cause: - large , ragged equatorial breaks - dialysis , or -macular hole . The most common injuries are dialyses, which may be as small as 1 ora bay. Dialyses are usually located at the posterior border of the vitreous base but can also occur at the anterior border

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10. . Pathognomonic feature of ocular contusion: Avulsion of the vitreous base. Less common types of breaks caused by blunt trauma are: - horseshoe-shaped tears - operculated holes.

11. Trauma In Young Eyes Rarely does retina detach immediately depite high incidence of eye injury. Vitreous hasn’t yet undergone syneresis With time: RD Xtics of Traumatic RD in young eyes: -Shallow -Multiple demarcation lines - Subretinal deposits - Intraretinal schisis Exception: if there is PVS, RD occurs acutely. Resembles non-traumatic breaks

12. POSTERIOR VITREOUS DETACHMENT DESCRIPTION A posterior vitreous detachment (PVD) is the physical separation of the cortical vitreous from the intemallimiting membrane (ILM) of the retina . • With improved imaging modalities such as high-resolution optical coherence tomography (OCT ), earlier stages of structural partial PVD are readily detectable before symptoms occur and before acomplete PVD is present

13. EPIDEMIOLOGY The incidence of PVD increases with age. Although some estimates have indicated that 50% of phakic eyes have PVD by the age of 50 years, this has been somewhat disputed in autopsy studies

14. Risk factors for PVD • Increasing age • Axial myopia • Trauma • Inflammation • Pseudophalda • Aphakia • Prior surgeries (especially cataract extraction complicated by vitreous loss) • Vitreous hemorrhage

15. Genetics • Axial myopia (caused by both genetic and environmental factors) correlates with an earlier onset of vitreous liquefaction and PVD . • An earlier onset of PVD and PVD-related complications are seen in Stickler's and Marfan's syndromes due to anomalous collagen metabolism

16. PATHOPHYSIOLOGY Liquefaction of the vitreous gel is clinically evident as optically empty vacuoles within the vitreous cavity . This may be accompanied by coalescence of collagen fibrils into visible strands. which may be visualized ophthalmoscopically . Decreased strength of the vitreoretinal interface is also believed to precipitate PVD

17. ETIOPATHOGENESIS Vitreous liquefaction is detectable from early childhood and increases with age . Significant vitreous liquefaction together with loss of cohesion of the vitreoretinal interface combine to facilitate PVD formation . In the earliest stages of a PVD, the vitreous and the retina gradually separate. This process often starts in the macular region, but often spares the fovea until a later stage.

18. . Once the posterior vitreous face degrades sufficiently , liquefied vitreous can pass abruptly through even a minute defect in the posterior vitreous face into the subhyaloid space and this is known as an acute PVD. In areas where the ILM is especially thin (i.e., optic nerve , foveola , vitreous base, retinal vessels), the vitreoretinal interface is especially strong. These areas are often the last to separate from the hyaloid face. A Weiss ring is aclinical sign that confirms separation of the vitreopapillary junction, and it typically confirms the completion of the PVD

19. Commonly associated conditions

20. Diagnosis Signs and symptoms Many patients do not present with acute symptoms when PVD occurs. Presenting symptoms include entoptic phenomena such as floaters, change in pattern of floaters and photopsias . An alteration in peripheral visual field may indicate a retinal detachment

21. Physical exam Indirect ophthalmoscopy with scleral indentation and slit lamp exam with a three-mirror lens are the preferred techniques to confirm PVD and to exclude retinal tears or retinal detachment. The presence of vitreous hemorrhage or pigment may indicate a retinal tear. If significant hemorrhage interferes with complete examination, bed rest with head at 45º for hours or days with optional bilateral ocular patching may help restore transparency in order to rule out retinal tears. If the source of bleeding cannot be found, the patient should be re-examined regularly and frequently with a vitrectomy considered to identify a source. Echography may be useful in detecting retinal tears with flap or retinal detachment, especially if haemorrhage or other opacification of media limits visualization. Patients are given strict return precautions and often re-examined within 2-6 weeks after presentation to assess for retinal breaks with a PVD in evolution.

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24. PVD on OCT

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26. Differential Diagnosis Retinal detachment Asteroid hyalosis / Synchysis scintillans Vitreous syneresis Vitreous inflammation (infectious and non infectious) Vitreous haemorrhage Vitreous amyloidosis Ocular large cell lymphoma

27. Management General treatment: Observation with strict retinal detachment precautions, and follow up exam to rule out retinal breaks. Vitrectomy can be considered for non-clearing vitreous hemorrhage, or vision threatening pathology. Medical therapy: There are no medical therapies recommended for a PVD. Medical follow up After the diagnosis of an acute PVD, a follow up dilated fundus examination should be performed approximately 1 month afterwards. It is possible for a new retinal tear or retinal detachment to occur during this dynamic period.

28. Surgery For unmmplicated PVD, no treatment is necessary. When a retinal tear or detachment Is present, prompt treatment is imperative. Rarely , pars plana vitrectomy may be offered to alleviate severe PV!Helated symptoms; however, this Is the exception Surgical follow up If surgery is performed, the recommended follow up intervals are day 1, week 1, month 1 and month 3. Serial OCT scans are recommended to assess for anatomic success and correlation with visual acuity outcomes.

29. ONGOING CARE Prompt evaluation by an ophthalmologist or optometrist when symptoms of acute PVD occur Prompt referral to an ophthalmologist skilled in the treatment of retinal tears and/or detachments In the event that one is detected

30. Patient education After an acute PVD, patients are often significantly bothered by floaters and flashes. tt is often reassuring to let patients know that symptoms will typically lessen within months . Patients should be educated to report the symptoms of a retinaI tear or detachment should they occur

31. PROGNOSIS • After an uncomplicated PVD, tile prognosis is excellent . In some cases. as in eyes with vitreomacular traction , visual acuity may improve. After a complicated PVD U.e ., with a retinal break ), there is an elevated risk of additional tears occurring . When a complicated PVD occurs in one eye, the fellow eye has ahigher risk of romplications from PVD likely due to the nature ofthe vitreoretinal interface .

32. Complications Retinal tears Rhegmatogenous retinal detachment VH Long term complications may include: vitreo -macular traction lamellar macular holes full-thickness macular holes epiretinal membrane

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34. Lesions Predisposing Eyes to Retinal Detachment Lattice Degeneration Vitreoretinal Tufts Meridional Folds, Enclosed Ora Bays, and Peripheral Retinal Excavations

35. Lattice Degeneration Vitreoretinal interface abnormality Epid : 6-10% of general population Bilateral on 1/3-1/2 of affected patients RFs: myopia, familial predilection Complications: Retinal breaks and RD

36. . Histology: 1. loss of ILM 2. Vitreous liquifies in pockets 3. Vitreous adheres to margins 4. inner retinal atrophy

37. . Features of RD caused by Lattice Degeneration: Tractional tear at the lateral or posterior margin of lattice lesion Atrophic hole within zone of lattice

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44. Vitreoretinal Tufts Definition: small, peripheral, focal areas of elevated glial hyperplasia Associations: vitreous or zonular attachment and traction Classification based on: Anatomical ppt Pathogenesis Clinical distinctions

45. . Groups: Noncystic retinal tufts Cystic retinal tufts Zonular traction retinal tufts Complications: Retinal tears and RD

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48. Meridional Folds, Enclosed Ora Bays and Peripheral Retinal Excavations Meridional folds: folds of redundant retina. Site; Superonasal . Tears assoc with PVD occur at the most posterior limit of the folds Enclosed ora bays: oval islands of pars plana epithelium. Site; immediately posterior to ora serrata . Retinal tears at the posterior limit. Peripheral retinal excavations: firmly attached to vitreoretinal adhesions. Site; 4 DD posterior to ora serrata . Significance; represent a mild form of lattice degeneration.

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50. Lesions not predisposing eyes to retinal detachment Paving-Stone Degeneration RPE hyperplasia RPE hypertrophy Peripheral cystoid degeneration

51. Paving-Stone Degeneration Description: peripheral, small, discrete areas of atrophy of outer retina. Single or in groups. Epid : in 22% > 20 years old Histology: atrophy of RPE and outer retinal layers Attenuation or absence of choriocapillaris Adhesions between remaining neuroepithelial layers and Bruch’s membrane

52. . CFs: Yellowish white, with rim of hypertrophic RPE Inferior quadrants, anterior to equator

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54. RPE Hyperplasia Cause: chronic low grade traction Sites: Ora serrata Pars plana Peripheral retina Areas of previous inflammation or trauma

55. RPE Hypertrophy Degenerative change Site: periphery. Pattern: reticular Histology: Large cells Large spherical melanin granules Ddx : Congenital hypertrophy of RPE (“break tracks”)

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57. Peripheral Cystoid Degeneration Typical Peripheral Cystoid Degeneration Reticular Peripheral Cystoid Degeneration

58. Typical Peripheral Cystoid Degeneration Zones of microcysts in far-peripheral retina Age: > 20 yrs Complications: retinal holes

59. Reticular Peripheral Cystoid Degeneration Site: posterior to typical PCD Description: in inner retina. Linear or reticular pattern along retinal vessels Age: adults Complication: reticular degenerative retinoschisis

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61. Clinical significance of Retinal Breaks Majority don’t cause any RD Some cause RD. Mech : fluid from vitreous thru it and separates sensory retina from the RPE

62. Prophylactic treatment of retinal breaks Prophylactic treatment aims to reduce risk of RD Options: -Laser -Cryotherapy Goals: create a chorioretinal adhesion around each break preventing fluid from entering the subretinal space If subretinal fluid present, treatment applied to surround area of subretinal fluid Contraindications: >-6 D Myopia >6 clock-hours lattice

63. Factors to consider when considering prophylaxis Symptoms Family history Residual traction Size and location of break Phakic status Refractive error Status of fellow eye Presence of subretinal fluid Availability of follow-up evaluation

64. Approach to prophylaxis Symptomatic retinal breaks Asymptomatic retinal breaks Lattice Degeneration Aphakia and Pseudophakia Fellow eye in patients with RD Subclinical RD

65. Symptomatic Retinal Breaks Risk of progress to RD, esp if there is VH Acute symptomatic flap tears: treated prophylactically Acute operculated holes: usually not treated. Less likely to cause RD. Indications for prophylaxis here: Persistent vitreous traction at margin of operculated hole If hole is large or located superiorly VH Atrophic holes: don’t require treatment. Incidental findings.

66. Asymptomatic Retinal Breaks Asymptomatic flap tears: not treated if in emmetrophic phakic eyes. When to treat them: Lattice degeneration Myopia Subclinical detachment Aphakia h/o RD in fellow eye Asymptomatic operculated holes and atrophic holes: rarely treated.

67. Lattice degeneration Limited data Doesn’t require prophylaxis if no risk factors Which additional risk factors warrant treatment? RD in fellow eye Flap tears Aphakia

68. Aphakia and pseudophakia Higher risks of RD than phakic eyes RFs for developing RD after cataract surgery: -Male sex -Younger age -Myopia -Increased axial length -Posterior capsular tear

69. Fellow eye in patients with RD If a patient has RD in one eye, fellow eye risk of RD is: 10% for phakic RD 25% for aphakic RD 35% for pseudophakic RD Rx: prophylactic treatment of flap tears and lattice degeneration

70. Subclinical Retinal Detachment Definition: a detachment where subretinal fluid extends > 1 DD from the break but not more than 2 DD posterior to the equator. Significance : 30% progress to RD Indications for treatment: -Symptomatic patients -Cases involving traction on the break

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74. RETINAL DETACHMENT Neuroepithelium and the pigmentary epithelium of the retina normally lie in apposition with the potential space bewtween the (original primary optic vesicle) Retinal detachment occurs when subretinal fluid accumulates in the potential space between the neurosensory retina and the underlying retinal pigment epithelium.

75. Epidemiology incidence of approximately 1 in 10000 very rare in children Most common between 40 to 70 years old. Natural ageing changes in the vitreous gel, known as PVD, can cause retinal tears and PVD is more common as you get older.

76. RISK FACTORS FOR RD Lattice degeneration Peripheral retinal breaks Pathologic myopia Previous intraocular surgery Trauma Previous retinal detachment Family history

77. CLASSIFICATION Depending on the mechanism of subretinal fluid accumulation, retinal detachments traditionally have been classifird into: -Rhegmatogenous -Tractional -Exudative Clinically: 1) Primary detachments: detachments due to the development of a break in the retina, in which case the state of this tissue is of primary importance (rhegmatogenous) 2) Secondary detachments: due to an obvious mechanical cause – when the detachment is because of another disease process in the eye

78. . A) Exudation: exudative choroiditis or retnopathy, angiomatous, toxemia of pregnancy fluid may be blood (as from a chroroidal hemorrhage) Pathophysiology: association of subretinal fluid to absence of traction and break. Retinal signs: convex configuration of RD, mobile detached retina, shifting fluid +

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80. . B) Traction: plastic cyclitis, proliferative retinopahty (diabetic mostly) or ROP, penetrating posterior segment trauma Pathophysiology: retina being mechanically pulled away from its bed by the contraction of fibrous tissue in the vitreous in absence of retinal tear Retinal signs: concave configuration o RD. Severely reduced retinal mobility and absence of drifting fluid Combined Tractional Rhegmatogenous RD – Retinal break is caused by traction from an adjacent area of fibrovascular proliferation.

81. Diagnosis History: significant photopsias and/or persistent new floaters constant fixed or slowly progressive visual field loss. Important information to elicit: - onset of symptoms - presence and duration of decreased central visual acuity - prior trauma - prior surgery - hemorrhage - complete past medical history and review of systems.

82. Physical examination Visual acuity, pupillary examination, visual field testing, intraocular pressure, color vision. Slit lamp examination of the anterior segment. Examination of the anterior vitreous for pigment (Schaffer's sign) or vitreous hemorrhage is critical. A thorough fundus examination to include indirect ophthalmoscopy with scleral depression and visualization to the ora serrata should be completed. A detailed drawing describing the detachment with location of retinal pathology may be documented. If there is no view to the posterior pole such as in hemorrhage or media opacity, B-scan ultrasound should be used to evaluate the retinal and vitreous status.

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84. RRD

85. Clinical diagnosis

86. . Differential diagnosis: A) Degenerative retinoschisis B) Choroidal detachment C) Uveal effusion syndrome

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89. Choroidal Detachment .

90. Uveal effusion syndrome .

91. Lab tests Indication: If a cause for the traction retinal detachment cannot be determined by history, further laboratory analysis may be required to determine if diabetes, sickle cell, carotid disease or another systemic or ocular process is the source for proliferative retinopathy. Since exudative detachments may be due to a systemic or ocular inflammatory process, laboratory investigation may be indicated. Here, fluorescein angiography may be indicated to further clarify exudative processes such as macular degeneration, central serous chorioretinopathy , and Vogt- Koyanagi -Harada syndrome or other uveitic processes. Ultrasound is a useful imaging modality to evaluate choroidal masses or posterior scleritis .

92. Rhegmatogenous RD Characterised by the presence of a retinal break in concert with vitreoretinal traction that allows accumulation of liquefied vitreous under the neurosensory retina, separating it from the RPE Even though a retinal break is present, a RD will almost never occur if the vitreous is not at least partially liquefied and traction is absent

93. RRD cont Risk factors: Myopia, PVD,Vitreous loss following cataract surgery and laer capsulotomy. Aphakia, RD in other eye. Persistent vitreoretinal traction, blunt and penetrating trauma. Retinal breaks: retinal breaks may be flat or associated with a surrounding cuff of SRF. The shape of such breaks varies. Breaks can be round holes, horseshoe-shaped tears, operculated tears or retinal disinsertion at the ora (dialysis)

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95. . A retinal break is identified and localized in most eyes with RRD, 50% have more than one break. More than half of all retinal breaks are located in the upper temporal quadrant, although any quadrant may be affected SRF spread is governed by gravity, by anatomical limits (ora serrata and optic nerve) and by the location of the primary retinal break The likely location of primary retinal break can be predicted by studying the shape of RD by Lincoff rule:

96. Lincoff rules A superior retinal detachment extending downwards equally on both sides of the macula is commonly found to have a retinal break present within a clock hour of 12 o’clock. An inferior retinal detachment extending upwards equally on both sides of the macula is commonly found to have a retinal break present within a clock hour of 6 o’clock Asymmetrical distribution of subretinal fluid (SRF) points to the presence of a retinal break within one to two clock hours of the edge of the more vertically extensive retinal detachment

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99. Bullous detachments are generally caused by superior breaks .

100. Symptoms Classic premonitory sumptoms in patients with complete RRD: flashing lights (photopsia) and floaters associated with acute PVD After a variable period of time a curtain-like relative peripheral visual field defect may ensue, and can progress to involve the central vision.

101. General signs RAPD: present in an eye with extensive RD IOP is often lower by about 5mmHg compared with the normal eye Iritis is very common but usually mild ‘Tobacco dust’ (Shaffer sign) consisting of pigment cells is commonly seen in the anterior vitreous, subretinal vitreous blood or inflammatory cells are also highly specific

102. . Retinal breaks appear as discontinuaties in the retinal surface. They are usually red. Retinal signs: Early stages: In the most typical condition it is white or gray, with folds which show a bright sheen at the summits and appear gray in the depressions During the slight movements of the eye the folds show oscillations and the retinal vessels are seen coursing over the surface.

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104. . Extensive detachment: great ballon-like folds may be seen, and then may cut off all view of the disc (bullous RD) Detached retina: slightly opaque colour secondary to intraretinal edema and the normal choroidal pattern of vessels is no longer seen. It has a convex configuration, and moves freely with eye movements unless proliferative vitreoretinopathy (PVR) is present

105. . At the edges of the detachment a considerable degree of pigmentary disturbance may appear, as well as white spots of exudation, hemorrhages and greyish-white lines due to the retinal folds. In total detachment the retina is funnel shaped, remaining attached at the disc and at the ora serrata. Still later it becomes largely bunched behind the lens, the part attached to the disc being pulled out into a straight cord.

106. Long-standing More fixed folds Retinal thinning Intraretinal cysts Subretinal fibrosis Subretinal demarcation lines: present usually at the junction of the attached and detached retina Represent areas of increased retinal adhesion to the RPE. Subretinal fluid may spread beyond the lines.

107. PROPHYLAXIS FOR RD Prophylaxis of retinal detachment is best done by identifying predisposing retinal breaks and other lesions, and treating them with cryotherapy or laser especially if other risk factors are present. Even after prophylactic treatment, a lifelong followup of such eyes is essential. Asymptomatic patients with peripheral retinal degenerations that could lead on to a retinal break, e.g lattice degeneration, have a low risk of retinal detachment and require only periodic review.

108. MANAGEMENT OF RD Operations for retinal detachment can be successfully performed only after accurate localization of all retinal breaks SURGICAL MANAGEMENT: Depends on the extent and duration of the condition and the condition of the retina.

109. PRINCIPLES OF SURGERY Common principles used in all types of surgery to treat a retinal detachment are as follows: 1. Identification of all retinal breaks and areas of vitreous or periretinal traction 2. Induction of aseptic chorioretinal inflammation around the breaks to seal them 3. Release of any vitreous or periretinal traction 4. Drainage of subretinal fluid and 5. Ensuring chorioretinal apposition for at least a couple of weeks by either or both of the following: A) External tamponade: silicone buckle, sponge, tyre, encircling band B) Internal tamponade; air, gases such as Sulphur hexafluoride (SF6), perfluoropropane (C3F8), or liquids such as silicone oil.

110. Pneumatic retinopexy I nvolves the injection of an intraocular gas bubble along with retinopexy using cryotherapy or laser, typically in a clinic setting. An important part in the successful repair of retinal detachment with pneumatic retinopexy involves head positioning so that the gas bubble tamponades the retinal tear. Pneumatic retinopexy is typically only used with retinal detachments due to retinal tears in the superior eight clock hours and involving a single break less than one clock hour.

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113. Scleral buckling Scleral buckles are silicone bands permanently placed around the outside of the globe under the extraocular rectus muscles to relieve any traction and support retinal tears. Scleral buckling is combined with retinopexy , typically cryotherapy. This is the oldest method of repair and still has excellent results in well-trained hands.

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115. Pars plana vitrectomy Pars plana vitrectomy with 20 gauge, 23 gauge, 25 gauge, or 27 gauge instruments involves removal of the vitreous by way of cutting the vitreous strands with a vitrectomy machine/ handpiece and flattening of the retina through a direct intraocular process

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117. Proliferative Vitreoretinopathy Most common complication following a RRD. Most common cause of failure of retinal repair. Caused by epiretinal and subretinal membrane formation, contraction leads to tangential retinal traction and fixed retinal fold formation Main features are retinal folds and rigidity so that retinal mobility induced by eye movements is decreased Noted as: Stage A: minimal Stage B: moderate Stage C: marked Stage D: massive and the number of quadrants is recorded as 1-4 This scar tissue exerts traction on the retina and may result in recurrence of the retinal detachment, even after an initially successful retinal reattachment procedure Rx: surgical intervention to release the traction caused by membranes

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119. Risk factors for PVR include Age Giant retinal tears Retinal detachments involving more than 2 quadrants Previous retinal detachment repair Use of cryotherapy Vitreous hemorrhage Choroidal detachment. Trauma

120. Macular Lesions Associated With Retinal Detachment Optic Pit Maculopathy Macular Holes in High Myopia

121. Optic Pit Maculopathy Definition: small , hypopigmented , yellow or whitish, oval or round, excavated colobomatous defects of the optic nerve; they are usually found within the inferior temporal portion of the optic disc margin Significance: may lead to serous macular detachments with a poor prognosis if left untreated Rx: vitrectomy with gas-bubble placement

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123. Macular Holes in High Myopia A distinct variant of RRD is caused by macular holes, almost always in the setting of a posterior staphyloma of highly myopic eyes Vitreous cavity fluid enters the subretinal space through the macular hole, and the relative recoil forces of the stretched macular retina lining the staphyloma help initiate the detachment. These macular holes with retinal detachment have a far lower success rate for surgical repair than do either macular holes or typical RRDs

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