Retinal detachment

retinal deatchment

1. RETINAL DETACHMENT Dr Nikhil R P

2. ANATOMY OF THE PERIPHERAL RETINA Pars Plana The ciliary body starts 1 mm from the limbus and extends posteriorly for about 6 mm. The first 2 mm consist of the pars plicata and the remaining 4 mm comprises the flattened pars plana . In order not to endanger the lens or retina , the optimal location for a pars plana surgical incision is 4 mm from the limbus in phakic eyes and 3.5 mm from the limbus in pseudophakic eyes.

3. Ora Serrata The ora serrata forms the junction between the retina and ciliary body and is characterized by the following

4.    1     Dentate processes  are teeth-like extensions of retina onto the pars plana ; they are more marked nasally than temporally and can have extreme variation in contour.    2     Oral bays  are the scalloped edges of the pars plana epithelium in between the dentate processes   3     A meridional fold  is a small radial fold of thickened retinal tissue in line with a dentate process, usually located in the superonasal quadrant . A fold may occasionally exhibit a small retinal hole at its apex.  

5. Normal variants of the ora serrata . (A)  Meridional fold with a small retinal hole at its base; (B) enclosed oral bay; (C) granular tissue 

6.   4     An enclosed oral bay  is a small island of pars plana surrounded by retina as a result of meeting of two adjacent dentate processes.    5     Granular tissue  characterized by multiple white opacities within the vitreous base can sometimes be mistaken for small peripheral opercula. At the ora , fusion of the sensory retina with the retinal pigment epithelium (RPE) and choroid limits forward extension of subretinal fluid. However, there being no equivalent adhesion between the choroid and sclera, choroidal detachments may progress anteriorly to involve the ciliary body ( ciliochoroidal detachment).

7. Vitreous base The vitreous base is a 3–4 mm wide zone straddling the ora serrata . The cortical vitreous is strongly attached at the vitreous base, so that following acute posterior vitreous detachment (PVD), the posterior hyaloid face remains attached to the posterior border of the vitreous base. Pre-existing retinal holes within the vitreous base do not lead to RD.

8. The vitreous base 

9. DEFINITIONS

10. Retinal Detachment A Retinal Detachment (RD) describes the separation of the neurosensory retina (NSR) from the retinal pigment epithelium (RPE). This results in the accumulation of subretinal fluid (SRF) in the potential space between the NSR and RPE. The main types of RD are: 

11.   1      Rhegmatogenous   ( rhegma  – break), occurs secondarily to a full-thickness defect in the sensory retina, which permits fluid derived from synchytic (liquefied) vitreous to gain access to the subretinal space.    2      Tractional  in which the NSR is pulled away from the RPE by contracting vitreoretinal membranes in the absence of a retinal break.   

12. 3      Exudative   (serous, secondary) is caused neither by a break nor traction; the SRF is derived from fluid in the vessels of the NSR or choroid, or both.    4      Combined tractional-rhegmatogenous , as the name implies, is the result of a combination of a retinal break and retinal traction. The retinal break is caused by traction from an adjacent area of fibrovascular proliferation and is most commonly seen in advanced proliferative diabetic retinopathy.

13. Vitreous adhesions     1      Normal.  The peripheral cortical vitreous is loosely attached to the internal limiting membrane (ILM) of the sensory retina. Stronger adhesions occur at the following sites:    •    Vitreous base, where they are very strong.    •    Around the optic nerve head, where they are fairly strong.    •    Around the fovea, where they are fairly weak, except in eyes with vitreomacular traction and macular hole formation.    •    Along peripheral blood vessels, where they are usually weak.   

14. 2      Abnormal  adhesions at the following sites may be associated with retinal tear formation as a result of dynamic vitreoretinal traction associated with acute PVD.   •    Posterior border of islands of lattice degeneration.    •    Retinal pigment clumps.    •    Peripheral paravascular condensations.    •    Vitreous base anomalies such as tongue-like extensions and posterior islands.    •    ‘White with pressure’ and ‘white without pressure’.

15. Vitreoretinal traction Vitreoretinal traction is a force exerted on the retina by structures originating in the vitreous, and may be dynamic or static. The difference between the two is crucial in understanding the pathogenesis of the various types of RD.     1      Dynamic  traction is induced by eye movements and exerts a centripetal force towards the vitreous cavity. It plays an important role in the pathogenesis of retinal tears and rhegmatogenous RD.    2      Static  traction is independent of ocular movements. It plays a key role in the pathogenesis of tractional RD and proliferative vitreoretinopathy .

16. Posterior vitreous detachment A posterior vitreous detachment (PVD) is a separation of the cortical vitreous from the internal limiting membrane (ILM) of the NSR posterior to the vitreous base. PVD can be classified according to the following characteristics:    1      Onset.   Acute PVD is by far the most common. It develops suddenly and usually becomes complete soon after onset. Chronic PVD occurs gradually and may take weeks or months to become complete.    2      Extent     a     Complete   PVD in which the entire vitreous cortex detaches up to the posterior margin of the vitreous base.    b      Incomplete  PVD in which residual vitreoretinal attachments remain posterior to the vitreous base. Rhegmatogenous RD is usually associated with acute PVD; tractional RD is associated with chronic, incomplete PVD; exudative RD is unrelated to the presence of PVD.

17. Retinal break A retinal break is a full-thickness defect in the sensory retina. Breaks can be classified according to (a)  pathogenesis , (b)  morphology  and (c)  location .    1      Pathogenesis     a     Tears   are caused by dynamic vitreoretinal traction and have a predilection for the superior fundus (temporal more than nasal).    b      Holes  are caused by chronic atrophy of the sensory retina and may be round or oval. They have a predilection for the temporal fundus (upper more than lower).

18.    2     Morphology     a     U-tears  (horseshoe, flap or arrowhead) consist of a flap, the apex of which is pulled anteriorly by the vitreous, the base remaining attached to the retina. The tear itself consists of two anterior extensions (horns) running forward from the apex.    b      Incomplete U-tears ,  which may be linear, L-shaped or J-shaped, are often paravascular .    c      Operculated tears  in which the flap is completely torn away from the retina by detached vitreous gel.    d     Dialyses  are circumferential tears along the ora serrata with vitreous gel attached to their posterior margins.    e      Giant tears  involve 90° or more of the circumference of the globe. They are most frequently located in the immediate post-oral retina or, less commonly, at the equator..

19. Retinal tears.   (A)  Complete U-shaped;   (B)   linear;  (C)   Lshaped ;  (D)   operculated ;  (E)  dialysis 

20.   (A)  Giant retinal tear involving the immediate post-oral retina;  (B)  vitreous cortex is attached to the anterior margin of the tear 

21. 3     Location     a     Oral  breaks are located within the vitreous base.    b     Post-oral  breaks are located between the posterior border of the vitreous base and the equator.    c     Equatorial  breaks are at or near the equator.   d      Post-equatorial  breaks are behind the equator.    e      Macular  breaks (invariably holes) are at the fovea.

22. CLINICAL EXAMINATION

23. Head-mounted Indirect Ophthalmoscopy 1     Principles . Indirect ophthalmoscopy provides a stereoscopic view of the fundus. The light emitted from the instrument is transmitted to the fundus through a condensing lens held at the focal point of the eye, which provides an inverted and laterally reversed image of the fundus. AS THE POWER OF THE CONDENSING LENS DECREASES THE WORKING DISTANCE AND THE MAGNIFICATION INCREASE BUT THE FIELD OF VIEW IS REDUCED, AND VICE VERSA.

24.   (A)  Principles of indirect ophthalmoscopy ;  (B)  condensing lenses  

25. 2     Condensing lenses  of various powers and diameters are available for indirect ophthalmoscopy .    •     20 D (magnifies ×3; field about 45°) is the most commonly used for general examination of the fundus.    •    25 D (magnifies ×2.5; field is about 50°).    •    30 D (magnifies ×2; field is 60°) has a shorter working distance and is useful when examining patients with small pupils.    •    40 D (magnifies ×1.5; field is about 65°) is used mainly to examine small children.    •     Panretinal 2.2 (magnifies ×3; field is about 55°).

26. 3      Technique     a    Both pupils are dilated with tropicamide 1% and, if necessary, phenylephrine 2.5% so that they will not constrict when exposed to a bright light during examination.    b    The patient should be in the supine position with one pillow, on a bed, reclining chair or couch and not sitting upright in a chair.    c    The examination room is darkened.    d    The eyepieces are set at the correct interpupillary distance and the beam aligned so that it is located in the centre of the viewing frame.

27. Position of patient during indirect ophthalmoscopy

28.    e    The patient is instructed to keep both eyes open at all times.    f    The lens is taken into one hand with the flat surface facing the patient and throughout the examination is kept parallel to the patient's iris plane.    g    If necessary, the patient's eyelids are gently separated with the fingers.    h    In order to enable the patient to adapt to the light he should be asked to look up and the superior peripheral fundus should be examined first.    i    The patient is asked to move the eyes and head into optimal positions for examination. For example, when examining the extreme retinal periphery, the patient is asked to look away from the examiner.

29. Scleral indentation 1     Purposes.   Scleral indentation should be attempted only after the art of indirect ophthalmoscopy has been mastered. Its main function is to enhance visualization of the peripheral retina anterior to the equator; it also permits a kinetic evaluation of the retina.

30. Appearance of retinal breaks in detached retina.  (A)  Without scleral indentation;  (B)  with indentation  

31. Technique of scleral indentation.  (A)  Insertion of indenter;  (B)  indentation;   (C)  mound created by indentation  

32. Goldmann Three-mirror Examination 1      Goldmann three-mirror lens  consists of four parts; the central lens and three mirrors set at different angles. Because the curvature of the contact surface of the lens is steeper than that of the cornea, a viscous coupling substance with the same refractive index as the cornea is required to bridge the gap between the cornea and the goniolens . It is important to be familiar with each part of the lens as follows :    •    The central part provides a 30° upright view of the posterior pole.    •    The equatorial mirror (largest and oblong-shaped) enables visualization from 30° to the equator.    •   

33.  The peripheral mirror (intermediate in size and square-shaped) enables visualization between the equator and the ora serrata .    •    The gonioscopy mirror (smallest and dome-shaped) may be used for visualizing the extreme retinal periphery and pars plana .    •    It is therefore apparent that the smaller the mirror, the more peripheral the view obtained.

34. 2     Mirror positioning    •    The mirror should be positioned opposite the area of the fundus to be examined; to examine the 12 o’clock position the mirror should be positioned at 6 o’clock.    •    When viewing the vertical meridian, the image is upside down but not laterally reversed, in contrast to indirect ophthalmoscopy . Lesions located to the left of 12 o’clock in the retina will therefore also appear in the mirror on the left-hand side    •    When viewing the horizontal meridian, the image is laterally reversed.

35. (A)  U-tear left of 12 o’clock and an island of lattice degeneration right of 12 o’clock;  (B)  the same lesions seen with the three-mirror lens positioned at 6 o’clock  

36. 3      Technique    a    The pupils are dilated.    b    The locking screw of the slit-lamp is unlocked to allow the illumination column to be tilted.    c     Anaesthetic drops are instilled.    d    Coupling fluid (high viscosity methylcellulose or equivalent) is inserted into the cup of the contact lens; it should be no more than half full.

37.  Preparation of the slit-lamp for fundus examination.  (A)  Unlocking the screw;  (B)  tilting the illumination column

38.    e    The patient is asked to look up; the inferior rim of the lens is inserted into the lower fornix and quickly pressed against the cornea so that the coupling fluid is retained.    f    The illumination column should always be tilted except when viewing the 12 o’clock position in the fundus (i.e. with the mirror at 6 o’clock).   

39. (A)  Insertion of the three-mirror lens into the lower fornix with the patient looking up;  (B)  three-mirror lens in position  

40.  The illumination column is tilted and positioned right of centre to view the oblique meridian at 1.30 and 7.30 o’clock  

41. Fundus Drawing 1      Technique.   The image seen with indirect ophthalmoscopy is vertically inverted and laterally reversed. This phenomenon can be compensated for when viewing the fundus if the top of the chart is placed towards the patient's feet (i.e. upside down).

42. In this way the inverted position of the chart in relation to the patient's eye corresponds to the image of the fundus obtained by the observer. For example, a U-tear at 11 o’clock in the patient's right eye will correspond to the 11 o’clock position on the chart; the same applies to the area of lattice degeneration between 1 o’clock and 2 o’clock.

43. Technique of drawing retinal lesions.  (A)  Position of the chart in relation to the eye;

44. 2      Colour Code      a    The boundaries of the RD are drawn by starting at the optic nerve and then extending to the periphery.    b    Detached retina is shaded blue and flat retina red.    c    The course of retinal veins is indicated with blue . Retinal arterioles are not usually drawn unless they serve as a specific guide to an important lesion.    d    Retinal breaks are drawn in red with blue outlines; the flat part of a retinal tear is also drawn in blue.    e    Thin retina is indicated by red hatching outlined in blue, lattice degeneration is shown as blue hatching outlined in blue, retinal pigment is black k , retinal exudates yellow , and vitreous opacities green .

45. (B)   colour coding for documenting retinal pathology

46. Finding the primary break The primary break is the one responsible for the RD. A secondary break is not responsible for the RD because it was either present before the development of the RD or formed after the retina is detached. Finding the primary break is of paramount importance and aided by the following considerations.   

47. 1      Distribution of breaks  in eyes with RD is approximately as follows: 60% in the upper temporal quadrant; 15% in the upper nasal quadrant; 15% in the lower temporal quadrant; 10% in the lower nasal quadrant. The upper temporal quadrant is therefore by far the most common site for retinal break formation and should be examined in great detail if a retinal break cannot be detected initially. It should also be remembered that about 50% of eyes with RD have more than one break, and in most eyes these are located within 90° of each other.

48. 2     Configuration of SRF  is of relevance because SRF spreads in a gravitational fashion, and its shape is governed by anatomical limits ( ora serrata and optic nerve) and by the location of the primary retinal break. If the primary break is located superiorly, the SRF first spreads inferiorly on the same side as the break and then spreads superiorly on the opposite side of the fundus. The likely location of the primary retinal break can therefore be predicted by studying the shape of the RD by Lincoff rules.     

49. a     A shallow inferior RD in which the SRF is slightly higher on the temporal side points to a primary break located inferiorly on that side.

50.   b    A primary break located at 6 o’clock will cause an inferior RD with equal fluid levels.  

51.   c    In a bullous inferior RD the primary break usually lies above the horizontal meridian.    d    If the primary break is located in the upper nasal quadrant the SRF will revolve around the optic disc and then rise on the temporal side until it is level with the primary break.

52.    e    A subtotal RD with a superior wedge of attached retina points to a primary break located in the periphery nearest its highest border.    f    When the SRF crosses the vertical midline above, the primary break is near to 12 o’clock, the lower edge of the RD corresponding to the side of the break .

53. The above points are important because they aid in prevention of the treatment of a secondary break whilst overlooking the primary break. It is therefore essential to ensure that the shape of the RD corresponds to the location of a presumed primary retinal break.     3     History . Although the location of light flashes is of no value in predicting the site of the primary break, the quadrant in which a visual field defect first appears may be of considerable value. For example, if a field defect started in the upper nasal quadrant the primary break is probably located in the lower temporal quadrant.

54. RHEGMATOGENOUS RETINAL DETACHMENT

55. Pathogenesis Rhegmatogenous RD affects about 1 in 10 000 of the population each year and both eyes may eventually be involved in about 10% of patients. It is characterized by the presence of a retinal break held open by vitreoretinal traction that allows accumulation of liquefied vitreous under the NSR, separating it from the RPE.

56. The retinal breaks responsible for RD are caused by interplay between dynamic vitreoretinal traction and an underlying weakness in the peripheral retina referred to as predisposing degeneration. Even though a retinal break is present, a RD will not occur if the vitreous is not at least partially liquefied and if the necessary traction is not present.

57. DYNAMIC VITREORETINAL TRACTION    1     Pathogenesis . Syneresis defines liquefaction of the vitreous gel. Some eyes with syneresis develop a hole in the posterior hyaloid membrane and fluid from within the centre of the vitreous cavity passes through this defect into the newly formed retrohyaloid space. 2. This process forcibly detaches the posterior vitreous and the posterior hyaloid membrane from the ILM of the sensory retina as far as the posterior border of the vitreous base. 3. The remaining solid vitreous gel collapses inferiorly and the retrohyaloid space is occupied entirely by synchytic fluid.   

58. 2     Age at onset  is typically 45–65 years in the general population but may occur earlier in myopic or otherwise predisposed individuals (e.g. trauma, uveitis). The fellow eye frequently becomes affected within 6 months to 2 years.

59.   (A)  Vitreous syneresis ;  (B)  uncomplicated posterior vitreous detachment

60. Complications Of Acute PVD Following PVD, the sensory retina is no longer protected by the stable vitreous cortex, and can be directly affected by dynamic vitreoretinal tractional forces. The vision-threatening complications of acute PVD are dependent on the strength and extent of pre-existing vitreoretinal adhesions.    1      No complications  occur in most eyes because vitreoretinal attachments are weak so that the vitreous cortex detaches completely without sequelae .   

61. 2      Retinal tears  may develop as a result of transmission of traction at sites of abnormally strong vitreoretinal adhesion as previously described .    3     Avulsion of a peripheral blood vessel  resulting in vitreous haemorrhage in the absence of retinal tear formation may occur.

62. (A)  U-tear and localized subretinal fluid associated with acute posterior vitreous detachment;  (B)  the vitreous shows syneresis , posterior vitreous detachment with partial collapse, and retained attachment of cortical vitreous to the flap of the tear  

63. About 60% of all breaks develop in areas of the peripheral retina that show specific changes. These lesions may be associated with a spontaneous breakdown of pathologically thin retinal tissue to cause a retinal hole, or they may predispose to retinal tear formation in eyes with acute PVD. Retinal holes are round or oval, usually smaller than tears and carry a lower risk of RD.

64. PREDISPOSING PERIPHERAL RETINAL DEGENERATION

65. Lattice degeneration     1     Prevalence . Lattice degeneration is present in about 8% of the population. It probably develops early in life, with a peak incidence during the second and third decades. It is found more commonly in moderate myopes and is the most important degeneration directly related to RD. It is usually bilateral and most frequently located in the temporal rather than the nasal fundus, and superiorly rather than inferiorly. Lattice is present in about 40% of eyes with RD.    

66. 2     Pathology.  There is discontinuity of the internal limiting membrane with variable atrophy of the underlying NSR. The vitreous overlying an area of lattice is synchytic but the vitreous attachments around the margins are exaggerated.

67. Vitreous changes associated with lattice degeneration  

68. 3     Signs     •    Spindle-shaped areas of retinal thinning, commonly located between the equator and the posterior border of the vitreous base.    •    A characteristic feature is an arborizing network of white lines within the islands.    •    Some lattice lesions may be associated with ‘snowflakes’ (remnants of degenerate Müller cells.)    •    Associated hyperplasia of the RPE is common.    •    Small holes within lattice lesions are common and usually innocuous.

69. Clinical features of lattice degeneration.  (A)  Small island of lattice with an arborizing network of white lines;  (B)  lattice associated with ‘snowflakes’;  (C)  lattice associated with RPE changes;  (D)  small holes within lattice seen on scleral indentation  

70. 4     Complications     a     No complications  are encountered in most patients.    b      Tears  may occasionally develop in eyes with acute PVD. They typically occur in myopes over the age of 50 years and the SRF progresses more rapidly than in RD caused by small round holes.    c      Atrophic holes   may rarely lead to RD, particularly in young myopes .

71.  Complications of lattice degeneration.  (A)  Atypical radial lattice without breaks;   (B)  two U-tears, the larger one of which shows a small patch of lattice on its flap and is surrounded by a small puddle of subretinal fluid;   (C)  linear tear along the posterior margin of lattice; (D)  multiple small holes within islands of lattice  

72. Snailtrack degeneration Snailtrack degeneration is characterized by sharply demarcated bands of tightly packed ‘snowflakes’ which give the peripheral retina a white frost-like appearance. The islands are usually longer than in lattice degeneration and may be associated with overlying vitreous liquefaction. However, marked vitreous traction at the posterior border of the lesions is seldom present so that tractional U-tears rarely occur, although round holes within the snailtracks may be present.

73.  Islands of snailtrack degeneration, some of which contain holes 

74. Degenerative retinoschisis 1     Prevalence . Degenerative retinoschisis is present in about 5% of the population over the age of 20 years and is particularly prevalent in Hypermetropes (70% of patients are hypermetropic ). Both eyes are frequently involved.   

75. 2     Pathology.   There is coalescence of cystic lesions as a result of degeneration of neuroretinal and glial supporting elements within areas of peripheral cystoid degeneration. This eventually results in separation or splitting of the NSR into an inner (vitreous) layer and an outer (choroidal) layer with severing of neurones and complete loss of visual function in the affected area. In typical retinoschisis the split is in the outer plexiform layer, and in reticular retinoschisis , which is less common, splitting occurs at the level of the nerve fibre layer.

76. 3     Signs   •    Early retinoschisis usually involves the extreme inferotemporal periphery of both fundi , appearing as an exaggeration of microcystoid degeneration with a smooth immobile elevation of the retina.    •    The lesion may progress circumferentially until it has involved the entire fundus periphery. The typical form usually remains anterior to the equator although the reticular type may spread beyond the equator.    •    The surface of the inner layer may show snowflakes as well as sheathing or ‘silver-wiring’ of blood vessels and the schisis cavity may be bridged by rows of torn grey-white tissue.   

77. Microcystoid degeneration.   (A)  Histology shows spaces in the nerve fibre layer delineated by delicate vertical columns of Müller cells;   (B)  circumferential microcystoid degeneration and mild retinoschisis in the inferotemporal and superotemporal quadrants 

78. 4     Complications     a     No complications  occur in most cases and the condition is asymptomatic and innocuous.    b     Breaks . Inner layer breaks are small and round, whilst the less common outer layer breaks are usually larger, with rolled edges and located behind the equator.   

79. C.)     RD  may occasionally develop in eyes with breaks in both layers, especially in the presence of PVD. Eyes with only outer layer breaks do not as a rule develop RD because the fluid within the schisis cavity is viscous and does not pass readily into the subretinal space . However, occasionally the schisis fluid loses its viscosity and passes through the break into the subretinal space, giving rise to a localized detachment of the outer retinal layer which is usually confined to the area of retinoschisis    D.)   Vitreous haemorrhage  is uncommon.

80. Retinoschisis .   (A)  Large breaks in both layers but absence of retinal detachment;  (B)  linear break in the outer layer associated with localized subretinal fluid  

81. Diffuse chorioretinal atrophy Diffuse chorioretinal atrophy is characterized by choroidal depigmentation and thinning of the overlying retina in the equatorial area of highly myopic eyes. Retinal holes developing in the atrophic retina may lead to RD. Because of lack of contrast between the depigmented choroid and sensory retina, small holes may be very difficult to visualize without the help of slit-lamp biomicroscopy .

82.  Diffuse chorioretinal atrophy with holes and localized subretinal fluid  

83. White with pressure’ and ‘white without pressure ’    1     ‘White with pressure’   T ranslucent grey appearance of the retina, induced by indenting the sclera. Each area has a fixed configuration which does not change when the scleral indenter is moved to an adjacent area. It is frequently seen in normal eyes and may be associated with abnormally strong attachment of the vitreous gel. It is also observed along the posterior border of islands of lattice degeneration, snailtrack degeneration and the outer layer of acquired retinoschisis .  

84.   2     ‘White without pressure’   same appearance but is present without scleral indentation. 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.

85.   (A)  ‘White with pressure’;  (B)  extensive vitreous syneresis and strong attachment of condensed vitreous gel to an area of ‘white without pressure’  

86. (A)   Pseudoholes within an area of ‘white without pressure’;   (B)  total retinal detachment caused by a giant tear  

87. PIGMENT CLUMPS Small,localised,irregular patches of pigmentation often associated with vitreoretinal traction tufts. Paravascular vitreoretinal attachments.

88. Significance of myopia Although myopes make up to 10% of the general population, over 40% of all RDs occur in myopic eyes; the higher the refractive error the greater is the risk of RD. The following interrelated factors predispose a myopic eye to RD:    1      Lattice degeneration  is more common in moderate myopes and may give rise to either tears or atrophic holes. Giant retinal tears may also develop along the posterior edge of long lattice islands. 2     Snailtrack degeneration  is common in myopic eyes and may be associated with atrophic holes.

89.   3      Diffuse chorioretinal atrophy  may give rise to small round holes in highly myopic eyes    4      Macular holes  may give rise to RD in highly myopic eyes    5      Vitreous degeneration and PVD  are more common    6      Vitreous loss during cataract surgery , particularly if inappropriately managed, is associated with an increased risk of subsequent RD, particularly in highly myopic eyes   

90. Inferior retinal detachment in a highly myopic eye caused by a giant tear which developed along the posterior border of extensive lattice degeneration; also note lattice in the superotemporal quadrant  

91. Macular hole surrounded by shallow subretinal fluid confined to the posterior pole 

92. SIGNIFICANCE OF APHAKIA About 30% of all RD’s occur in aphakic eyes. MECHANISM-Loss of hyaluronic acid from vitreous gel causes synchysis and PVD which may result in retinal tear. Vitreous loss if inappropriately managed is associated with a 7% risk of RD.

93. SIGNIFICANCE OF BLUNT TRAUMA Severe blunt trauma AP length decreasesSimultaneous expansion at equatorial plane-Relatively inelastic vitreous causes traction along the posterior border of vitreous base-Traumatic retinal dialysis,RD develops months later. Upper nasal quadrant is the most common site.

94. SIGNIFICANCE OF PENETRATING TRAUMA It may be rhegmatogenous,due to retinal tears caused by foreign bodies or tractional .

95. INNOCUOUS PERIPHERAL RETINAL DEGENERATIONS The peripheral retina extends from the equator to the ora serrata and may show the following innocuous lesions.    1     Microcystoid degeneration  consists of tiny vesicles with indistinct boundaries on a greyish -white background which make the retina appear thickened and less transparent. The degeneration always starts adjacent to the ora serrata and extends circumferentially and posteriorly with a smooth undulating posterior border. Microcystoid degeneration is present in all adult eyes, increasing in severity with age, and is not in itself causally related to RD, although it may give rise to retinoschisis .      

96. 2     Pavingstone degeneration  is characterized by discrete yellow-white patches of focal chorioretinal atrophy which is present to some extent in 25% of normal eyes . 3. Honeycomb (reticular) degeneration  is an age-related change characterized by a fine network of perivascular pigmentation which may extend posterior to the equator.    4      Peripheral drusen  are characterized by clusters of small pale lesions which may have hyperpigmented borders. They are similar to drusen at the posterior pole and usually occur in the eyes of elderly individuals.

97.  Innocuous peripheral retinal degenerations.   (A)   Microcystoid seen on scleral indentation;  (B)   pavingstone ;  (C)  honeycomb (reticular);   (D)   drusen   

98. Symptoms The classic premonitory symptoms reported in about 60% of patients with spontaneous rhegmatogenous RD are flashing lights and vitreous floaters caused by acute PVD with collapse . After a variable period of time the patient notices a relative peripheral visual field defect which may progress to involve central vision.

99.    1     Photopsia  is the subjective sensation of a flash of light. In eyes with acute PVD it is probably caused by traction at sites of vitreoretinal adhesion. The cessation of photopsia is the result of either separation of the adhesion or complete tearing away of a piece of retina (operculum). In PVD the photopsia is often described as an arc of golden or white light induced by eye movements and is more noticeable in dim illumination. It tends to be projected into the patient's temporal peripheral visual field. Occasionally photopsia precedes PVD by 24–48 hours.

100. 2     Floaters  are moving vitreous opacities which are perceived when they cast shadows on the retina. Vitreous opacities in eyes with acute PVD are of the following three types:   a     Weiss ring  is a solitary floater consisting of the detached annular attachment of vitreous to the margin of the optic disc. Its presence does not necessarily indicate total PVD, nor does its absence confirm absence of PVD since it may be destroyed during the process of separation.    

101. b     Cobwebs  are caused by condensation of collagen fibres within the collapsed vitreous cortex .     c     A sudden shower  of minute red- coloured or dark spots usually indicates vitreous haemorrhage secondary to tearing of a peripheral retinal blood vessel. Vitreous haemorrhage associated with acute PVD is usually sparse due to the small calibre of peripheral retinal vessels.

102.   (A)  Weiss ring;   (B)  B-scan shows a Weiss ring associated with posterior vitreous detachment

103. 3     A visual field defect  is perceived as a ‘black curtain’. In some patients it may not be present on waking in the morning, due to spontaneous absorption of SRF while lying inactive overnight, only to reappear later in the day. A lower field defect is usually appreciated more quickly by the patient than an upper field defect.

104. The quadrant of the visual field in which the field defect first appears is useful in predicting the location of the primary retinal break, which will be in the opposite quadrant. Loss of central vision may be due either to involvement of the fovea by SRF or, less frequently, obstruction of the visual axis by a large upper bullous RD.

105. Signs General     1     Marcus Gunn pupil  (relative afferent pupillary defect) is present in an eye with an extensive RD irrespective of the type.     2     Intraocular pressure  is usually lower by about 5 mmHg compared with the normal eye. If the intraocular pressure is extremely low, an associated choroidal detachment may be present.     3     Iritis  is very common but usually mild. Occasionally it may be severe enough to cause posterior synechiae . In these cases the underlying RD may be overlooked and the poor visual acuity incorrectly ascribed to some other cause.    

106. 4     ‘ Tobacco dust’  consisting of pigment cells is seen in the anterior vitreous .    5     Retinal breaks  appear as discontinuities in the retinal surface. They are usually red because of the colour contrast between the sensory retina and underlying choroid. However, in eyes with hypopigmented choroid (as in high myopia), the colour contrast is decreased and small breaks may be overlooked unless careful slit-lamp and indirect ophthalmoscopic examination is performed .     6     Retinal signs  depend on the duration of RD and the presence or absence of proliferative vitreoretinopathy (PVR) as described below.

107. ‘Tobacco dust’ in the anterior vitreous

108. Fresh retinal detachment    C onvex configuration Mobile S lightly opaque and corrugated appearance as a result of retinal oedema . L oss of the underlying choroidal pattern and retinal blood vessels appear darker than in flat retina, so that colour contrast between venules and arterioles is less apparent. SRF  extends up to the ora serrata , except in the rare cases caused by a macular hole in which the SRF is initially confined to the posterior pole.      

109.   Fresh retinal detachment.   (A)  U-tear in detached retina;  (B)  superior bullous retinal detachment;   (C)  shallow temporal retinal detachment;   (D)  B-scan shows a totally detached retina with linear echogenic structures inserting onto the optic nerve head to form an open funnel

110. Long-standing retinal detachment The following are the main features of a long-standing rhegmatogenous RD:    1     Retinal thinning   and surface appears smooth secondary to atrophy is a characteristic finding which must not be mistaken for retinoschisis .    2     Secondary intraretinal cysts  may develop if the RD has been present for about 1 year; these tend to disappear after retinal reattachment.  

111.   3      Subretinal demarcation lines  (‘high water marks’) caused by proliferation of RPE cells at the junction of flat and detached retina are common and take about 3 months to develop . They are initially pigmented but tend to lose this with time. Demarcation lines are convex with respect to the ora serrata and, although they represent sites of increased adhesion, they do not invariably limit spread of SRF.

112. Long-standing retinal detachment.   (A)  Secondary retinal cyst;   (B)  B-scan shows a retinal cyst;  (C)  ‘high water mark’ in an eye with an inferior retinal detachment

113. Proliferative vitreoretinopathy Proliferative vitreoretinopathy (PVR) is caused by epiretinal and subretinal membrane formation. Cell-mediated contraction of these membranes causes tangential retinal traction and fixed retinal folds. Usually, PVR occurs following surgery for rhegmatogenous RD or penetrating injury.

114. However, it may also occur in eyes with rhegmatogenous RD that have not had previous vitreoretinal surgery . The main features are retinal folds and rigidity so that retinal mobility induced by eye movements or scleral indentation is decreased . Classification is as follows although it should be emphasized that progression from one stage to the next is not inevitable.

115. B-scan ultrasonography  in advanced disease shows gross reduction of retinal mobility with retinal shortening and the characteristic triangular sign

116. Differential Diagnosis R etinoschisis 1     Symptoms.   Photopsia and floaters are absent because there is no vitreoretinal traction. A visual field defect is seldom observed because spread posterior to the equator is rare. If present it is absolute and not relative as in RD. Occasionally symptoms occur as a result of either vitreous haemorrhage or the development of progressive RD.

117.       2     Signs    •    Breaks may be present in one or both layers.    •    The elevation is convex, smooth, thin and relatively immobile, unlike the opaque and corrugated appearance of a rhegmatogenous RD.    •    The thin inner leaf of the schisis cavity may be mistaken, on cursory examination, for an atrophic long-standing rhegmatogenous RD but demarcation lines and secondary cysts in the inner leaf are absent.

118. (A)  Degenerative retinoschisis showing peripheral vascular sheathing and ‘snowflakes’;   (B)   uveal effusion characterized by choroidal detachment and exudative retinal detachment  

119. Ultrasonography B-scan ultrasonography (US) is very useful in the diagnosis of RD in eyes with opaque media, particularly severe vitreous haemorrhage that precludes visualization of the fundus. Utilises high frequency sound waves ranging from 8-10 MHz . B stands for bright echoes.

120. Types of frequency Low frequency : orbital tissue Medium frequency : ( 7 – 10 mhz ) Retinal , vitreous , optic nerve High frequency : ( 30 – 50 mhz) : ant chamber upto 5 mm

121. Examination technique The patient is either reclining on a chair or lying on a couch. The probe can be placed directly over the conjunctiva or the lids.

122. Probe positions Transverse : Lateral extent, 6 clock hours Longitudinal : radial ,1 clock hours Axial : lesion in relation to lens and optic nerve .

123. Gain adjusts the amplification of the echo signal, similar to volume control of a radio. Higher gain increases the sensitivity of the instrument in displaying weak echoes such as vitreous opacities. Lower gain only allows display of strong echoes such as the retina and sclera, though improves resolution because it narrows the beam.

124. Appearance of Normal Ocular Structures LENS : oval highly reflective structure with intralesional echoes with none to highly reflective echoes. Vitreous is echolucent. Retina, choroid and sclera : single reflective high structure. OPTIC NERVE : Wedge shaped acoustic void in the retrobulbar region . EXTRA OCULAR MUSCLES : Echolucent to low reflective fusiform structures. The SR- LPS complex is the thickest. IR is the thinnest. IO is generally not seen except in pathological conditions.

125. ORBIT -highly reflective due to orbital fat. Always examine the other eye before coming to a conclusion regarding the lesion . Opacities produce dots or short lines Membranous lesions produce an echogenic line

126. USES Vitreous haemorrhage Vitreous exudation Retinal detachment (type / extent) Posterior vitreous detachment (extent) Tumour (size/ site/ post treatment follow up) Retinal detachment (solid / exudative)

127. ULTRASONOGRAPHIC CHARACTERISTICS

128. VITREOUS HAEMORRHAGE To detect extent, density, location and cause Fresh haemorrhage shows dots or lines Old haemorrhage the dots gets brighter

129. POSTERIOR VITREOUS DETACHMENT membranous lesion with no/some attachments to the optic disc

130. POSTERIOR VITREOUS DETACHMENT Mobility of PVD is more than RD. The spike of RD is more than PVD. PVD becomes more prominent in higher gain settings

131. RETINAL DETACHMENT The detachment produces a bright continuous, folded appearance with insertion into the disc and ora serrata. It is to determine the configuration of the detachment as shallow, flat or bullous

132. RHEGMATOGENOUS RD

133. CLOSED FUNNEL RD WITH RETINAL CYST Retinal Tear

134. Appears as RD but it is a PVD Clues : non uniform thickness of membrane very thin attachment to the disc.

135.   (C)  B-scan image showing vitreous haemorrhage and flat retina;  (D)  B-scan image showing vitreous haemorrhage and funnel-shaped retinal detachment  

136. TRACTIONAL RETINAL DETACHMENT

137. The main causes of tractional RD are (a)  proliferative retinopathy  due to diabetes (b)  penetrating posterior segment trauma

138. Pathogenesis of diabetic tractional retinal detachment    Tractional RD is caused by progressive contraction of fibrovascular membranes over large areas of vitreoretinal adhesion. In contrast to acute PVD in eyes with rhegmatogenous RD, PVD in diabetic eyes is gradual and frequently incomplete. It is thought to be caused by leakage of plasma constituents into the vitreous gel from a fibrovascular network adherent to the posterior vitreous surface.

139. 2     Static vitreoretinal traction  of the following three types is recognized.    a     Tangential  traction is caused by the contraction of epiretinal fibrovascular membranes with puckering of the retina and distortion of retinal blood vessels.    b     Anteroposterior  traction is caused by the contraction of fibrovascular membranes extending from the posterior retina, usually in association with the major arcades, to the vitreous base anteriorly .    c     Bridging  (trampoline) traction is the result of contraction of fibrovascular membranes which stretch from one part of the posterior retina to another or between the vascular arcades, tending to pull the two involved points together.

140. Tractional retinal detachment associated with anteroposterior and bridging traction  

141. Diagnosis    1     Symptoms.   Photopsia and floaters are usually absent because vitreoretinal traction develops insidiously and is not associated with acute PVD. The visual field defect usually progresses slowly and may become stationary for months or even years. 2     Signs .    •    The RD has a concave configuration and breaks are absent .    •    Retinal mobility is severely reduced and shifting fluid is absent .    •    The SRF is shallower than in a rhegmatogenous RD and seldom extends to the ora serrata .   

142.    •    The highest elevation of the retina occurs at sites of vitreoretinal traction .    •    If a tractional RD develops a break it assumes the characteristics of a rhegmatogenous RD and progresses more quickly (combined tractional-rhegmatogenous RD).

143. (A)   Tractional retinal detachment in severe proliferative diabetic retinopathy;  (B)  B-scan image of another patient shows a shallow tractional retinal detachment

144. EXUDATIVE RETINAL DETACHMENT

145. Pathogenesis Exudative RD is characterized by the accumulation of SRF in the absence of retinal breaks or traction. It may occur in a variety of vascular, inflammatory and neoplastic diseases involving the NSR, RPE and choroid in which fluid leaks outside the vessels and accumulates under the retina.

146. As long as the RPE is able to compensate by pumping the leaking fluid into the choroidal circulation, no fluid accumulates in the subretinal space and RD does not occur. However, when the normal RPE pump is overwhelmed, or if the RPE activity is decreased, then fluid starts to accumulate in the subretinal space

147. The main causes are the following:   1     Choroidal tumours  such as melanomas, haemangiomas and metastases; it is therefore very important to consider that exudative RD is caused by an intraocular tumour until proved otherwise.    2     Inflammation  such as Harada disease and posterior scleritis .    3     Bullous central serous chorioretinopathy  is a rare cause.    4     Iatrogenic  causes include retinal detachment surgery and panretinal photocoagulation.   

148. 5     Subretinal neovascularization  which may leak and give rise to extensive subretinal accumulation of fluid at the posterior pole .   6     Hypertensive choroidopathy ,  as may occur in toxaemia of pregnancy, is a very rare cause .   7     Idiopathic  such as the uveal effusion syndrome.

149. Diagnosis    1      Symptoms.   Photopsia is absent F loaters may be present if there is associated vitritis . The visual field defect may develop suddenly and progress rapidly.    2     Signs    •    The RD has a convex configuration, just like a rhegmatogenous RD, but its surface is smooth and not corrugated.    •    The detached retina is very mobile E xhibits the phenomenon of ‘shifting fluid’ in which SRF responds to the force of gravity and detaches the area of retina under which it accumulates.   

150. Exudative retinal detachment with shifting fluid.  (A)  Inferior collection of subretinal fluid with the patient sitting;  (B)  the subretinal fluid shifts upwards when the patient assumes the supine position

151. Exudative retinal detachment caused by a choroidal melanoma 

152.  ‘Leopard spot’ pigmentation following resolution of exudative retinal detachment  

153. EXUDATIVE RETINAL DETACHMENT

154. Choroidal detachment    1     Symptoms.   Photopsia and floaters are absent A visual field defect may be noticed if the choroidal detachment is extensive.    2     Signs     •    Low intraocular pressure is common as a result of concomitant detachment of the ciliary body.    •    The anterior chamber may be shallow in eyes with extensive choroidal detachments.    •    The elevations are brown, convex, smooth and relatively immobile.

155. •    Large ‘kissing’ choroidal detachments may obscure the view of the fundus .    •    The elevations do not extend to the posterior pole because they are limited by the firm adhesion between the suprachoroidal lamellae where the vortex veins enter their scleral canals.

156. (A)  Choroidal detachment.   (B)  B-scan image of extensive choroidal detachment almost touching in the middle of the vitreous cavity

157. TREATMENT The choice of treatment to resolve the secondary subretinal accumulation of fluid should be directed toward the primary pathology. L aser treatment may be effective to treat focal breakdown of the blood-retina barrier, as seen in central serous chorioretinopathy , exudative diabetic retinopathy, Coats’ disease, or vascular malformations.

158. PROPHYLACTIC TREATMENT Criteria for selection Characteristics of break Tear is more dangerous than a hole Large break is more dangerous than a small break Location-Superior tears,Upper temporal tears,equatorial breaks are more dangerous. A retinal break in an aphakic eye,myopia .

159. Family history of RD. If patient cannot be relied upon to report new synptoms indicative of RD. In patients with Marfan’s syndrome,Stickler’s syndrome or Ehlers danlos syndrome.

160. In the absence of breaks, neither of predisposing degeneration is treated prophylactically unless associated with following risk factors 1.RD in fellow eye 2.Aphakia 3.High myopia 4.Strong family history of RD. 5. Marfan’s syndrome,Stickler’s syndrome or Ehlers danlos syndrome.

161. TREATMENT MODALITIES Cryotherapy v/s Photocoagulation 1.Location of lesion Equatorial lesions- cryo or Photocoagulation Postequatorial lesions-Photocoagulation Peripheral lesions-Cryotherapy

162. Clarity of media-In hazy media cryotherapy preferred. Pupil size-Small pupils easier to treat with cryotherapy.

163. Laser photocoagulation 200 microns spot size,duration of 0.1-0.2 seconds. Two rows of confluent burns surrounding the lesion. LASER used- Argon Green, Krypton Red, Diode Laser

164. Cornea- Burns,endothelial damage. Iritis,iris atrophy Anterior capsular opacities Cystoid macular edema Exudative RD New retinal tears Retinal haemorrhage. Complications

165. Cryotherapy PRINCIPLE T he normal microvillous interdigitations seen between retina and RPE are missing . If both the RPE and overlying retina are frozen, the adhesion that results after reattachment demonstrates cellular connections between the NSR and RPE consisting of desmosome formation between retinal glia and RPE or direct contact between retinal glia and Bruch’s membrane.

166. Current cryotherapy instrumentation employs expansion of high-pressure nitrous oxide at the tip of a probe generating temperatures as low as −89°C. Temperature effect is confined to the tip of the probe by an insulating sleeve. A probe 2.0 to 2.5 mm in diameter usually is used for retinal work. Treatment of retinal breaks & pathologic conditions requires accurate placement of the cryoprobe tip .

167. The goal is to surround all retinal breaks with 1 to 2 mm of contiguous treatment. Treatment should include freezing of overlying retina, because this results in a stronger adhesion than does treatment of RPE alone . To avoid damage of refreezing, treatment should not significantly overlap.

168. The treatment end point is retinal whitening without ice crystal formation . Cryoprobe should not be removed until it has defrosted completely because premature removal may crack the choroid and give rise to choroidal haemorrhage .

169. COMPLICATIONS Chemosis Diplopia if rectus muscle is frozen. Vitritis if treatment is excessively heavy. CAUSES OF FAILURE Failure to surround the entire lesion Failure to release vitreoretinal traction New breaks within or adjacent to treated area due to excessively heavy treatment.

170. Cryotherapy vs LASER Retinopexy Cryotherapy Use of external probe & IDO Can be used with moderate media opacities Promotes dispersion of viable RPE cells CME, wrinkling of ILM Increased Postoperative flare, extensive retinal oedema , necrosis LASER Retinopexy Endolaser / IDO with laser Difficult in moderate media opacities Ideal for posteriorly located breaks

171. Father of RD surgery

172. Retinal Reattachment Surgery Scleral Buckling Surgery with or without drainage Encircling S egmental Temporary scleral buckle Lincoff balloon Absorbable material Vitrectomy Classical Sutureless Pneumoretinopexy Routine With drainage of SRF/intravitreal liquid

173. INDICATIONS FOR BED REST To prevent macular involvement by subretinal fluid. To promote resorption of SRF. To unroll mobile flap of giant retinal tear.

174. INSPECTION OF SCLERA To detect areas of thinning-It may be associated with problems such as penetration of choroid and retina during insertion of scleral sutures, cutting of sutures, scleral rupture during localisation or cryotherapy

175. Retinopexy The indent from the explant closes retinal breaks but retinopexy is required to produce an enduring bond between the retina & retinal pigment epithelium that will persist even if the indent disappears. Retinopexy was initially achieved using diathermy in association with lamellar scleral dissection and scleral implants. Cryotherapy has supplanted diathermy because it can be performed without scleral dissection . Intraoperative cryopexy remains a quick and simple technique .

176. Cryopexy remains the choice of most retinal surgeons for the intraoperative treatment of retinal breaks during scleral buckling

177. Scleral Buckling Surgery AIM I s to close retinal breaks by indenting eye wall, preventing the passage of liquefied vitreous into the subretinal space.

178. How scleral buckle works??? Gold standard for uncomplicated RD Relieves vitreous traction along the surface of the buckle The buckle displaces the retinal break centrally, where the break becomes tamponaded by cortical vitreous It displaces SRF away from the break & alters the shape of eyewall, thus reducing the effects of the intraocular fluid currents

179. EXPLANT-Material sutured directly onto the sclera to create a buckle. IMPLANT-Material placed within the sclera to create a buckle.

180. Scleral Buckles EXPLANT MATERIAL Soft silicone( silastic )sponge Hard silicone straps Hard silicone tyre

181. Buckle configuration Radial explants- right angle to limbus- to seal U tears/posterior breaks Segmental circumferential- parallel to limbus Encircling- entire circumference of globe for 360˚ buckle

182. INDICATIONS Radial buckling Large U shaped tears Posterior breaks because sutures are easier to insert. Segmental circumferential buckling Multiple breaks Anterior breaks Wide breaks such as dialysis and giant tears.

183. ENCIRCLING BUCKLE Breaks involving three or more quadrants. Extensive RD without detectable breaks. PVR Grade C Failed local procedures.

184. PROCEDURE VIDEO

185. Complications Scleral perforation Choroidal Haemorrhage Buckle infection, migration, extrusion Failed retinal reattachment Redetachment - PVR Anterior segment ischemia Choroidal edema, detachment Secondary Glaucoma Suboptimal visual recovery- CME, persistent subfoveal SRF Diplopia and motility disturbances

186. FISHMOUTHING

187. Fish mouth Retinal Tears Typically large U shaped equatorial tears located superiorly in a bullous RD open widely following scleral buckling and drainage of SRF. Management- Prevented by using a radial buckle instead of circumferential Extra radially oriented buckling material can be added. Air can be injected into the vitreous cavity so that bubble will close the tear.

188. Radial retinal folds If encircling buckle is too tight,radial folds form over the retina. Prevents retinal reattachment Management Loosen the buckle,if too tight Air injection into the vitreous cavity.

189. Lincoff’s balloon Can be inserted under LA Minimal surgical trauma No scleral suturing No changes in refractive status of the eye

190. DRAINAGE OF SUBRETINAL FLUID INDICATIONS Difficulty in localization of retinal breaks in highly elevated bullous RDs. In immobile retina due to PVR, eye is first softened by draining SRF to achieve a high buckle. Long standing RD as they tend to have viscous SRF. Inferior tears. Coexisting glaucoma

191. Technique Fundus examined to make sure SRF has not shifted. Radial Sclerotomy, beneath the area of deepest SRF, 4mm long, sufficient depth to allow herniation of small dark knuckle of choroid. Insert a 5-0 dacron mattress suture across the lips of the sclerotomy .

192. If large vessel is present , suture the sclerotomy and choose another site Gentle low-heat cautery to the knuckle 27 G hypodermic needle bent at 2mm from tip, full thickness perforation . Sclerotomy site inspected-Presence of small pigment granules means all the SRF has been drained.

193. Complications Failure of drainage- dry tap Retinal perforation Intraocular haemorrhage Ocular hypotony Vitreous loss Retinal incarceration(star shaped puckering at the drainage site) Endophthalmitis

194. PNEUMATIC RETINOPEXY Sulfur hexafluoride (SF6) and perfluoropropane (C3F8) are the gases most frequently used with PR. Success also has been reported with sterile room air . The value of the intraocular bubble is based on three features: buoyancy, surface tension, and isolation of retinal tears from intraocular currents.

195. Buoyancy applies upward pressure on the detached retina . The surface tension of the bubble closes the retinal break and prevents the bubble from passing into the subretinal space. With the break closed, the retinal pigment epithelial pump removes the subretinal fluid.

196. Because of their low solubility in water, SF6 and C3F8 tend to diffuse from the eye very slowly. But, the nitrogen and oxygen that are in solution in surrounding tissues of the eye are much more soluble and pass relatively quickly into the gas bubble, following the law of partial pressures. The net result is the initial expansion of a bubble of pure SF6 or C3F8 within the vitreous, followed by gradual resorption.

197. Short, minimally invasive, OPD procedure Indications Retinal break smaller than one clock hour Multiple breaks within one clock hour All breaks in superior 8 clock hours Hypotony following drainage of SRF. Fishmouthing of large retinal tear Radial retinal folds Macular hole giving rise to RD.

198. Gases tried in vitreoretinal surgery Non-expansile Expansile Air SF 6 Nitrogen C 4 F 10 Helium CF 4 Oxygen C 2 F 6 Argon C 3 F 8 Xenon C 4 F 10 Krypton C 5 F 12

199. Properties of intraocular gases Gas Average Duration Largest size of the bubble (duration) Average expansion Nonexpansile concentration Typical Dose Air 3 days Immediate No expansion -- 0.8ml SF6 12 days 36 hours 2 times 18% 0.5ml C3F8 38 days 72 hours 4 times 14% 0.3ml

200. Procedure Anaesthesia - Topical/LA Needle is inserted 4mm behind the limbus to avoid the vitreous base. Aimed at the center of the globe, stopped when the tip of needle is just visible through the pupil. Single, expansile gas bubble injected in vitreous cavity through pars plana using sterile 30 G needle Paracentesis Positioning- to ensure max. tamponade, retinal break should remain at the top

201. CASE SELECTION AVOIDED IN 1. Breaks larger than 1 clock-hour or multiple breaks extending over more than 1 clock-hour of the retina. 2. Breaks in the inferior 4 clock-hours retina. 3. Presence of PVR grade C or D . 4. Disability precluding maintenance of the required positioning. 5. Severe or uncontrolled glaucoma. 6. Cloudy media precluding full assessment of the retina.

202. PR presents a advantage IN 1. Macular breaks and other posterior retinal breaks. Posterior retinal breaks are difficult to treat with SB, optic pits with macular detachment. 2 . Redetachment or persistent detachment after SB .

203. PR presents a advantage IN 3. Isolated tears under the superior rectus. Placing a segmental buckle under a vertically acting muscle runs the risk of iatrogenic diplopia; this is eliminated with PR . 4. Filtering blebs. If a functioning filtering bleb is present, or if a filtering procedure may be necessary in future, PR should be considered .

204. PR presents a advantage IN 5. Impending macular detachment. 6. Bullous detachment. When RD is highly bullous, retinal tears can be difficult to localize and treat with SB, a problem which is avoided by two-session PR.

205. One-session / two-session procedure PR can be done in one session, with cryopexy applied to the retinal breaks just before gas injection, or as a two-session procedure, with initial gas injection followed by laser 1 or 2 days later, when the retina is reattached. One-session procedures always involve cryopexy , since laser cannot be applied to detached retina. Two-session procedures are usually, but not always, done with the laser.

206. Disadvantages Poor visualisation due to formation of minute air bubbles in the vitreous. Excessive elevation of IOP.

207. Silicone Oil in RD Repair FDA approved for VR surgery in 1994 Highly viscous, transparent liquid with high surface tension, lighter than water Viscosity 1000-5000 centistokes Indications Detachment with inferior breaks Extensive PVR One eyed patient with need of early visual recovery Giant retinal tears

208. Advantages Prolonged tamponading effect Less strict requirement of post-operative positioning Early visual rehabilitation No restriction on air travel Hypotony less common Disadvantages Needs repeat surgery for removal Cataract, raised IOP,band shaped keratopathy Inadequate tamponading for inferior breaks Post-operative change in refraction Perisilicone oil membrane & macular pucker Redetachment after oil removal (15-20%)

209. Advantages of intraocular gases vs use of silicon oil No need of repeat surgery for removal Absence of complications related to long-term presence of silicone oil Disadvantages of intraocular gases Requirement of strict postoperative positioning Risk of postoperative rise in IOP Restriction of air travel Delayed visual rehabilitation Short duration of tamponading effect

210. Primary Vitrectomy in Rhegmatogenous RD

211. Pars Plana Vitrectomy Indicated in Media opacities- cataract , VH & advanced PVR Posteriorly located breaks RD with giant retinal tear or macular hole Tractional RD Relative contraindications Relatively simple phakic RD

212. PRINCIPLES OF VITRECTOMY The principles of vitrectomy to treat RRD are release of tractional forces that precipitated the retinal break, and the closure and reattachment of breaks to the underlying RPE . The surgical procedure requires: (1) removal of the vitreous gel and preretinal tractional membrane; (2) intraoperative flattening of the detached retina; (3) application of retinopexy; and (4) placement of a tamponade in vitreous cavity.

213. PPV Compared to SB, PPV offers several advantages. The view of the retinal periphery is enhanced , I dentification of retinal breaks is rendered easier, A chievement of complete intraoperative retinal attachment is possible, the risks of hemorrhage or retinal incarceration inherent to external drainage procedure applied during SB is eliminated, and the technique is less likely to cause a refractive change .

214. Procedure video

215. Sutureless Microincision Vitrectomy Transconjunctival sutureless MIVS using 23G/ 25G instrumentation Advantages Shorter surgical time Less surgically induced astigmatism Reduced risk of post-operative corneal astigmatism Greater rigidity, better illumination, improved fluidics with 23 G IOP compensation via direct control of infusion pressure Wide angle viewing systems

216. Management of Tractional Retinal Detachment TRD progresses very slowly, may reattach spontaneously Localized TRD away from macula- observation Indications for surgery Macular threatened or detached Vitreous haemorrhage Retinal holes Surgical Principles To relax the vitreoretinal traction Closure of retinal holes Drainage of SRF

217. PPV- to clear media, release of AP & tangential traction ERM- peeling/ segmentation/ delamination Enblock excision of traction membranes Retinotomy with internal drainage of SRF, internal tamponade with gas/silicone oil injection Endodiathermy & endophotocoagulation - new vessels & retinopexy

218. Comparison of various surgical techniques Method Reattachment Rate Limitations/Complications Benefits Scleral Buckling 94% Morbidity, infection, buckle extrusion, ocular motility disturbances Excellent long term anatomic success, good visual outcome Pars Plana Vitrectomy 71-92% (1˚ success rate) 94% (2˚ success rate) Iatrogenic retinal breaks, PVR, lens trauma, cataract progression Visualization of all breaks, removal of opacities/synechiae, anatomic success in complicated detachments Pneumatic Retinopexy 64% (1˚ success rate) 91% (2˚ success rate) Limited use only in uncomplicated RRD with superior breaks Post-op positioning, iatrogenic breaks In-office procedure, minimally invasive, ↓ Recovery time, better post-op VA

219. SB / PR / PPV Complicated detachments are usually managed with PPV , whereas localized, relatively simple cases are usually managed with a “walling-off” (demarcating) procedure employing laser or cryotherapy , with PR, or with a small and localized scleral buckling procedure.

220. Pneumatic  retinopexy  versus scleral buckle for repairing simple rhegmatogenous retinal detachments . Hatef E et al The objectives of this review were to assess the effectiveness and safety of  pneumatic  retinopexy  versus scleral buckle or pneumatic  retinopexy  versus a combination treatment of scleral buckle and vitrectomy for people with RRD.

221. The evidence suggests that pneumatic  retinopexy  may result in lower rates of reattachment and higher rates of recurrence than scleral buckle for eyes with RRD, but does not rule out no difference between procedures. The relative safety of the procedures is uncertain and the relative effects of these procedures in terms of other patient-important outcomes, such as visual acuity and quality of life, is unknown.

222. Outcomes after Failed Pneumatic  Retinopexy  for Retinal Detachment. Anaya et al Abstract PURPOSE: To provide visual and anatomic outcomes for patients with retinal detachment (RD) in whom primary pneumatic  retinopexy  (PR) failed. DESIGN: Retrospective, single- center , consecutive case series. PARTICIPANTS: Eyes with RD that failed a primary PR .

223. METHODS: Anatomic and functional outcomes were evaluated for patients receiving treatment for failed PR. Three secondary procedures were compared, including repeat PR, pars plana vitrectomy (PPV), and combined scleral buckle (SB) plus PPV (SB+PPV). MAIN OUTCOME MEASURES: Anatomic reattachment and visual acuity (VA) at 1 year. Anatomic success rates for secondary PR, PPV, and SB+PPV after failed PR were lower than published success rates for their use in primary RD.

224. Macular choroidal thickness after vitreoretinal surgery: Long-term effect of pars plana vitrectomy with and without encircling scleral buckling surgery. Gama et al . PURPOSE : To evaluate the macular choroidal thickness (CT) of eyes subjected to pars plana vitrectomy (PPV) whether or not combined with encircling scleral buckling (ESB) surgery for primary rhegmatogenous retinal detachment repair at 6 months or more after surgery.

225. The CT of the eyes subjected to combined ESB and PPV was significantly increased at 6 months or more after surgery compared to the CT of their FE and to the CT of the eyes subjected to PPV alone, which could be explained by a venous engorgement caused by the ESB.

226. Scleral buckling in phakic uncomplicated primary rhegmatogenous retinal detachment: long-term outcomes . Quijano C et al The aim of this study was to report the long-term anatomical and functional outcomes of SB surgery in phakic patients with uncomplicated primary rhegmatogenous retinal detachment (PRRD ).

227. Retrospective studyof 90 phakic eyes with PRRD treated with SB surgery that had a minimum of 5 years follow-up. High single operation success rate over time in phakic PRRD, repaired through SB surgery. Functional and anatomical success was maintained throughout the follow-up without complications.

228. Anatomical and Functional Results Following 23-Gauge Primary Pars Plana Vitrectomy for Rhegmatogenous Retinal Detachment: Superior versus Inferior Breaks Panagiotis Stavrakas et al In this retrospective study, they evaluated the anatomical and functional outcomes of patients with rhegmatogenous retinal detachment primarily treated with pars plana vitrectomy in regard to the location of the breaks.

229. Conclusion This study supports that acceptable reattachment rates can be achieved using PPV for uncomplicated RRD irrespective of the breaks location and inferior breaks do not constitute an independent risk factor for worse anatomical or functional outcome.

230. REFERENCES RETINAL DETACHMENT-JACK KANSKI RETINAL DETACHMENT SURGERY-CHIGNELL AAO YANOFF

231. THANK YOU