Intravitreal in opthamology

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A presentation from Dr. Atul Dhavan from Dr. Agarwal's Eye Hospital , Chennai in Kalpavriksha 2012- Chennai

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Intravitreal in opthamology

  1. 1. Retinal Lasers in Ophthalmology Dr. Atul Dhawan (M.S., F.E.R.C.) Vitreo-Retina Consultant Dr. Agarwal’s Retina Foundation Chennai
  2. 2. INTRODUCTIONLASER is an acronym for:• L : Light• A : Amplification (by)• S : Stimulated• E : Emission (of)• R : RadiationTerm coined by Gordon Gould.Lase means to absorb energy in one form and to emit a new form oflight energy which is more useful.
  3. 3. Gordon Gould [1959]
  4. 4. The Electromagnetic Spectrum
  5. 5. Incandescent vs. Laser Light1. Many wavelengths 1. Monochromatic2. Multidirectional 2. Directional3. Incoherent 3. Coherent
  6. 6. These three properties of laser light arewhat can make it more hazardous thanordinary light. Laser light can deposit alot of energy within a small area.
  7. 7. Two things to produce laser1. Population inversion2. Stimulated emission
  8. 8. Stimulated emission• Suppose an electron is in a higher energy level and a photon comes along with an energy equal to the difference between the electrons energy and a lower energy. What will happen is that the photon will stimulate the electron to fall into the lower energy state, thereby emitting a photon. This is pictured below.• The emitted photon will have the same energy as the original photon, and viewed as waves we will then have two waves emerging from the atom in phase with the same frequency. Such waves will constructively interfere, leading to a more intense wave.
  9. 9. Types of Lasers LASERS Gas Solid State Metal EXCIMER Dye Diode Vapour Argon Ruby Copper Argon Fluoride Krypton Nd Yag Gold Helium NeonCarbon Dioxide
  10. 10. Factors effecting retinal photocoagulation• Degree of scattering• Absorption of energy by ocular pigments• Spot size• Power used• Exposure time
  11. 11. Ocular pigments• Melanin:  RPE, Choroid  Argon Blue, Krypton  Pan Retinal Photocoagulation Haemoglobin: Absorb blue,green and yellow but poor for red light.  Argon Green are absorbed, Krypton yellow. These laser are found to be useful to coagulate the blood vessels.• Xanthophyll:  Macular area  Maximum absorption is blue
  12. 12. Laser effects LASER TISSUE Thermal Photo- Ionizing Effect Effect chemical Photocoagulation  Photoradation  Photoablation. Photovaporization
  13. 13. THREE BASIC LIGHT TISSUE INTERACTIONS(1) Photocoagulation: Laser Light transfer energy Target Tissue[absorption by ocular pigments] Generate Heat[transfer to tissue by thermal conduction] Denatures Proteins (Coagulation)Rise in temperature of about 10 to 20 0C will cause coagulation of tissue.
  14. 14. PHOTOCHEMICAL EFFECTPHOTORADIATION :• Hematoporphyrin Derivatives administerd i.v. are selectively taken up by metabolically active tissue. subsequently irradiated by rhodamine dye laser[630 nm] 72 hours injection .This leads to formation of singlet oxygen which is cytotoxic.e.g. Treatment of ocular tumour and CNV
  15. 15. THREE BASIC COMPONENTS A Laser Exciting Optical Cavity Medium Methods (Laser Tube)• e.g. Solid, • for exciting • around the Liquid or Gas atoms or medium molecules in which act as the medium a resonator e.g. Light, Electricity
  16. 16. MODES OF LASER OPERATIONContinuous Wave • It deliver their energy in a (CW) Laser: continuous stream of photons. • Produce energy pulses of a few Pulsed Lasers: tens of micro to few mili second. Q Switches • Deliver energy pulses of extremely Lasers: short duration (nano second). A Mode-locked • Emits a train of short duration Lasers: pulses (picoseconds).
  17. 17. Laser delivery system• SLIT LAMP• LASER INDIRECT OPHTHALMOSCOPE• ENDOLASER
  18. 18. Lenses for laser
  19. 19. PRP Lens Image magnification: 1.96 FOV : 165 degree LSMF: 0.51
  20. 20. VOLK AREA CENTRALIS IImage magnification: 1.05 LSMF : 0.95 FOV : 82 degree
  21. 21. CLASSIFICATION OF CHORIORETINAL BURN INTENSITY• Light : Barely visible retinal blanching• Mild : Faint white retinal burn• Moderate : Opaque dirty white retinal burn• Heavy : Dense white retinal burn
  22. 22. Pan Retinal Photocoagulation
  23. 23. LASER TREATMENT OF FUNDUS DISORDERS• Diabetic Retinopathy• Retinal Vascular Diseases• Choroidal Neovascularization (CNV)• Eales disease• Central Serous Retinopathy (CSR)• Retinal Break/Detachment• Tumour
  24. 24. India-Diabetic capital of the worldINCIDENCE BETWEEN 20-79 YRS HAS GONE UP 6 FOLD IN THE LAST DECADEYear No. of people 2006 41 millions 2025 80 millions Data Source Dr J Brown,Chair,IDF Task Force
  25. 25. DIABETES CHALLANGE EVERY ONE KNOWS SOMEONE WHO HAS DIABETES.“IT IS THAT COMMON IN INDIA”
  26. 26. Diabetic retinopathyTYPE OF RETINOPATHY THERAPYMaculopathy Focal photocoagulationCSMEDiffuse leakage around macula Grid laserCircinate Focal photocoagulationPre-proliferative Retinopathy Frequent reviewProliferative retinopathy Pan retinal photocoagulation Vitreoretinal surgery withAdvanced diabetic eye disease photocoagulation
  27. 27. How it works?
  28. 28. Diabetic macular oedma LEAK DIFFUSE MIXED FOCALSRF/NSD IVTA MODIFIED GRID FOCAL TO MA ,ANTIVEGF GRID Periodic Periodic FFA,OCT after evaluation evaluation 2-3 4wks 3mths mths
  29. 29. ETDRS PROTOCOL Focal Grid.• 50 to 100u size 50 to 200u size.• 0.05 to 0.1sec. 0.05 to 0.1 sec.• Moderate intensity. Light to medium int ( mild RPE whitening)
  30. 30. Pan retinal photocoagulationcomprises of :1. 2000-3000 application2. in a scatter pattern of3. 500 size with goldmann lense and 200-300 m size with panfunduscopic lens.4. duration 0.05-0.10 sec.
  31. 31. Retinal Vein Occlusion
  32. 32. IntroductionVascular obstructive disease of retina is a common vascular disorder, second only toDiabetic Retinopathy in incidence RVO Central retinal vein Branch retinal vein obstruction obstructionIschemic non ischemic
  33. 33. Venous Occlusion Causes elevation of venous and capillary pressure Stagnation of blood flow Hypoxia of involved retina Damage of capillaries endothelium Extra vasation of blood More pressure Further more stagnation Viscous cycle starts
  34. 34. C.R.V.O StudyQn. What is the natural history of eyes with perfused CRVO (<10 DD CNP areas) ?Ans. 1/3rd of eyes with perfused CRVO became non- perfused by 3 years Majority of eyes classified as indeterminate were non-perfused
  35. 35. C.R.V.O StudyQn. Does early PRP prevent NVI in non- perfused CRVO (>10 DD area CNP) ?Ans. Prophylactic PRP does not prevent Neovascularisation of iris or angle Careful monitoring of INV/ANV and prompt PRP is needed
  36. 36. C.R.V.O StudyQn. Does early PRP is more effective than delaying the Tt until ant. Segment neovascularization is first seen in preventing NVG?Ans. NO
  37. 37. C.R.V.O StudyQn. Does macular grid PHC improve V.A. in macular oedema due to perfused macular edema ?Ans. Grid PHC not recommended in perfused macular oedema.
  38. 38. PRP Protocol• 500 or 1000 µ size, duration 0.2 sec• Burns 0.5 – 1 burn width apart• More than 2 DD from center of the fovea till equator or beyond in all quadrants, nasally >500 µ from disc• Around 2000 spots• Avoid retinal hemorrhages or large retinal vessels
  39. 39. Treatment Recommendations – Non-perfused CRVO Nonperfused CRVO Nonperfused CRVO with TC-INV without INV/ANV or any ANV Panretinal PHCNo PRP unless monthly followup not possible Follow up every 2-4weeks If INV/ANV increases Supplemental panretinal PHC
  40. 40. Neovascularisation B.R.V.O In BRVO• Areas of CNP >5DD (NVD or NVE : first 3 yrs) – 60% do not develop NVE• 40% develop : NVE• 60% of NVE Vit. hge
  41. 41. • For this reason it is recommended that laser photocoagulation should be delayed till NVE develops.
  42. 42. B.R.V.O Recommendations 1. Vision 20/40 or less 2. Wait for 3-6 months: Clearance of Hges : Good FFA 3. Evaluation of FFA: Macular oedema Vs Ischaemia 4. Recommend grid treatment : Macular oedema FFA proven 5. Macular Non perfusion : No laser
  43. 43. Eale’s DiseaseHENRY EALES – 1980
  44. 44. Etiopathogenesis• Unknown• Factors - Tuberculosis - Focal sepsis - Berger’s disease - Leprosy - Brusellosis - Sarcoidosis - Behcet’s disease
  45. 45. Clinical featuresSIGNS –1. Inflammation- Venous dilatation, tortuosity of veins- Perivascular exudates, sheathing- Superficial retinal haemorrhage- Cells in vitreous, aqueous- Keratic precipitates
  46. 46. Clinical features2. Nonperfusion- Intraretinal haemorrhage- Collaterals around occluded vessels- Microaneurysms- A-V shunts- Venous beading- Hard exudates , cotton wool spots
  47. 47. Clinical features3. Neovascularisation - 10% Patients - NVD - NVE - Rubiosis iridis - Neovascular glaucoma
  48. 48. Clinical features4. Other abnormalities- Pigmentation – healed chorioretinitis- Vitreous codensation, PVD- Macular changes – Macular oedema - Ischaemia - Hole - ERM
  49. 49. ManagementAIMS - Reduce perivasculitis - Reduce Vitritis - Reduce chance of vitreous haemorrhage
  50. 50. Management1. Corticosteroids2. Anterior Retinal Cryotherapy3. Photocoagulation4. Vitrectomy
  51. 51. Photocoagulation• Flat new retinal vessel: direct laser to vessel• Elevated neovascularization: laser the feeder vessel• NVD: Pan retinal photocoagulation• Capillary non perfusion area: scatter laser
  52. 52. Central Serous Retinopathy
  53. 53. HISTORY• First recognized by von Graefe in 1866 & named central recurrent retinitis• Different names given by diff. persons• ICSC given by Gass et al in 1967s
  54. 54. Idiopathic central serous chorioretinopathy (ICSC)• Patient is usually of Type A personality• Organ transplantation , pregnancy• Less common in high degree of myopia• Young 20—50 yrs• Male : Female 10 : 1 [ Age 30 – 50 yrs ]• Male : Female 2 : 1 [ Age > 50 yrs ]• WHITE > BLACK
  55. 55. SYMPTOMS• Sudden onset Blurring of vision• Metamorphopsia, micropsia• Seeing a dark patch (central scotoma )
  56. 56. Signs• Ophthalmoscopy—circumscribed round or oval area of retinal elevation at post. pole , outlined by a glistening reflex• Foveal reflex—Absent / attenuated
  57. 57. Central serous retinopathy ( CSR )
  58. 58. FFA• Pin-points site of RPED & site of leakage of serous fluid from RPE into SR space• In 95% of cases one area of leakage of dye are seen -INK BLOT APPEARANCE• Only in 10% cases the classic “smoke stack pattern” is seen due to convection currents & high sp. gr. of SR exudate
  59. 59. FFA• Majority of leaking sites are within 1 DD of fovea, but foveola is affected in < 10%• Incidence of leakage sites is greatest in upper nasal quadrant >lower nasal >lower temporal• 25% of leaks in PM bundle
  60. 60. Smoke-stack appearance
  61. 61. Smoke-stack appearanceLater dye passes intosubretinal space and Subsequent lateral spreadvertical ascend until entire area filled
  62. 62. FFA of CSREarly hyperfluorescent spot Subsequent concentric spread until entire area filled Ink-blot appearance
  63. 63. TREATMENT• Laser Photocoagulation at the site of leak destroying leaky vessels, debrides diseased RPE, allows growth of healthy RPE.• Laser causes early recovery but final VA is same.
  64. 64. Laser Photocoagulation• Vn of less then 6/12• Well defined leakage point on FFA atleast 500 micron from the fovea• More then 4 month• Recurrent CSR• Bilateral CSR• OCCUPATIONAL NEED of the Pt
  65. 65. AGE RELATED MACULAR DEGENERATION
  66. 66. TYPES OF ARMD• NON EXUDATIVE – (dry / non neovascular) – slowly progressive – 90% of ARMD• EXUDATIVE – (wet / neovascular) – less common – 88% of legal blindness due to ARMDBoth may occur in combination
  67. 67. Exudative AMDDrusen and AMD - progressionAtrophic AMD
  68. 68. Classical CNV•Well defined memb. fills with dye in “LACY”pattern in early phase, fluoresces brightly duringpeak dye transit then leaks into subretinal spaceand around CNV within 1—2 min•Fibrous tissue of CNV stain to give late Hyperf.•Subdivided into 3, with relation to foveola
  69. 69. Classical CNV 1. EXTRA-foveal >200 um from FAZ center 2. JUXTA-foveal <200 um from FAZ but sparing the foveola 3. SUB-foveal Involving foveola either by nearby extension or direct origin underneath(70% of CNV extend to subfoveal position within 1 yr)
  70. 70. Occult CNV • Poorly defined membrane gives late leakage Occult divided into two By MPS1. Fibrovascular RPED2. Late leakage of fluorescein from undetermined source
  71. 71. TREATMENT OF WET ARMD1. Photocoagulation2. Radiation therapy3. TTT4. TSDLP5. Photodynamic therapy (PDT)
  72. 72. TREATMENT OF ARMD6. Pharmacological agents7. Micronutrients8. Gene therapy9. Foveal translocation/ Macular rotation10. RPE / IPE cell transplantation
  73. 73. TREATMENT OF ARMD1. PHOTOCOAGULATIONFor complete oblitn of CNVFocal—Extra, Juxta, selected subfoveal CNVFor recurrent CNV similar parametersArgon Green laser(514 nm) recommended by MPS. Diode infrared if covered by thin haemorrhage
  74. 74. Disadvantages of laser T/t• Only for well defined CNV• Significant fall in VA depending on site• High recurrence rates• Benefit occurs after long period (months)• Breach of Bruch’s membrane can trigger similar pathgenesis as the ds. itself.
  75. 75. PHOTODYNAMIC THERAPY• Photochemical injury to the target• Drug is conc. in rapidly dividing cells & NV tissue• T1/2 of dye 5—6 hrs• Excreted in stools (urine not discolored)
  76. 76. • Singlet oxygen & free radicals damage cellular str. by platelet activation, vessel occlusion, destruction of fibrovascular tissue
  77. 77. PDT Photosensitizers— working at wave length• Benzoporphyrin derivatives (vertiporfin)-690• Tin ethyl etiopuritin (Purlytin)-664 nm• Lutetiutexaphyrin (Lu-tex)-732 nm
  78. 78. Eligibility criteria for PDT1. Lesions involving FAZ2. Lesion size < 5400 um3. CNV > 50% of the lesion4. Classic component >50% of CNV5. > 200 um from disc edge6. VA 20/200—20/40
  79. 79. C/I of PDT S/E of PDT Extravasation• Allergic to the dye Rash• H/O porphyria Headache• Severe liver disease VA reduction• Severe Heart disease Decreased fields Dry eye• Uncontrolled HT Conjunctivitis Cataract Hemorrhages
  80. 80. Procedure of PDT1. 15 mg visudyne powder + 7 ml dist. water2. Dark green soln (protect from light)3. Store at 20-25o C, use within 4 hrs4. Dose 6 mg/m2 . Dilute in 5% DNS to make 30 ml soln5. Inject 3 ml/min over 10 minutes6. Rinse IV line by 5 ml of 5% DNS7. After 15 min (the vessels fill completely)
  81. 81. Procedure of PDT8. Diode laser 689 nm9. 50—60 J/cm2 at intensity of 600 mw/cm210. Duration—83 seconds11. Spot size—GLD + 1000 um (GLDgreatest linear dimension of lesion by FFA)12. Protective dark glasses, hat, clothing & avoiding sunlight/bright light for 5 days

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