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Retinal Lasers in Ophthalmology




       Dr. Atul Dhawan (M.S., F.E.R.C.)
               Vitreo-Retina Consultant
           Dr. Agarwal’s Retina Foundation
                       Chennai
INTRODUCTION

LASER is an acronym for:
•   L   : Light
•   A   : Amplification (by)
•   S   : Stimulated
•   E   : Emission (of)
•   R   : Radiation
Term coined by Gordon Gould.
Lase means to absorb energy in one form and to emit a new form of
light energy which is more useful.
Gordon Gould [1959]
The Electromagnetic Spectrum
Incandescent vs. Laser Light




1.   Many wavelengths   1.   Monochromatic
2.   Multidirectional   2.   Directional
3.   Incoherent         3.   Coherent
These three properties of laser light are
what can make it more hazardous than
ordinary light. Laser light can deposit a
lot of energy within a small area.
Two things to produce laser
1. Population inversion
2. Stimulated emission
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 electron's 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.
Types of Lasers
                                   LASERS

    Gas          Solid State    Metal   EXCIMER          Dye   Diode
                               Vapour

    Argon           Ruby       Copper   Argon Fluoride


   Krypton         Nd Yag       Gold


   Helium


    Neon


Carbon Dioxide
Factors effecting retinal
             photocoagulation

•   Degree of scattering
•   Absorption of energy by ocular pigments
•   Spot size
•   Power used
•   Exposure time
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
Laser effects
                            LASER


                            TISSUE




  Thermal                   Photo-         Ionizing Effect
   Effect                  chemical

 Photocoagulation        Photoradation
                          Photoablation
. Photovaporization
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.
PHOTOCHEMICAL EFFECT


PHOTORADIATION :

•   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
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
MODES OF LASER OPERATION

Continuous 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).
Laser delivery system
• SLIT LAMP
• LASER INDIRECT OPHTHALMOSCOPE
• ENDOLASER
Lenses for laser
PRP Lens
    Image magnification: 1.96

    FOV :     165 degree

    LSMF:     0.51
VOLK AREA CENTRALIS

          IImage magnification: 1.05

          LSMF : 0.95

          FOV :   82 degree
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
Pan Retinal Photocoagulation
LASER TREATMENT OF
                     FUNDUS DISORDERS
•   Diabetic Retinopathy

•   Retinal Vascular Diseases

•   Choroidal Neovascularization (CNV)

•   Eales disease

•   Central Serous Retinopathy (CSR)

•   Retinal Break/Detachment

•   Tumour
India-Diabetic capital of the world
INCIDENCE BETWEEN 20-79 YRS HAS GONE UP 6 FOLD
              IN THE LAST DECADE
Year
                            No. of people
 2006
                            41 millions
 2025
                            80 millions

                            Data Source
                            Dr J Brown,Chair,IDF Task Force
DIABETES CHALLANGE


 EVERY ONE KNOWS SOMEONE
       WHO HAS DIABETES.
“IT IS THAT COMMON IN INDIA”
Diabetic retinopathy
TYPE OF RETINOPATHY               THERAPY




Maculopathy
                                  Focal photocoagulation
CSME

Diffuse leakage around macula     Grid laser
Circinate                         Focal photocoagulation
Pre-proliferative Retinopathy     Frequent review
Proliferative retinopathy         Pan retinal photocoagulation

                                  Vitreoretinal surgery with
Advanced diabetic eye disease
                                  photocoagulation
How it works?
Diabetic macular oedma

                                          LEAK




                    DIFFUSE                  MIXED       FOCAL
SRF/
NSD

                                 IVTA      MODIFIED
        GRID                                          FOCAL TO MA
                              ,ANTIVEGF     GRID



        Periodic                                         Periodic
                          FFA,OCT after
       evaluation                                     evaluation 2-3
                              4wks
         3mths                                            mths
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)
Pan retinal photocoagulation



comprises of :
1.   2000-3000 application
2.   in a scatter pattern of
3.   500 size with goldmann lense and 200-300
      m size with panfunduscopic lens.
4.   duration 0.05-0.10 sec.
Retinal Vein Occlusion
Introduction
Vascular obstructive disease of retina is a common vascular disorder, second only to
Diabetic Retinopathy in incidence




                                        RVO


       Central retinal vein                              Branch retinal vein
          obstruction                                       obstruction



Ischemic                    non ischemic
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
C.R.V.O Study

Qn. 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
C.R.V.O Study
Qn. 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
C.R.V.O Study

Qn. Does early PRP is more effective than delaying
    the Tt until ant. Segment neovascularization is
    first seen in preventing NVG?


Ans. NO
C.R.V.O Study
Qn. Does macular grid PHC improve V.A. in
 macular oedema due to perfused macular
 edema ?


Ans. Grid PHC not recommended in perfused
  macular oedema.
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
Treatment Recommendations –
                   Non-perfused CRVO

   Nonperfused CRVO              Nonperfused CRVO with TC-INV
   without INV/ANV               or any ANV




                                      Panretinal
                                      PHC
No PRP unless monthly follow
up not possible                Follow up every 2-4weeks
                               If INV/ANV increases



                                Supplemental panretinal
                                PHC
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
• For this reason it is recommended that laser
  photocoagulation should be delayed till NVE
  develops.
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
Eale’s Disease

HENRY EALES – 1980
Etiopathogenesis
• Unknown
• Factors - Tuberculosis
        -   Focal sepsis
        -   Berger’s disease
        -   Leprosy
        -   Brusellosis
        -   Sarcoidosis
        -   Behcet’s disease
Clinical features
SIGNS –
1. Inflammation
- Venous dilatation, tortuosity of veins
- Perivascular exudates, sheathing
- Superficial retinal haemorrhage
- Cells in vitreous, aqueous
- Keratic precipitates
Clinical features
2. Nonperfusion
- Intraretinal haemorrhage
- Collaterals around occluded vessels
- Microaneurysms
- A-V shunts
- Venous beading
- Hard exudates , cotton wool spots
Clinical features

3. Neovascularisation
 -   10% Patients
 -   NVD
 -   NVE
 -   Rubiosis iridis
 -   Neovascular glaucoma
Clinical features
4. Other abnormalities
- Pigmentation – healed chorioretinitis
- Vitreous codensation, PVD
- Macular changes – Macular oedema
               - Ischaemia
               - Hole
               - ERM
Management
AIMS - Reduce perivasculitis
     - Reduce Vitritis
     - Reduce chance of vitreous
       haemorrhage
Management

1. Corticosteroids

2. Anterior Retinal Cryotherapy

3. Photocoagulation

4. Vitrectomy
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
Central Serous Retinopathy
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
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
SYMPTOMS

• Sudden onset Blurring of vision
• Metamorphopsia, micropsia
• Seeing a dark patch (central scotoma )
Signs
• Ophthalmoscopy—circumscribed round
 or oval area of retinal elevation at post. pole
 , outlined by a glistening reflex

• Foveal reflex—Absent / attenuated
Central serous retinopathy ( CSR )
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
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
Smoke-stack appearance
Smoke-stack
               appearance




Later dye passes into
subretinal space and         Subsequent lateral spread
vertical ascend              until entire area filled
FFA of CSR




Early hyperfluorescent spot   Subsequent concentric spread until entire area filled




                       Ink-blot appearance
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.
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
AGE RELATED MACULAR
    DEGENERATION
TYPES OF ARMD
• NON EXUDATIVE
  – (dry / non neovascular)
  – slowly progressive
  – 90% of ARMD
• EXUDATIVE
  – (wet / neovascular)
  – less common
  – 88% of legal blindness due to ARMD


Both may occur in combination
Exudative AMD
Drusen and AMD - progression
Atrophic AMD
Classical CNV

•Well defined memb. fills with dye in “LACY”
pattern in early phase, fluoresces brightly during
peak dye transit then leaks into subretinal space
and around CNV within 1—2 min
•Fibrous tissue of CNV stain to give late Hyperf.
•Subdivided into 3, with relation to foveola
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)
Occult CNV

 • Poorly defined membrane gives late leakage


         Occult divided into two By MPS

1. Fibrovascular RPED

2. Late leakage of fluorescein from
   undetermined source
TREATMENT OF WET ARMD

1. Photocoagulation

2. Radiation therapy

3. TTT

4. TSDLP

5. Photodynamic therapy (PDT)
TREATMENT OF ARMD

6. Pharmacological agents

7. Micronutrients

8. Gene therapy

9. Foveal translocation/ Macular rotation

10. RPE / IPE cell transplantation
TREATMENT OF ARMD

1. PHOTOCOAGULATION
For complete oblitn of CNV
Focal—Extra, Juxta, selected subfoveal CNV
For recurrent CNV similar parameters
Argon Green laser(514 nm) recommended by
  MPS. Diode infrared if covered by thin
  haemorrhage
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.
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)
• Singlet oxygen & free radicals damage cellular
  str. by platelet activation, vessel occlusion,
  destruction of fibrovascular tissue
PDT

 Photosensitizers— working at wave length


• Benzoporphyrin derivatives (vertiporfin)-690
• Tin ethyl etiopuritin (Purlytin)-664 nm
• Lutetiutexaphyrin (Lu-tex)-732 nm
Eligibility criteria for PDT
1.   Lesions involving FAZ
2.   Lesion size < 5400 um
3.   CNV > 50% of the lesion
4.   Classic component >50% of CNV
5.   > 200 um from disc edge
6.   VA 20/200—20/40
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
Procedure of PDT

1. 15 mg visudyne powder + 7 ml dist. water
2. Dark green soln (protect from light)
3. Store at 20-25o C, use within 4 hrs
4. Dose 6 mg/m2 . Dilute in 5% DNS to make 30
   ml soln
5. Inject 3 ml/min over 10 minutes
6. Rinse IV line by 5 ml of 5% DNS
7. After 15 min (the vessels fill completely)
Procedure of PDT

8.   Diode laser 689 nm
9.   50—60 J/cm2 at intensity of 600 mw/cm2
10.  Duration—83 seconds
11.  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
Intravitreal in opthamology
Intravitreal in opthamology
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Intravitreal in opthamology

  • 1. Retinal Lasers in Ophthalmology Dr. Atul Dhawan (M.S., F.E.R.C.) Vitreo-Retina Consultant Dr. Agarwal’s Retina Foundation Chennai
  • 2. INTRODUCTION LASER is an acronym for: • L : Light • A : Amplification (by) • S : Stimulated • E : Emission (of) • R : Radiation Term coined by Gordon Gould. Lase means to absorb energy in one form and to emit a new form of light energy which is more useful.
  • 5. Incandescent vs. Laser Light 1. Many wavelengths 1. Monochromatic 2. Multidirectional 2. Directional 3. Incoherent 3. Coherent
  • 6. These three properties of laser light are what can make it more hazardous than ordinary light. Laser light can deposit a lot of energy within a small area.
  • 7.
  • 8. Two things to produce laser 1. Population inversion 2. Stimulated emission
  • 9. 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 electron's 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.
  • 10.
  • 11. Types of Lasers LASERS Gas Solid State Metal EXCIMER Dye Diode Vapour Argon Ruby Copper Argon Fluoride Krypton Nd Yag Gold Helium Neon Carbon Dioxide
  • 12. Factors effecting retinal photocoagulation • Degree of scattering • Absorption of energy by ocular pigments • Spot size • Power used • Exposure time
  • 13. 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
  • 14. Laser effects LASER TISSUE Thermal Photo- Ionizing Effect Effect chemical  Photocoagulation  Photoradation  Photoablation . Photovaporization
  • 15. 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.
  • 16. PHOTOCHEMICAL EFFECT PHOTORADIATION : • 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
  • 17. 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
  • 18.
  • 19. MODES OF LASER OPERATION Continuous 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).
  • 20.
  • 21. Laser delivery system • SLIT LAMP • LASER INDIRECT OPHTHALMOSCOPE • ENDOLASER
  • 23. PRP Lens Image magnification: 1.96 FOV : 165 degree LSMF: 0.51
  • 24. VOLK AREA CENTRALIS IImage magnification: 1.05 LSMF : 0.95 FOV : 82 degree
  • 25. 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
  • 27. LASER TREATMENT OF FUNDUS DISORDERS • Diabetic Retinopathy • Retinal Vascular Diseases • Choroidal Neovascularization (CNV) • Eales disease • Central Serous Retinopathy (CSR) • Retinal Break/Detachment • Tumour
  • 28.
  • 29. India-Diabetic capital of the world INCIDENCE BETWEEN 20-79 YRS HAS GONE UP 6 FOLD IN THE LAST DECADE Year No. of people 2006 41 millions 2025 80 millions Data Source Dr J Brown,Chair,IDF Task Force
  • 30. DIABETES CHALLANGE EVERY ONE KNOWS SOMEONE WHO HAS DIABETES. “IT IS THAT COMMON IN INDIA”
  • 31. Diabetic retinopathy TYPE OF RETINOPATHY THERAPY Maculopathy Focal photocoagulation CSME Diffuse leakage around macula Grid laser Circinate Focal photocoagulation Pre-proliferative Retinopathy Frequent review Proliferative retinopathy Pan retinal photocoagulation Vitreoretinal surgery with Advanced diabetic eye disease photocoagulation
  • 33.
  • 34.
  • 35. Diabetic macular oedma LEAK DIFFUSE MIXED FOCAL SRF/ NSD IVTA MODIFIED GRID FOCAL TO MA ,ANTIVEGF GRID Periodic Periodic FFA,OCT after evaluation evaluation 2-3 4wks 3mths mths
  • 36. 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)
  • 37.
  • 38. Pan retinal photocoagulation comprises of : 1. 2000-3000 application 2. in a scatter pattern of 3. 500 size with goldmann lense and 200-300 m size with panfunduscopic lens. 4. duration 0.05-0.10 sec.
  • 40. Introduction Vascular obstructive disease of retina is a common vascular disorder, second only to Diabetic Retinopathy in incidence RVO Central retinal vein Branch retinal vein obstruction obstruction Ischemic non ischemic
  • 41. 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
  • 42. C.R.V.O Study Qn. 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
  • 43. C.R.V.O Study Qn. 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
  • 44. C.R.V.O Study Qn. Does early PRP is more effective than delaying the Tt until ant. Segment neovascularization is first seen in preventing NVG? Ans. NO
  • 45. C.R.V.O Study Qn. Does macular grid PHC improve V.A. in macular oedema due to perfused macular edema ? Ans. Grid PHC not recommended in perfused macular oedema.
  • 46. 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
  • 47. Treatment Recommendations – Non-perfused CRVO Nonperfused CRVO Nonperfused CRVO with TC-INV without INV/ANV or any ANV Panretinal PHC No PRP unless monthly follow up not possible Follow up every 2-4weeks If INV/ANV increases Supplemental panretinal PHC
  • 48. 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
  • 49. • For this reason it is recommended that laser photocoagulation should be delayed till NVE develops.
  • 50. 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
  • 52. Etiopathogenesis • Unknown • Factors - Tuberculosis - Focal sepsis - Berger’s disease - Leprosy - Brusellosis - Sarcoidosis - Behcet’s disease
  • 53. Clinical features SIGNS – 1. Inflammation - Venous dilatation, tortuosity of veins - Perivascular exudates, sheathing - Superficial retinal haemorrhage - Cells in vitreous, aqueous - Keratic precipitates
  • 54. Clinical features 2. Nonperfusion - Intraretinal haemorrhage - Collaterals around occluded vessels - Microaneurysms - A-V shunts - Venous beading - Hard exudates , cotton wool spots
  • 55. Clinical features 3. Neovascularisation - 10% Patients - NVD - NVE - Rubiosis iridis - Neovascular glaucoma
  • 56. Clinical features 4. Other abnormalities - Pigmentation – healed chorioretinitis - Vitreous codensation, PVD - Macular changes – Macular oedema - Ischaemia - Hole - ERM
  • 57. Management AIMS - Reduce perivasculitis - Reduce Vitritis - Reduce chance of vitreous haemorrhage
  • 58. Management 1. Corticosteroids 2. Anterior Retinal Cryotherapy 3. Photocoagulation 4. Vitrectomy
  • 59.
  • 60. 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
  • 62. 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
  • 63. 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
  • 64. SYMPTOMS • Sudden onset Blurring of vision • Metamorphopsia, micropsia • Seeing a dark patch (central scotoma )
  • 65. Signs • Ophthalmoscopy—circumscribed round or oval area of retinal elevation at post. pole , outlined by a glistening reflex • Foveal reflex—Absent / attenuated
  • 67. 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
  • 68. 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
  • 70. Smoke-stack appearance Later dye passes into subretinal space and Subsequent lateral spread vertical ascend until entire area filled
  • 71. FFA of CSR Early hyperfluorescent spot Subsequent concentric spread until entire area filled Ink-blot appearance
  • 72.
  • 73. 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.
  • 74. 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
  • 75. AGE RELATED MACULAR DEGENERATION
  • 76. TYPES OF ARMD • NON EXUDATIVE – (dry / non neovascular) – slowly progressive – 90% of ARMD • EXUDATIVE – (wet / neovascular) – less common – 88% of legal blindness due to ARMD Both may occur in combination
  • 77. Exudative AMD Drusen and AMD - progression Atrophic AMD
  • 78. Classical CNV •Well defined memb. fills with dye in “LACY” pattern in early phase, fluoresces brightly during peak dye transit then leaks into subretinal space and around CNV within 1—2 min •Fibrous tissue of CNV stain to give late Hyperf. •Subdivided into 3, with relation to foveola
  • 79. 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)
  • 80. Occult CNV • Poorly defined membrane gives late leakage Occult divided into two By MPS 1. Fibrovascular RPED 2. Late leakage of fluorescein from undetermined source
  • 81. TREATMENT OF WET ARMD 1. Photocoagulation 2. Radiation therapy 3. TTT 4. TSDLP 5. Photodynamic therapy (PDT)
  • 82. TREATMENT OF ARMD 6. Pharmacological agents 7. Micronutrients 8. Gene therapy 9. Foveal translocation/ Macular rotation 10. RPE / IPE cell transplantation
  • 83. TREATMENT OF ARMD 1. PHOTOCOAGULATION For complete oblitn of CNV Focal—Extra, Juxta, selected subfoveal CNV For recurrent CNV similar parameters Argon Green laser(514 nm) recommended by MPS. Diode infrared if covered by thin haemorrhage
  • 84. 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.
  • 85. 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)
  • 86. • Singlet oxygen & free radicals damage cellular str. by platelet activation, vessel occlusion, destruction of fibrovascular tissue
  • 87. PDT Photosensitizers— working at wave length • Benzoporphyrin derivatives (vertiporfin)-690 • Tin ethyl etiopuritin (Purlytin)-664 nm • Lutetiutexaphyrin (Lu-tex)-732 nm
  • 88. Eligibility criteria for PDT 1. Lesions involving FAZ 2. Lesion size < 5400 um 3. CNV > 50% of the lesion 4. Classic component >50% of CNV 5. > 200 um from disc edge 6. VA 20/200—20/40
  • 89. 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
  • 90. Procedure of PDT 1. 15 mg visudyne powder + 7 ml dist. water 2. Dark green soln (protect from light) 3. Store at 20-25o C, use within 4 hrs 4. Dose 6 mg/m2 . Dilute in 5% DNS to make 30 ml soln 5. Inject 3 ml/min over 10 minutes 6. Rinse IV line by 5 ml of 5% DNS 7. After 15 min (the vessels fill completely)
  • 91. Procedure of PDT 8. Diode laser 689 nm 9. 50—60 J/cm2 at intensity of 600 mw/cm2 10. Duration—83 seconds 11. 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