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Retinal Lasers in Ophthalmology
Dr. Atul Dhawan (M.S., F.E.R.C.)Vitreo-Retina Consultant
Dr. Agarwal’s Retina FoundationChennai
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
2. Multidirectional
3. Incoherent
1. Monochromatic
2. Directional
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 inversion2. 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
Carbon Dioxide
Neon
Helium
Krypton
Argon
Gas
Nd Yag
Ruby
Solid State
Gold
Copper
MetalVapour
Argon Fluoride
EXCIMER Dye Diode
LASERS
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 effectsLASER
TISSUE
Thermal Effect Photo-chemical
Ionizing Effect
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 Medium
•e.g. Solid, Liquid or Gas
Exciting Methods
•for exciting atoms or molecules in the medium e.g. Light, Electricity
Optical Cavity (Laser Tube)
•around the medium which act as a resonator
MODES OF LASER OPERATION
•It deliver their energy in a continuous stream of photons.
Continuous Wave (CW) Laser:
•Produce energy pulses of a few tens of micro to few mili second.Pulsed Lasers:
•Deliver energy pulses of extremely short duration (nano second).
Q Switches Lasers:
•Emits a train of short duration pulses (picoseconds).
A Mode-locked Lasers:
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 worldINCIDENCE BETWEEN 20-79 YRS HAS GONE UP 6 FOLD
IN THE LAST DECADE
No. of people
41 millions
80 millions
Data SourceDr J Brown,Chair,IDF Task Force
Year 2006 2025
DIABETES CHALLANGE
EVERY ONE KNOWS SOMEONE
WHO HAS DIABETES.“IT IS THAT COMMON IN INDIA”
Diabetic retinopathyTYPE OF RETINOPATHY THERAPY
Maculopathy CSME Focal photocoagulation
Diffuse leakage around macula Grid laser
Circinate Focal photocoagulation
Pre-proliferative Retinopathy Frequent review
Proliferative retinopathy Pan retinal photocoagulation
Advanced diabetic eye disease Vitreoretinal surgery with photocoagulation
How it works?
Diabetic macular oedma
LEAK
DIFFUSE
GRID
Periodic evaluation
3mths
IVTA ,ANTIVEGF
FFA,OCT after 4wks
MIXED
MODIFIED GRID
FOCAL
FOCAL TO MA
Periodic evaluation 2-3
mths
SRF/NSD
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 m size with goldmann lense and 200-300 mm size with panfunduscopic lens.
4. duration 0.05-0.10 sec.
Retinal Vein Occlusion
IntroductionVascular obstructive disease of retina is a common vascular disorder, second only to Diabetic Retinopathy in incidence
RVO
Central retinal vein obstruction
Branch retinal vein 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 without INV/ANV
No PRP unless monthly follow up not possible
Panretinal PHC
Follow up every 2-4weeks If INV/ANV increases
Supplemental panretinal PHC
Nonperfused CRVO with TC-INV or any ANV
NeovascularisationIn BRVO
• Areas of CNP >5DD(NVD or NVE : first 3 yrs)
– 60% do not develop NVE
• 40% develop : NVE
• 60% of NVE Vit. hge
B.R.V.O
• For this reason it is recommended that laser photocoagulation should be delayed till NVE develops.
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
B.R.V.O
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 vertical ascend
Subsequent lateral spread 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
Atrophic AMD Exudative AMDDrusen and AMD - progression
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)
6. Pharmacological agents
7. Micronutrients
8. Gene therapy
9. Foveal translocation/ Macular rotation
10. RPE / IPE cell transplantation
TREATMENT OF ARMD
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.
• 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)
PHOTODYNAMIC THERAPY
• Singlet oxygen & free radicals damage cellular str. by platelet activation, vessel occlusion, destruction of fibrovascular tissue
Photosensitizers— working at wave length
• Benzoporphyrin derivatives (vertiporfin)-690 • Tin ethyl etiopuritin (Purlytin)-664 nm • Lutetiutexaphyrin (Lu-tex)-732 nm
PDT
Eligibility criteria for PDT
1. 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
C/I of PDT
• Allergic to the dye• H/O porphyria• Severe liver disease• Severe Heart disease• Uncontrolled HT
S/E of PDT
ExtravasationRashHeadacheVA reductionDecreased fieldsDry eyeConjunctivitisCataractHemorrhages
Procedure of PDT
1. 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 soln
5. Inject 3 ml/min over 10 minutes6. Rinse IV line by 5 ml of 5% DNS7. After 15 min (the vessels fill completely)
Procedure of PDT
8. Diode laser 689 nm9. 50—60 J/cm2 at intensity of 600 mw/cm2
10. Duration—83 seconds11. Spot size—GLD + 1000 um
(GLDgreatest linear dimension of lesion by FFA)
12. Protective dark glasses, hat, clothing & avoiding sunlight/bright light for 5 days