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