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FFA and ICG
Presenter-
Dr. Sulabh Sahu
Learning Objectives
• INTRODUCTION
• BASIC PRINCIPLES
• FLUOROSCENE
• TECHNIQUE
• CONTRAINDICATION
• NORMAL FFA
• ABNORMAL FINDING
• INDICATIONS
Fundus Fluorescein Angiography
• Photography of the fundus performed in rapid sequence following
intravenous injection of fluorescein dye.
• Provides :
- Flow characteristics in the blood vessels
- Assessment of functional integrity of retinal vessels
- Records fine details of retinal pigment epithelium and retinal circulation.
- Check the integrity of the blood ocular barrier.
- outer blood retinal barrier breaks in CSR
- inner blood retinal barrier breaks in NVD,NVE
HISTORY OF FFA
• The technique of using intravenous fluorescein to evaluate the ocular
circulation was introduced 40 years ago by Mac Lean and Maumenee.
• Chao and Flocks provided the earliest description of fluorescein
angiography in 1958.
• Finally, it was introduced into clinical use in 1961 by Novotny and Alvis,
who demonstrated the photographic documentation of the fluorescein
dynamics.
• Over the last 3 decades advances have occurred in this sphere, digital
imaging has made possible the generation of high resolution angiography
of the retina and choroid.
Basic principles
• Luminescence:
Emission of light from any source other than high
temperature.
• Fluorescence:
Luminescence that is maintained only by continuous
excitation. Property of certain molecules to emit
light energy of longer wavelength when stimulated
by a shorter wavelength.
• Phosphorescence:
Luminescence where the emission continues long
after the excitation has stopped.
Fluorescent
chemical
absorbs
Radiant
energy
release
Free
electron
Jump
to
higher
level
Becomes
unstable
Returns
To
Lower
level
Emit
energy
fluorescence
UNDERSTANDING FLUORESCENCE
OUTER AND INNER RETINAL BLOOD
BARRIER
• The major choroidal vessels are impermeable to
both bound and free fluorescein.
• The walls of the choriocapillaris contain
fenestrations through which unbound molecules
escape into the extravascular space.
• It crosses Bruch membrane but on reaching the
RPE are blocked by intercellular complexes termed
tight junctions or zonula occludens.
OUTER BLOOD–RETINAL BARRIER
INNER BLOOD–RETINAL BARRIER
 It composed principally of the tight junctions
between retinal capillary endothelial cells.
 Across which neither bound nor free fluorescein
can pass.
 The basement membrane and pericytes play only a
minor role in this regard.
 Disruption of the blood–retinal barrier permits
leakage of both bound and free fluorescein into the
extravascular space.
PRINCIPLE OF FFA
• Based on
 Luminescence
 Fluorescence
 Phosphorescence
• Two filters are used:
 COBALT BLUE EXCITATION FILTER
 YELLOW GREEN BARRIER FILTER
EXCITATION AND EMISSION SPECTRUM
OF FLUORESCEIN
EXCITATION FILTER
• Absorption spectrum lies between 465-490 nm.
• Excitation peak = 490nm(blue part of spectrum)
• The blue flash excites the unbound fluorescein within the blood vessels or
the leaked out fluorescein.
• The blue light is reflected off of the fundus structures that do not have
fluorescein.
BARRIER FILTER
• Emission spectrum lies between 520 – 530 nm
• Emission peak = 530 nm
• Just in front of the film a filter is placed that allows the green-yellow
fluorescent light through but keeps out the blue reflected light.
• Thus, even though the excitation and emission spectra are quite close, as
long as suitably matched excitation and barrier filters are used, only
substances capable of fluorescence are detected.
SODIUM FLUORESCEIN
• Sodium fluorescein (C20H10O5Na2)
• Orange red crystalline hydrocarbon.
• Low molecular weight (376.27 Daltons).
• Nontoxic, inexpensive, safe, alkaline solution.
• Fluoresces at Blood pH (7.37-7.45).
• Absorbs blue light (480-500 nm).
• Emits yellow-green (500-600 nm) (Peak 525 nm).
• 80% bound to plasma protein and also with RBC.
• Can’t pass through tight retinal barriers so allows
study of retinal circulation
CLEARANCE
• Within 24 hours
• Sodium Fluorescein is metabolised to fluorescein glucuronide.
• The plasma half-life of fluorescein is 11 minutes
• Mainly –urine ( yellow orange coloration)
• Small amount-bile
• Some absorbed by kidney
• Skin staining may remain up to 24 hours
• Urine discoloration –24-36 hours
DOSASGE AND ADMINISTRATION
• Solutions containing 500 mg of fluorescein are
available in vials of:
- 10 ml of 5% fluorescein
- 5 ml of 10% fluorescein
- 3 ml of 25% fluorescein solution (750 mg)
• Solution above 25% precipitates.
• For children, the dose is calculated on the
basis of 35mg for each 5kg of body weight.
• Dye is injected as a bolus into the vein of the
patient's arm.
• With a greater volume the injection time increases, with a smaller volume,
more fluorescein remains in the dead space between the arm and the heart.
• Therefore, 5 ml of 10% solution (500 mg) fluorescein is generally
preferred.
• The venous dead space between the hand or the antecubital vein and the
heart may be 5 to 10 ml, leading to sluggish or reduced flow of fluorescein
into the central circulation.
• The fluorescein can be flushed with 5 to 10 ml of normal saline.
• An alternative is to elevate the patient’s arm above the level of the heart
using an adjustable armrest, reducing the fluorescein transit time to the
heart.
TECHNIQUE AND EQUIPMENTS
• The materials needed for fluorescein angiography are as follows:
1. Fundus camera and auxiliary equipment
2. 23 gauge scalp vein needle
3. 5 ml syringe
4. Fluorescein solution
5. 20 gauge 1 ½ inch needle to draw the dye
6. Armrest for fluorescein injection
7. Tourniquet
8. Alcohol
9. Bandage
10. Standard emergency equipment
EQUIPMENT
• The traditional fluorescein angiography unit has two 35 mm cameras, one
for color fundus photography while the other (black & white) for
fluorescein angiography.
• Most fundus cameras take 30° photographs (magnification of 2.5X on a
35mm film), which are adequate for a study of posterior pole lesions
especially macular diseases.
• Many camera units provide variable magnification at 20, 30 and 50 degrees.
• The 50° view is most useful for lesions involving a large area of the fundus.
PROCEDURE
• Informed consent – explain the procedure to the patient.
• Dilate patient’s pupil.
• Fluorescein solution, scalp vein needle, 5 ml syringe
and the emergency tray is prepared.
• Check fundus camera for any fault.
• Observe lens and fundus camera for any dust or opacity.
• Feed the machine with patient information – Name,
MRD no, age, sex, clinical diagnosis etc.
• The patient is positioned and the camera aligned.
• Color photography of both eyes.
• Red free photograph of the posterior pole is taken.
• Insert the scalp-vein needle, preferably at anticubital vein
and inject the fluorescein dye 5ml of 10% solution in 5-
10 seconds.
• Simultaneously inject fluorescein dye and start
Fluorescein mode in machine.
• Once machine is set at Fluorescein mode timer will start
and exciter and barrier filter will be activated.
• Oral administration at a dose of 30 mg/kg; and pictures should be taken over 20–
60 minutes following ingestion.
• Images are taken at 1–2 second intervals initially to capture the critical early
transit phases, beginning 5–10 seconds after injection, tapering frequency through
subsequent phases.
• Start fluorescein photograph 8 seconds after start of injection in young and after
10 seconds in older patients.
• Images may be captured as late as 10–20 minutes.
• When photography is done, reassure the patient that all went well and remind him
or her that the urine will be discolored for a day or so (24-36 hours). Make patient
wait an additional 20 minutes for observation for possible reactions to fluorescein.
FLUORESCEIN PATHWAY
• Arm-to-retina circulation time is 8-10 sec.
• Normally 10-15 seconds elapse between dye injection
and arrival of dye in the short ciliary arteries.
• Choroidal circulation precedes retinal circulation by
1second.
• Transit of dye through the retinal circulation takes
approximately 15 to 20 seconds.
Peripheral vein
Venous circulation
Heart
Arterial system
INTERNAL CAROTID ARTERY
Ophthalmic artery
Short posterior ciliary artery Central retinal Artery
(choroidal circulation) (retinal circulation)
Circulation
MILD MODERATE SEVERE
Staining of skin, sclera
and mucous membrane
Nausea and vomiting
(10%)
Respiratory- laryngeal
edema, bronchospasm
Stained secretion
Tear, saliva
Vasovagal response
(1%)
Circulatory shock, MI,
cardiac arrest (<0.01%)
Vision tinged with
yellow
Urtricaria (<1%) Generalized convulsion
Orange-yellow urine Fainting Skin necrosis
Skin flushing, tingling
lips pruritis
Periphlebitis Extravasation of dye and
local tissue necrosis
COMPLICATIONS
CONTRAINDICATIONS
• ABSOLUTE
1) Known allergy to iodine containing compounds.
2) H/O adverse reaction to FFA in the past.
• RELATIVE
1) Asthma
2) Hay fever
3) Renal failure
4) Hepatic failure
5) Cardiac disease – cardiac failure, Myocardial infarction
6) Previous mild reaction to dye.
7) Tonic-clonic seizures
6) Pregnancy ( especially 1st trimester)
EMERGENCY TRAY FOR FFA
An emergency tray including such items as:
• 0.1% Epinephrine for intravenous or
intramuscular use;
• Antihistaminic,
• Soluble steroid,
• Aminophylline for IV use;
• Oxygen should always be available in the event
of possible reaction to fluorescein injection.
SEQUENCE OF PHOTOGRAPHS
DURING FFA
• Color photograph of Each eye.
• Red free photograph of each eye.
• Room light to be kept dim.
• Activate Barrier and exciter filter , change the flash
intensity and take control photographs.
• Once dye is being injected set the machine at
fluorescein mode and start the timer.
ANGIOGRAPHIC PHASES
• Precise details of the choroidal circulation are typically
not discernible, mainly because of rapid leakage of free
fluorescein from the choriocapillaris.
• Melanin in the RPE cells also blocks choroidal
fluorescence.
• The angiogram consists of the following overlapping
phase:
1. Choroidal
2. Arterial
3. Arteriovenous
4. Venous
5. Late( recirculation) phase
6. The dark appearance of fovea.
CHOROIDAL PHASE
• The choroidal (pre-arterial) phase
typically occurs 9–15 seconds after dye
injection.
• It is longer in patients with poor general
circulation.
• It is characterized by patchy lobular
filling of the choroid due to leakage of
free fluorescein from the fenestrated
choriocapillaris.
• A cilioretinal artery, if present, will
fill at this time because it is derived
from the posterior ciliary circulation.
Arterial phase
• 10–15 seconds after injection
• The central retinal artery fluoresce
• Choroidal filling continues
Arteriovenous phase
• Complete filling of the arteries and
capillaries
• Early laminar flow in the veins
• Choroidal filling continues
Venous phase
• Early phase -complete arterial and capillary
filling with marked venous filling
• Mid-phase -complete venous filling
• Late phase -complete venous filling with
reducing concentration of dye in the arteries
• Maximal peri foveal capillary filling is reached
at around 20–25 seconds and the first pass of
fluorescein circulation is generally completed
by approximately 30 seconds.
Late phase
• Elimination phase
• Reduced intensity of fluorescence
• Staining of disc
• Fluorescein absent after 5-10 min
LATE EXTRAVASCULAR
HYPERFLUOROSCENE CONSIDERED
NORMAL
• Fluorosence of Disc margins from surrounding capillaries
• Fluorosence of lamina cribrosa
• Fluorosence of Sclera at disc margin if RPE terminates away from disc
as in Optic crescent
• Fluoresence of Sclera if RPE is lightly pigmented.
DARK APPEARANCE OF FOVEA
• The dark appearance of the fovea is caused by three factors:
Absence of blood vessels in the FAZ.
 Blockage of background choroidal fluorescence due to the high
density of xanthophyll at the fovea.
 Blockage of background choroidal fluorescence by the RPE cells at
the fovea, which are larger and contain more melanin and lipofuscin
than else where in the retina.
PHASE TIME ( IN Secs)
Choroidal phase 10
Arterial 10-12
Arterio venous 13
Early venous 14-15
Mid venous 16-17
Late venous 18-20
Late ( elimination) 5 MINS
KEY TERMINOLOGY IN FFA
• Hyper fluorescence: An area of abnormally high fluorescence (due to
increased density of the dye molecule)
• Hypo fluorescence: An area of abnormally poor fluorescence ( due to
a paucity of dye molecules or due to masking of the fluorescence)
CAUSES OF HYPERFLOURESCENCE
1. AUTOFLUORESCENCE
Auto fluorescent compounds absorb blue light and emit yellow–green
light in a similar fashion to fluorescein, but much more weakly.
• Auto fluorescent lesions classically include:
- Optic nerve head drusen.
- Astrocytic Hamartoma.
AUTOFLOURESCENCE
2. PSEUDO-FLUORESCENCE
• It refers to non-fluorescent reflected light visible prior to fluorescein
injection; this passes through the filters due to the overlap of
wavelengths passing through the excitation then the barrier filters.
• It is more evident when filters are wearing out.
INCREASED FLUORESCENCE
It may be caused by;
(a) Enhanced visualization of normal fluorescein density.
(b) An increase in fluorescein content of tissues.
3.WINDOW DEFECT
• It is caused by atrophy or absence of the
RPE as in :
 Atrophic age-related macular
degeneration.
 A full-thickness macular hole.
 RPE tears.
• Unmasking of normal background
choroidal fluorescence, characterized by
very early hyperfluorescence that
increases in intensity and then fades
without changing size or shape.
4. POOLING
• Pooling in an anatomical space occurs due to breakdown of the outer
blood–retinal barrier.
• A type of hyperfluorescence in which the dye accumulates within a
closed space. (e.g. RPED)
CENTRAL SEROUS
CHRIORETINOPATHY
PED
5. STAINING
• It is a late phenomenon consisting of the
prolonged retention of dye in entities such
as
 Drusen,
 Fibrous tissue,
 Exposed sclera
 Normal optic disc
• It is seen in the later phases of the
angiogram, particularly after the dye has
left the choroidal and retinal circulations.
STAINING
6. LEAKAGE
• Leakage of dye is characterized by fairly early hyperfluorescence, increasing with
time in both area and intensity. It occurs as a result of breakdown of the inner
blood–retinal barrier due to:
• Dysfunction or loss of existing vascular endothelial tight junctions as in
 Diabetic retinopathy
 Retinal vein occlusion
 Cystoid macular oedema
 Papilloedema.
• Primary absence of vascular endothelial tight junctions as
 CNV
 Proliferative diabetic retinopathy
 Tumours
LEAKAGE
CAUSES OF HYPERFLOURESCENCE
Microaneurysm, Telangiectasia,
Anastomosis
Retinal Abnormal Vessels in DR
Retinal Neovascularization
CAUSES OF HYPERFLOURESCENCE
Subretinal neovascularization
Tumor: Choroidal Hemangioma
CAUSES OF HYPERFLOURESCENCE
Vitreous
Disc
CYSTOID MACULAR EDEMA
NON CYSTOID
HYPOFLOURESCENCE
• Reduction or absence of fluorescence may be due to:
(a) Optical obstruction (masking or blockage) of normal fluorescein
density.
(b) Inadequate perfusion of tissue (filling defect).
• Masking of retinal fluorescence- Preretinal lesions such as blood will
block all fluorescence
• Masking of background choroidal fluorescence allows persistence
of fluorescence from superficial retinal vessels:
 Deeper retinal lesions, e.g. intraretinal haemorrhages, dense exudates.
 Subretinal or sub-RPE lesions, e.g. blood
 Increased density of the RPE, e.g. congenital hypertrophy
 Choroidal lesions, e.g. naevi.
BLOCKED FLUORESCENCE
BLOCKED FLUORESCENCE
CAPILLARY NON-PERFUSION
• A type of hypofluorescence that results
from non-filling of the retinal capillaries
due to the anatomical or functional
reasons.
FILLING DEFECTS
They may result from:
 Vascular occlusion, which may involve the retinal arteries, veins or
capillaries or the choroidal circulation.
 Optic nerve head filling defects as in anterior ischaemic optic
neuropathy.
 Loss of the vascular bed as in myopic degeneration and
choroideremia.
VASCULAR FILLING DEFECT - BRVO
CAUSES OF HYPOFLOURESCENCE
CAUSES OF HYPOFLOURESCENCE
PRE RETINAL HAEMORRHAGE
INTRA RETINAL HAEMORRHAGE
SUB RETINAL HAEMORRHAGE
RPE HYPERTROPHY
SYSTEMATIC APPROACH TO FLUORESCEIN
ANGIOGRAM ANALYSIS
• A fluorescein angiogram should be interpreted methodically to optimize
diagnostic accuracy.
1. Note the clinical findings, patient’s age and gender, before assessing the
images.
2. Note whether images of right, left or both eyes have been taken.
3. Comment on any colour and red-free images and on any pre-injection
demonstration of pseudo- or autofluorescence.
4. Looking at the post-injection images, indicate whether the overall timing of
filling, especially arm-to-eye transit time, is normal.
SYSTEMATIC APPROACH TO FLUORESCEIN
ANGIOGRAM ANALYSIS
5. Briefly scan through the sequence of images in time order for each eye in
turn, concentrate on the eye with the greatest number of shots as this is likely
to be the one with greater concern. Look for any characteristic major
diagnostic features.
6. Go through the run for each eye in greater detail, provide a description of
any other findings using the methodical consideration of the causes of hyper-
and hypofluorescence set out above.
INDOCYANINE GREEN ANGIOGRAPHY
INDOCYANINE GREEN ANGIOGRAPHY
• Indocyanine green (ICG) angiography (ICGA) is fast emerging as a popular
and useful adjunct to the traditional fundus fluorescein angiography (FFA)
in the diagnosis of macular, choroidal and outer retinal disorders.
• This technique was introduced in ophthalmology in 1973 by Flower and
Hochheimer.
• FDA approved the ophthalmic use of ICG dye in 1975.
• It remained largely unpopular owing mainly to technical difficulties. With
the advent of videoangiogram recordings and the recognition of its potential
in delineating occult choroidal neovascular membranes, the clinical use of
ICGA has increased tremendously .
PRINCIPLES OF ICG
• ICG fluorescence is only 1/25th that of fluorescein.
• So modern digital ICGA uses high-sensitivity videoangiographic image capture
by means of an appropriately adapted camera.
• Both the excitation (805 nm) and emission (835 nm) filters are set at infrared
wavelengths.
• Alternatively, scanning laser ophthalmoscopy (SLO) systems provide high
contrast images, with less scattering of light and fast image acquisition rates
facilitating high quality ICG video.
It also exhibits a phenomenon referred to as concentration quenching. After a
period of increasing fluorescence with increasing serum concentration, that
results in peak fluorescence, further increase in concentration, paradoxically
leads to decreased fluorescence. This is thought to result from dimer formation.
EXCITATION AND EMISSION SPECTRUM
OF INDOCYANINE GREEN
INDOCYANINE GREEN
• The indocyanine green(ICG) is a tricarbocyanine dye that comes
packaged as a sterile lyophilized powder and is supplied with an
aqueous solvent.
• Molecular weight :774.97
• It contains less than 5% sodium iodide (in order to increase its
solubility).
• It has a pH of 5.5 to 6.5 in the dissolved state, has limited stability, and
hence must be used within 10 hours after reconstitution.
• 98% of the injected dye is bound to plasma proteins, with 80% being
bound to globulins, especially alpha- 1 lipoproteins.
CLEARANCE
• The dye is secreted unchanged by the liver into the bile.
• There is no renal excretion of the dye
• It does not cross the placenta.
• The dye also has a high affinity for vascular endothelium, and hence
persists in the large choroidal veins, long after injection.
ADVERSE EFFECTS
• Nausea, vomiting are uncommon.
• Anaphylaxis, approximately equal incidence to FA.
• Serious reactions are exceptionally rare.
• ICG contains iodide and so should not be given to patients allergic to
iodine or possibly shellfish.
• Iodine-free preparations such as infracyanine green are available.
CONTRAINDICATIONS
• ICGA is relatively contraindicated in liver disease (excretion is
hepatic)
• In patients with a history of a severe reaction to any allergen.
• Moderate or severe asthma
• Significant cardiac disease.
• Its safety in pregnancy has not been established.
TECHNIQUE AND DOSAGE
• The technique is similar to that of FA.
• There is an increased emphasis on the acquisition of later images (up
to about 45 minutes) than with FA
• A dose of 25–50 mg in 1–2 ml water for injection is used.
PHASES OF ICGA
 Early – up to 60 seconds post-injection
 Early mid-phase – 1–3 minutes
 Late mid-phase –3–15 minutes
 Late phase – 15–45 minute
EARLY PHASE
• Up to 60 seconds post-injection.
• Showing prominent choroidal arteries and poor early perfusion of the
‘choroidal watershed’ zone adjacent to the disc.
EARLY MID-PHASE
• 1–3 minutes post-injection.
• Showing greater prominence of choroidal veins as well as retinal
vessels.
LATE MID-PHASE
• 3–15 minutes post injection.
• Showing fading of choroidal vessels but retinal vessels are still
visible; diffuse tissue staining is also present.
LATE PHASE
• 15–45 minutes post injection
• Showing hypofluorescent choroidal vessels and gradual fading of diffuse
hyperfluorescence
HYPERCYANESCENE
• A window defect similar to those seen with FA.
• Leakage from retinal or choroidal vessels the optic nerve head or the
RPE gives rise to tissue staining or to pooling.
• Abnormal retinal or choroidal vessels with an anomalous morphology
exhibiting greater fluorescence than normal.
HYPORCYANESCENE
• Blockage (masking) of fluorescence.
• Pigment and blood are self-evident causes, but fibrosis, infiltrate, exudate and
serous fluid also block fluorescence.
• A particular phenomenon to note is that in contrast to its FA appearance, a
pigment epithelial detachment appears predominantly hypofluorescent on
ICGA.
• Filling defect due to obstruction or loss of choroidal or retinal circulation.
INDICATIONS OF ICGA
• Polypoidal choroidal vasculopathy (PCV): ICGA is far superior to FA for
the imaging of PCV.
• Exudative age-related macular degeneration (AMD): Conventional FA
remains the primary method of assessment, but ICGA can be a useful
adjunct.
• Chronic central serous chorioretinopathy often difficult to interpret
areas of leakage on FA. ICGA shows choroidal leakage and the presence of
dilated choroidal vessels.
• Posterior uveitis. ICGA can provide useful information beyond that
available from FA in relation to diagnosis and the extent of disease
involvement.
INDICATIONS OF ICGA
• Choroidal tumors may be imaged effectively but ICGA is inferior to
clinical assessment for diagnosis.
• Breaks in Bruch membrane such as lacquer cracks and angioid
streaks are more effectively defined on ICGA than FA
• If FA is contraindicated.
ADVANTAGES OF ICGA OVER FFA
• FA is of limited use in delineating the choroidal vasculature, due to masking by
the RPE.
• In contrast, the near-infrared light utilized in indocyanine green angiography
(ICGA) penetrates ocular pigments such as melanin and xanthophyll, as well as
exudate and thin layers of subretinal blood, making this technique eminently
suitable.
• ICGA can be used even when the ocular media are too hazy for FFA. This is due
to the phenomenon of Rayleigh scatter .
• ICG fluorescence can be imaged even in the presence of considerable blood, due
to the phenomenon of Mie or forward scatter.
Fundus fluorescein
angiography
ICG angiography
For retinal circulation For choroidal circulation
Dye used – sodium fluorescein Dye used – indocyanin green
80% plasma protein bound and low
MW
98% plasma protein bound and high
MW
Light of visible spectrum used Infrared spectrum of light used
Blue green filters used Infrared filters used
More side effects Less side effects
LIMITATIONS OF ICGA
• The choriocapillaris cannot be imaged separately with ICGA since their
average cross-sectional diameter (21 μm) is much smaller than that of their
feeding and draining vessels, and hence the fluorescence of the former
cannot be differentiated from that arising from the latter.
• The phenomenon of Mie scatter also masks the unfilled retinal vessels that
cannot be visualized well in low speed angiography systems.
• Bright areas do not necessarily signify dye leakage due to the phenomenon
of additive fluorescence
• ICGA is poorer than FFA in the imaging of classic CNVM since the early
hyper fluorescence of the CNVM is overwhelmed by the intense background
choroidal filling.
RECENT ADVANCES IN INDOCYANINE
• GREEN ANGIOGRAPHY
• Wide-angle angiography: This is carried out by performing ICGA
with the aid of wide angle contact lenses, such as Volk SuperQuad and
a traditional Topcon fundus camera. This allows real-time imaging of a
wide field of the choroidal circulation up to 160 degrees of field of
view.
• Overlay technique: This technique allows lesion on one image to be
traced on to another color or red-free image.
• Digital stereo imaging: Elevated lesions such as PEDs can be better
imaged in this way.
• ICG as a photo sensitizer: It is considered to be a cheaper alternative
to vertoporfin in photodynamic therapy of neovascularAMD & other
disorders .
• Digital subtraction ICGA: It uses digital subtraction of sequentially
acquired ICG images along with pseudo color imaging. It shows
occult CNVM in greater detail and within a shorter time than
conventional ICGA.
HEIDELBERG RETINALANGIOGRAPHY
• Preferred imaging device of retinal specialist
in research centers and apex institutes.
• Unique feature is dynamic high speed
angiography and higher resolution.
• Also called as Confocal scanning laser
ophthalmoscope.
 16 frames per second motion images
 It is used in the following basic modes like
• Fluorescein angiography (FA mode) 488nm
• ICGA mode 790nm
• Red free reflection 488nm
• Infrared reflection 820nm
SCHEMATIC STRUCTURE OF CSLO
MODIFIED FUNDUS CAMERA CONFOCAL SCANNING LASER
OPHTHALMOSCOPE
One single flash at maximum Intensity, hence
a single image of the fundus is captured
Continuous scanning at low light intensities,
so scans are obtained in raster fashion through
a pin hole aperture
Entire Cone of light Confocal System
True color Image Pseudo color Image
Bandwidth filters for excitation and emission One Excitation wavelength (laser source)
Large emission spectrum (cut off filter)
Slower image acquisition capability Faster acquisition speed, faster after image
processing and thus decreased motion artifacts
Uses shorter wavelengths for FAF and ICG
images
cSLO uses longer wavelengths, hence
captures higher resolution images
Difficult to use in media opacity and poor
dilation
Penetrates media opacity and possible in eyes
with poor dilation
Thank you

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FFA and ICG

  • 2. Learning Objectives • INTRODUCTION • BASIC PRINCIPLES • FLUOROSCENE • TECHNIQUE • CONTRAINDICATION • NORMAL FFA • ABNORMAL FINDING • INDICATIONS
  • 3. Fundus Fluorescein Angiography • Photography of the fundus performed in rapid sequence following intravenous injection of fluorescein dye. • Provides : - Flow characteristics in the blood vessels - Assessment of functional integrity of retinal vessels - Records fine details of retinal pigment epithelium and retinal circulation. - Check the integrity of the blood ocular barrier. - outer blood retinal barrier breaks in CSR - inner blood retinal barrier breaks in NVD,NVE
  • 4. HISTORY OF FFA • The technique of using intravenous fluorescein to evaluate the ocular circulation was introduced 40 years ago by Mac Lean and Maumenee. • Chao and Flocks provided the earliest description of fluorescein angiography in 1958. • Finally, it was introduced into clinical use in 1961 by Novotny and Alvis, who demonstrated the photographic documentation of the fluorescein dynamics. • Over the last 3 decades advances have occurred in this sphere, digital imaging has made possible the generation of high resolution angiography of the retina and choroid.
  • 5. Basic principles • Luminescence: Emission of light from any source other than high temperature. • Fluorescence: Luminescence that is maintained only by continuous excitation. Property of certain molecules to emit light energy of longer wavelength when stimulated by a shorter wavelength. • Phosphorescence: Luminescence where the emission continues long after the excitation has stopped.
  • 7. OUTER AND INNER RETINAL BLOOD BARRIER • The major choroidal vessels are impermeable to both bound and free fluorescein. • The walls of the choriocapillaris contain fenestrations through which unbound molecules escape into the extravascular space. • It crosses Bruch membrane but on reaching the RPE are blocked by intercellular complexes termed tight junctions or zonula occludens. OUTER BLOOD–RETINAL BARRIER
  • 8. INNER BLOOD–RETINAL BARRIER  It composed principally of the tight junctions between retinal capillary endothelial cells.  Across which neither bound nor free fluorescein can pass.  The basement membrane and pericytes play only a minor role in this regard.  Disruption of the blood–retinal barrier permits leakage of both bound and free fluorescein into the extravascular space.
  • 9. PRINCIPLE OF FFA • Based on  Luminescence  Fluorescence  Phosphorescence • Two filters are used:  COBALT BLUE EXCITATION FILTER  YELLOW GREEN BARRIER FILTER
  • 10. EXCITATION AND EMISSION SPECTRUM OF FLUORESCEIN
  • 11. EXCITATION FILTER • Absorption spectrum lies between 465-490 nm. • Excitation peak = 490nm(blue part of spectrum) • The blue flash excites the unbound fluorescein within the blood vessels or the leaked out fluorescein. • The blue light is reflected off of the fundus structures that do not have fluorescein.
  • 12. BARRIER FILTER • Emission spectrum lies between 520 – 530 nm • Emission peak = 530 nm • Just in front of the film a filter is placed that allows the green-yellow fluorescent light through but keeps out the blue reflected light. • Thus, even though the excitation and emission spectra are quite close, as long as suitably matched excitation and barrier filters are used, only substances capable of fluorescence are detected.
  • 13. SODIUM FLUORESCEIN • Sodium fluorescein (C20H10O5Na2) • Orange red crystalline hydrocarbon. • Low molecular weight (376.27 Daltons). • Nontoxic, inexpensive, safe, alkaline solution. • Fluoresces at Blood pH (7.37-7.45). • Absorbs blue light (480-500 nm). • Emits yellow-green (500-600 nm) (Peak 525 nm). • 80% bound to plasma protein and also with RBC. • Can’t pass through tight retinal barriers so allows study of retinal circulation
  • 14. CLEARANCE • Within 24 hours • Sodium Fluorescein is metabolised to fluorescein glucuronide. • The plasma half-life of fluorescein is 11 minutes • Mainly –urine ( yellow orange coloration) • Small amount-bile • Some absorbed by kidney • Skin staining may remain up to 24 hours • Urine discoloration –24-36 hours
  • 15. DOSASGE AND ADMINISTRATION • Solutions containing 500 mg of fluorescein are available in vials of: - 10 ml of 5% fluorescein - 5 ml of 10% fluorescein - 3 ml of 25% fluorescein solution (750 mg) • Solution above 25% precipitates. • For children, the dose is calculated on the basis of 35mg for each 5kg of body weight. • Dye is injected as a bolus into the vein of the patient's arm.
  • 16. • With a greater volume the injection time increases, with a smaller volume, more fluorescein remains in the dead space between the arm and the heart. • Therefore, 5 ml of 10% solution (500 mg) fluorescein is generally preferred. • The venous dead space between the hand or the antecubital vein and the heart may be 5 to 10 ml, leading to sluggish or reduced flow of fluorescein into the central circulation. • The fluorescein can be flushed with 5 to 10 ml of normal saline. • An alternative is to elevate the patient’s arm above the level of the heart using an adjustable armrest, reducing the fluorescein transit time to the heart.
  • 17. TECHNIQUE AND EQUIPMENTS • The materials needed for fluorescein angiography are as follows: 1. Fundus camera and auxiliary equipment 2. 23 gauge scalp vein needle 3. 5 ml syringe 4. Fluorescein solution 5. 20 gauge 1 ½ inch needle to draw the dye 6. Armrest for fluorescein injection 7. Tourniquet 8. Alcohol 9. Bandage 10. Standard emergency equipment
  • 18. EQUIPMENT • The traditional fluorescein angiography unit has two 35 mm cameras, one for color fundus photography while the other (black & white) for fluorescein angiography. • Most fundus cameras take 30° photographs (magnification of 2.5X on a 35mm film), which are adequate for a study of posterior pole lesions especially macular diseases. • Many camera units provide variable magnification at 20, 30 and 50 degrees. • The 50° view is most useful for lesions involving a large area of the fundus.
  • 19.
  • 20. PROCEDURE • Informed consent – explain the procedure to the patient. • Dilate patient’s pupil. • Fluorescein solution, scalp vein needle, 5 ml syringe and the emergency tray is prepared. • Check fundus camera for any fault. • Observe lens and fundus camera for any dust or opacity. • Feed the machine with patient information – Name, MRD no, age, sex, clinical diagnosis etc.
  • 21. • The patient is positioned and the camera aligned. • Color photography of both eyes. • Red free photograph of the posterior pole is taken. • Insert the scalp-vein needle, preferably at anticubital vein and inject the fluorescein dye 5ml of 10% solution in 5- 10 seconds. • Simultaneously inject fluorescein dye and start Fluorescein mode in machine. • Once machine is set at Fluorescein mode timer will start and exciter and barrier filter will be activated.
  • 22. • Oral administration at a dose of 30 mg/kg; and pictures should be taken over 20– 60 minutes following ingestion. • Images are taken at 1–2 second intervals initially to capture the critical early transit phases, beginning 5–10 seconds after injection, tapering frequency through subsequent phases. • Start fluorescein photograph 8 seconds after start of injection in young and after 10 seconds in older patients. • Images may be captured as late as 10–20 minutes. • When photography is done, reassure the patient that all went well and remind him or her that the urine will be discolored for a day or so (24-36 hours). Make patient wait an additional 20 minutes for observation for possible reactions to fluorescein.
  • 23. FLUORESCEIN PATHWAY • Arm-to-retina circulation time is 8-10 sec. • Normally 10-15 seconds elapse between dye injection and arrival of dye in the short ciliary arteries. • Choroidal circulation precedes retinal circulation by 1second. • Transit of dye through the retinal circulation takes approximately 15 to 20 seconds.
  • 24. Peripheral vein Venous circulation Heart Arterial system INTERNAL CAROTID ARTERY Ophthalmic artery Short posterior ciliary artery Central retinal Artery (choroidal circulation) (retinal circulation) Circulation
  • 25. MILD MODERATE SEVERE Staining of skin, sclera and mucous membrane Nausea and vomiting (10%) Respiratory- laryngeal edema, bronchospasm Stained secretion Tear, saliva Vasovagal response (1%) Circulatory shock, MI, cardiac arrest (<0.01%) Vision tinged with yellow Urtricaria (<1%) Generalized convulsion Orange-yellow urine Fainting Skin necrosis Skin flushing, tingling lips pruritis Periphlebitis Extravasation of dye and local tissue necrosis COMPLICATIONS
  • 26. CONTRAINDICATIONS • ABSOLUTE 1) Known allergy to iodine containing compounds. 2) H/O adverse reaction to FFA in the past. • RELATIVE 1) Asthma 2) Hay fever 3) Renal failure 4) Hepatic failure 5) Cardiac disease – cardiac failure, Myocardial infarction 6) Previous mild reaction to dye. 7) Tonic-clonic seizures 6) Pregnancy ( especially 1st trimester)
  • 27. EMERGENCY TRAY FOR FFA An emergency tray including such items as: • 0.1% Epinephrine for intravenous or intramuscular use; • Antihistaminic, • Soluble steroid, • Aminophylline for IV use; • Oxygen should always be available in the event of possible reaction to fluorescein injection.
  • 28. SEQUENCE OF PHOTOGRAPHS DURING FFA • Color photograph of Each eye. • Red free photograph of each eye. • Room light to be kept dim. • Activate Barrier and exciter filter , change the flash intensity and take control photographs. • Once dye is being injected set the machine at fluorescein mode and start the timer.
  • 29. ANGIOGRAPHIC PHASES • Precise details of the choroidal circulation are typically not discernible, mainly because of rapid leakage of free fluorescein from the choriocapillaris. • Melanin in the RPE cells also blocks choroidal fluorescence. • The angiogram consists of the following overlapping phase: 1. Choroidal 2. Arterial 3. Arteriovenous 4. Venous 5. Late( recirculation) phase 6. The dark appearance of fovea.
  • 30. CHOROIDAL PHASE • The choroidal (pre-arterial) phase typically occurs 9–15 seconds after dye injection. • It is longer in patients with poor general circulation. • It is characterized by patchy lobular filling of the choroid due to leakage of free fluorescein from the fenestrated choriocapillaris.
  • 31. • A cilioretinal artery, if present, will fill at this time because it is derived from the posterior ciliary circulation.
  • 32. Arterial phase • 10–15 seconds after injection • The central retinal artery fluoresce • Choroidal filling continues
  • 33. Arteriovenous phase • Complete filling of the arteries and capillaries • Early laminar flow in the veins • Choroidal filling continues
  • 34. Venous phase • Early phase -complete arterial and capillary filling with marked venous filling • Mid-phase -complete venous filling • Late phase -complete venous filling with reducing concentration of dye in the arteries • Maximal peri foveal capillary filling is reached at around 20–25 seconds and the first pass of fluorescein circulation is generally completed by approximately 30 seconds.
  • 35. Late phase • Elimination phase • Reduced intensity of fluorescence • Staining of disc • Fluorescein absent after 5-10 min
  • 36. LATE EXTRAVASCULAR HYPERFLUOROSCENE CONSIDERED NORMAL • Fluorosence of Disc margins from surrounding capillaries • Fluorosence of lamina cribrosa • Fluorosence of Sclera at disc margin if RPE terminates away from disc as in Optic crescent • Fluoresence of Sclera if RPE is lightly pigmented.
  • 37. DARK APPEARANCE OF FOVEA • The dark appearance of the fovea is caused by three factors: Absence of blood vessels in the FAZ.  Blockage of background choroidal fluorescence due to the high density of xanthophyll at the fovea.  Blockage of background choroidal fluorescence by the RPE cells at the fovea, which are larger and contain more melanin and lipofuscin than else where in the retina.
  • 38. PHASE TIME ( IN Secs) Choroidal phase 10 Arterial 10-12 Arterio venous 13 Early venous 14-15 Mid venous 16-17 Late venous 18-20 Late ( elimination) 5 MINS
  • 39. KEY TERMINOLOGY IN FFA • Hyper fluorescence: An area of abnormally high fluorescence (due to increased density of the dye molecule) • Hypo fluorescence: An area of abnormally poor fluorescence ( due to a paucity of dye molecules or due to masking of the fluorescence)
  • 40. CAUSES OF HYPERFLOURESCENCE 1. AUTOFLUORESCENCE Auto fluorescent compounds absorb blue light and emit yellow–green light in a similar fashion to fluorescein, but much more weakly. • Auto fluorescent lesions classically include: - Optic nerve head drusen. - Astrocytic Hamartoma.
  • 42. 2. PSEUDO-FLUORESCENCE • It refers to non-fluorescent reflected light visible prior to fluorescein injection; this passes through the filters due to the overlap of wavelengths passing through the excitation then the barrier filters. • It is more evident when filters are wearing out. INCREASED FLUORESCENCE It may be caused by; (a) Enhanced visualization of normal fluorescein density. (b) An increase in fluorescein content of tissues.
  • 43. 3.WINDOW DEFECT • It is caused by atrophy or absence of the RPE as in :  Atrophic age-related macular degeneration.  A full-thickness macular hole.  RPE tears. • Unmasking of normal background choroidal fluorescence, characterized by very early hyperfluorescence that increases in intensity and then fades without changing size or shape.
  • 44. 4. POOLING • Pooling in an anatomical space occurs due to breakdown of the outer blood–retinal barrier. • A type of hyperfluorescence in which the dye accumulates within a closed space. (e.g. RPED)
  • 46. PED
  • 47. 5. STAINING • It is a late phenomenon consisting of the prolonged retention of dye in entities such as  Drusen,  Fibrous tissue,  Exposed sclera  Normal optic disc • It is seen in the later phases of the angiogram, particularly after the dye has left the choroidal and retinal circulations.
  • 49. 6. LEAKAGE • Leakage of dye is characterized by fairly early hyperfluorescence, increasing with time in both area and intensity. It occurs as a result of breakdown of the inner blood–retinal barrier due to: • Dysfunction or loss of existing vascular endothelial tight junctions as in  Diabetic retinopathy  Retinal vein occlusion  Cystoid macular oedema  Papilloedema. • Primary absence of vascular endothelial tight junctions as  CNV  Proliferative diabetic retinopathy  Tumours
  • 60. Disc
  • 63. HYPOFLOURESCENCE • Reduction or absence of fluorescence may be due to: (a) Optical obstruction (masking or blockage) of normal fluorescein density. (b) Inadequate perfusion of tissue (filling defect).
  • 64. • Masking of retinal fluorescence- Preretinal lesions such as blood will block all fluorescence • Masking of background choroidal fluorescence allows persistence of fluorescence from superficial retinal vessels:  Deeper retinal lesions, e.g. intraretinal haemorrhages, dense exudates.  Subretinal or sub-RPE lesions, e.g. blood  Increased density of the RPE, e.g. congenital hypertrophy  Choroidal lesions, e.g. naevi. BLOCKED FLUORESCENCE
  • 66. CAPILLARY NON-PERFUSION • A type of hypofluorescence that results from non-filling of the retinal capillaries due to the anatomical or functional reasons.
  • 67. FILLING DEFECTS They may result from:  Vascular occlusion, which may involve the retinal arteries, veins or capillaries or the choroidal circulation.  Optic nerve head filling defects as in anterior ischaemic optic neuropathy.  Loss of the vascular bed as in myopic degeneration and choroideremia.
  • 75. SYSTEMATIC APPROACH TO FLUORESCEIN ANGIOGRAM ANALYSIS • A fluorescein angiogram should be interpreted methodically to optimize diagnostic accuracy. 1. Note the clinical findings, patient’s age and gender, before assessing the images. 2. Note whether images of right, left or both eyes have been taken. 3. Comment on any colour and red-free images and on any pre-injection demonstration of pseudo- or autofluorescence. 4. Looking at the post-injection images, indicate whether the overall timing of filling, especially arm-to-eye transit time, is normal.
  • 76. SYSTEMATIC APPROACH TO FLUORESCEIN ANGIOGRAM ANALYSIS 5. Briefly scan through the sequence of images in time order for each eye in turn, concentrate on the eye with the greatest number of shots as this is likely to be the one with greater concern. Look for any characteristic major diagnostic features. 6. Go through the run for each eye in greater detail, provide a description of any other findings using the methodical consideration of the causes of hyper- and hypofluorescence set out above.
  • 78. INDOCYANINE GREEN ANGIOGRAPHY • Indocyanine green (ICG) angiography (ICGA) is fast emerging as a popular and useful adjunct to the traditional fundus fluorescein angiography (FFA) in the diagnosis of macular, choroidal and outer retinal disorders. • This technique was introduced in ophthalmology in 1973 by Flower and Hochheimer. • FDA approved the ophthalmic use of ICG dye in 1975. • It remained largely unpopular owing mainly to technical difficulties. With the advent of videoangiogram recordings and the recognition of its potential in delineating occult choroidal neovascular membranes, the clinical use of ICGA has increased tremendously .
  • 79. PRINCIPLES OF ICG • ICG fluorescence is only 1/25th that of fluorescein. • So modern digital ICGA uses high-sensitivity videoangiographic image capture by means of an appropriately adapted camera. • Both the excitation (805 nm) and emission (835 nm) filters are set at infrared wavelengths. • Alternatively, scanning laser ophthalmoscopy (SLO) systems provide high contrast images, with less scattering of light and fast image acquisition rates facilitating high quality ICG video.
  • 80. It also exhibits a phenomenon referred to as concentration quenching. After a period of increasing fluorescence with increasing serum concentration, that results in peak fluorescence, further increase in concentration, paradoxically leads to decreased fluorescence. This is thought to result from dimer formation.
  • 81. EXCITATION AND EMISSION SPECTRUM OF INDOCYANINE GREEN
  • 82. INDOCYANINE GREEN • The indocyanine green(ICG) is a tricarbocyanine dye that comes packaged as a sterile lyophilized powder and is supplied with an aqueous solvent. • Molecular weight :774.97 • It contains less than 5% sodium iodide (in order to increase its solubility). • It has a pH of 5.5 to 6.5 in the dissolved state, has limited stability, and hence must be used within 10 hours after reconstitution. • 98% of the injected dye is bound to plasma proteins, with 80% being bound to globulins, especially alpha- 1 lipoproteins.
  • 83. CLEARANCE • The dye is secreted unchanged by the liver into the bile. • There is no renal excretion of the dye • It does not cross the placenta. • The dye also has a high affinity for vascular endothelium, and hence persists in the large choroidal veins, long after injection.
  • 84. ADVERSE EFFECTS • Nausea, vomiting are uncommon. • Anaphylaxis, approximately equal incidence to FA. • Serious reactions are exceptionally rare. • ICG contains iodide and so should not be given to patients allergic to iodine or possibly shellfish. • Iodine-free preparations such as infracyanine green are available.
  • 85. CONTRAINDICATIONS • ICGA is relatively contraindicated in liver disease (excretion is hepatic) • In patients with a history of a severe reaction to any allergen. • Moderate or severe asthma • Significant cardiac disease. • Its safety in pregnancy has not been established.
  • 86. TECHNIQUE AND DOSAGE • The technique is similar to that of FA. • There is an increased emphasis on the acquisition of later images (up to about 45 minutes) than with FA • A dose of 25–50 mg in 1–2 ml water for injection is used.
  • 87. PHASES OF ICGA  Early – up to 60 seconds post-injection  Early mid-phase – 1–3 minutes  Late mid-phase –3–15 minutes  Late phase – 15–45 minute
  • 88. EARLY PHASE • Up to 60 seconds post-injection. • Showing prominent choroidal arteries and poor early perfusion of the ‘choroidal watershed’ zone adjacent to the disc.
  • 89. EARLY MID-PHASE • 1–3 minutes post-injection. • Showing greater prominence of choroidal veins as well as retinal vessels.
  • 90. LATE MID-PHASE • 3–15 minutes post injection. • Showing fading of choroidal vessels but retinal vessels are still visible; diffuse tissue staining is also present.
  • 91. LATE PHASE • 15–45 minutes post injection • Showing hypofluorescent choroidal vessels and gradual fading of diffuse hyperfluorescence
  • 92. HYPERCYANESCENE • A window defect similar to those seen with FA. • Leakage from retinal or choroidal vessels the optic nerve head or the RPE gives rise to tissue staining or to pooling. • Abnormal retinal or choroidal vessels with an anomalous morphology exhibiting greater fluorescence than normal.
  • 93. HYPORCYANESCENE • Blockage (masking) of fluorescence. • Pigment and blood are self-evident causes, but fibrosis, infiltrate, exudate and serous fluid also block fluorescence. • A particular phenomenon to note is that in contrast to its FA appearance, a pigment epithelial detachment appears predominantly hypofluorescent on ICGA. • Filling defect due to obstruction or loss of choroidal or retinal circulation.
  • 94. INDICATIONS OF ICGA • Polypoidal choroidal vasculopathy (PCV): ICGA is far superior to FA for the imaging of PCV. • Exudative age-related macular degeneration (AMD): Conventional FA remains the primary method of assessment, but ICGA can be a useful adjunct. • Chronic central serous chorioretinopathy often difficult to interpret areas of leakage on FA. ICGA shows choroidal leakage and the presence of dilated choroidal vessels. • Posterior uveitis. ICGA can provide useful information beyond that available from FA in relation to diagnosis and the extent of disease involvement.
  • 95. INDICATIONS OF ICGA • Choroidal tumors may be imaged effectively but ICGA is inferior to clinical assessment for diagnosis. • Breaks in Bruch membrane such as lacquer cracks and angioid streaks are more effectively defined on ICGA than FA • If FA is contraindicated.
  • 96. ADVANTAGES OF ICGA OVER FFA • FA is of limited use in delineating the choroidal vasculature, due to masking by the RPE. • In contrast, the near-infrared light utilized in indocyanine green angiography (ICGA) penetrates ocular pigments such as melanin and xanthophyll, as well as exudate and thin layers of subretinal blood, making this technique eminently suitable. • ICGA can be used even when the ocular media are too hazy for FFA. This is due to the phenomenon of Rayleigh scatter . • ICG fluorescence can be imaged even in the presence of considerable blood, due to the phenomenon of Mie or forward scatter.
  • 97. Fundus fluorescein angiography ICG angiography For retinal circulation For choroidal circulation Dye used – sodium fluorescein Dye used – indocyanin green 80% plasma protein bound and low MW 98% plasma protein bound and high MW Light of visible spectrum used Infrared spectrum of light used Blue green filters used Infrared filters used More side effects Less side effects
  • 98. LIMITATIONS OF ICGA • The choriocapillaris cannot be imaged separately with ICGA since their average cross-sectional diameter (21 μm) is much smaller than that of their feeding and draining vessels, and hence the fluorescence of the former cannot be differentiated from that arising from the latter. • The phenomenon of Mie scatter also masks the unfilled retinal vessels that cannot be visualized well in low speed angiography systems. • Bright areas do not necessarily signify dye leakage due to the phenomenon of additive fluorescence • ICGA is poorer than FFA in the imaging of classic CNVM since the early hyper fluorescence of the CNVM is overwhelmed by the intense background choroidal filling.
  • 99. RECENT ADVANCES IN INDOCYANINE • GREEN ANGIOGRAPHY • Wide-angle angiography: This is carried out by performing ICGA with the aid of wide angle contact lenses, such as Volk SuperQuad and a traditional Topcon fundus camera. This allows real-time imaging of a wide field of the choroidal circulation up to 160 degrees of field of view. • Overlay technique: This technique allows lesion on one image to be traced on to another color or red-free image. • Digital stereo imaging: Elevated lesions such as PEDs can be better imaged in this way.
  • 100. • ICG as a photo sensitizer: It is considered to be a cheaper alternative to vertoporfin in photodynamic therapy of neovascularAMD & other disorders . • Digital subtraction ICGA: It uses digital subtraction of sequentially acquired ICG images along with pseudo color imaging. It shows occult CNVM in greater detail and within a shorter time than conventional ICGA.
  • 101. HEIDELBERG RETINALANGIOGRAPHY • Preferred imaging device of retinal specialist in research centers and apex institutes. • Unique feature is dynamic high speed angiography and higher resolution. • Also called as Confocal scanning laser ophthalmoscope.
  • 102.  16 frames per second motion images  It is used in the following basic modes like • Fluorescein angiography (FA mode) 488nm • ICGA mode 790nm • Red free reflection 488nm • Infrared reflection 820nm
  • 104. MODIFIED FUNDUS CAMERA CONFOCAL SCANNING LASER OPHTHALMOSCOPE One single flash at maximum Intensity, hence a single image of the fundus is captured Continuous scanning at low light intensities, so scans are obtained in raster fashion through a pin hole aperture Entire Cone of light Confocal System True color Image Pseudo color Image Bandwidth filters for excitation and emission One Excitation wavelength (laser source) Large emission spectrum (cut off filter) Slower image acquisition capability Faster acquisition speed, faster after image processing and thus decreased motion artifacts Uses shorter wavelengths for FAF and ICG images cSLO uses longer wavelengths, hence captures higher resolution images Difficult to use in media opacity and poor dilation Penetrates media opacity and possible in eyes with poor dilation