FUNDUS ANGIOGRAPHY

1. FLUORESCEIN ANGIOGRAPHY
AND INDOCYANINE GREEN
ANGIOGRAPHY
• PRESENTER – Dr. KRATI GUPTA
• MODERATOR – Dr. RONEL SOIBAM

2. FLUORESCEIN ANGIOGRAPHY
• The study and diagnosis of retinal, macular and choroidal pathologic
lesions have been greatly revolutionized with the advent of fundus
fluorescein angiography (FFA).
• From an initial laboratory tool, it has now become a useful
diagnostic tool that has aided the diagnosis and monitoring of the treatment
of retinal vascular and macular diseases.
• Although the retina can be readily examined by direct and indirect
ophthalmoscopy and slit-lamp bio microscopy, the fluorescein angiography
provides a valuable addition to these techniques.

3. 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.

4. INTRODUCTION
• 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.

5. OUTER AND INNER RETINAL BLOOD
BARRIER
OUTER BLOOD–RETINAL 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.

6. 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.

7. PRINCIPLE OF FFA
• Based on
 Luminescence
 Fluorescence
 Phosphorescence
• Two filters are used:
 COBALT BLUE EXCITATION FILTER
 YELLOW GREEN BARRIER FILTER
.

8. EXCITATION FILTER
 The dye absorbs light in the blue range of the visible spectrum with
absorption peaking at 465 to 490 nm. The blue flash excites the unbound
fluorescein within the blood vessels or the leaked out fluorescein.
 The blue filter shields out all other light and allows through only the blue
excitation light.
 Structures containing fluorescein within the eye emit green-yellow light.
 The blue light is reflected off of the fundus structures that do not have
fluorescein.

9. BARRIER FILTER
 The flourescein dye emits light from 500 to 600 nm with a maximum
intensity at 520 to 530 nm (green-yellow).
 The blue reflected light and green-yellow fluorescent light are directed back
toward the film of the fundus camera.
 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.

10. EXCITATION AND EMISSION SPECTRUM
OF FLUORESCEIN

11. 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

12. CLEARANCE
• Complete removal from blood by kidneys and liver in 24-36 hrs.
Metabolism
• Sodium Fluorescein is metabolised to fluorescein glucuronide.
• 60% of fluorescein is present in the form of metabolites 30 minutes after
injection, and 80% is metabolized after 60 minutes. 96% of the active
substance is glucuronized after five hours.
Elimination
• The plasma half-life of fluorescein is 11 minutes. Elimination is
predominantly via the kidneys, but also via the liver and in the faeces.
Renal clearance is 1.75 ml/minute/kg bodyweight. A dose of fluorescein is
excreted almost completely within 36 hours of administration.

13. 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 20% fluorescein
solution (750 mg)
 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.

14. • 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.

15. 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)

16. USE IN PREGNANCYAND LACTATION
• Controversial
• Avoid angiography on patients who are pregnant, especially those in first
trimester.
• Fluorescein Crosses the placenta
• Fluorescein is secreted in milk.
• Has been done in pregnancy with no adverse effect
• There have been no reports of fetal complications for fluorescein injection
during pregnancy.

17. INTERACTIONS
• Combination with beta-blockers may in rare cases cause lethal anaphylactic
reactions.
• Therefore, particularly in at-risk patients undergoing beta-blocker therapy
for whom fluorescein angiography is essential- the procedure must be
carried out under medical supervision, and with access to the necessary
resuscitation equipment during the whole examination.
• It should be born in mind that if such patients require resuscitation
measures, they may not respond fully to the use of adrenaline.
• The patient should be monitored for at least 30 minutes after completion of
fluorescein angiography.

18. COMPLICATIONS
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

19. EMERGENCY TRAY FOR FFA
An emergency tray including such
items as:
• 0.1% epinephrine for
intravenous or intramuscular
use;
• an antihistaminic,
• soluble steroid,
• aminophylline for IV use;
• oxygen should always be
available in the event of
possible reaction to fluorescein
injection.

21. 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

22. 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 35
mm film), which are adequate for a detailed 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.

25. 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.

26. • 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 3ml of
20% 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.

27. • Oral administration at a dose of 30 mg/kg is an alternative if venous access
cannot be obtained or is refused; a 5 ml vial of 10% (100 mg/ml) sodium
fluorescein contains 500 mg, 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.

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. FFA PROVIDES THREE MAIN
INFORMATION:
1. The flow characteristics in the blood vessels as the dye reaches and
circulates through the retina and choroid .
2. It records fine details of the pigment epithelium and retinal circulation
that may not otherwise be visible
3. Give a clear picture of the retinal vessels and assessment of
their functional integrity

30. 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 1 second.
• Transit of dye through the retinal
circulation takes approximately 15 to 20
seconds.

31. 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.

32. 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.

33. • A cilioretinal artery, if
present, will fill at this
time because it is derived
from the posterior ciliary
circulation.

34. ARTERIAL PHASE
• The arterial phase starts
about a second after the onset
of choroidal fluorescence, and
shows retinal arteriolar filling
and the continuation of
choroidal filling.

35. ARTERIOVENOUS PHASE
• The arteriovenous (capillary)
phase shows complete filling of
the arteries and capillaries with
early laminar flow in the veins
in which the dye appears to line
the venous wall leaving an axial
hypofluorescent strip.

36. This phenomenon (laminar
flow) reflects initial
drainage from posterior
pole capillaries filling the
venous margins, as well as
the small vessel velocity
profile, with faster plasma
flow adjacent to vessel
walls where cellular
concentration is lower.

37. VENOUS PHASE
• Laminar venous flow
progresses to complete filling,
with late venous phase
featuring reducing arterial
fluorescence.

38. • Maximal peri foveal capillary
filling is reached at around
20–25 seconds in patients
with normal cardiovascular
function, and the first pass of
fluorescein circulation is
generally completed by
approximately 30 seconds.

39. LATE PHASE
• The late (recirculation) phase
demonstrates the effects of
continuous recirculation, dilution
and elimination of the dye.
• With each succeeding wave, the
intensity of fluorescence becomes
weaker although the disc shows
staining.
• Fluorescein is absent from the
retinal vasculature after about 10
minutes .

40. 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.

41. 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

42. KEY TERMINOLOGY IN FFA
• Hyperfluorescence: An area of abnormally high fluorescence (due to
increased density of the dye molecule)
• Hypofluorescence: An area of abnormally poor fluorescence ( due to a
paucity of dye molecules or due to masking of the fluorescence)

43. CAUSES OF HYPERFLOURESCENCE
• AUTOFLUORESCENCE
Autofluorescent compounds absorb blue light and emit yellow–green light in a
similar fashion to fluorescein, but much more weakly.
Autofluorescent lesions classically include:
 Optic nerve head drusen.
 Drusens.

44. AUTOFLOURESCENCE

45. • 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.

46. 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.
This results in unmasking of normal
background choroidal fluorescence,
characterized by very early
hyperfluorescence that increases in
intensity and then fades without
changing size or shape.

47. • 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)

48. • 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
 Coats disease.

49. LEAKAGE

50. • 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.

51. 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.

52. BLOCKED FLUORESCENCE

53. CAPILLARY NON-PERFUSION
A type of hypofluorescence
that results from non-filling of
the retinal capillaries due to
the anatomical or functional
reasons.

54. • 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.

55. 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.

56. 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.

57. 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 .

58. 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.
 The technique is similar to that of FA, but with 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.

59. 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.

61. 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.

62. 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.

63. 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.

64. 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.

65. 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.

66. 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

67. 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.

68. EARLY MID-PHASE
(1–3 MINUTES)
• showing greater prominence of choroidal veins as well as retinal
vessels.

69. LATE MID-PHASE (3–15 MINUTES)
• showing fading of choroidal vessels but retinal vessels are still
visible; diffuse tissue staining is also present.

70. LATE PHASE (15–45 MINUTES)
• showing hypofluorescent choroidal vessels and gradual fading of
diffuse hyperfluorescence

71. HYPERFLOURESCENE
 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.

72. HYPOFLOURECENCE
 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.

73. 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, particularly if PCV is suspected.
 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.
 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.

74. ADVANTAGES OF ICGA OVER FFA
 FA is an excellent method of studying the retinal circulation, it 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.

75.  The peak absorption of ICG coincides with the emission spectrum of diode
laser, which allows the selective ablation of chorioretinal lesions using ICG
dye-enhanced laser photocoagulation wherein a target tissue containing
ICG is exposed to the diode laser beam.
 Photophobic patients tolerate ICGA better than FFA.
 ICGA accurately measures the size of an occult choroidal neovascular
membrane(CNVM).

76. 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.
 Although superior to FFA in the imaging of occult CNVM, ICGA may
underestimate the size of the CNVM.

77. 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

78. 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 neovascular AMD& 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.

79. FUTURE APPLICATIONS OF
INDOCYANINE GREEN ANGIOGRAPHY
In the future, ICGA is expected to play a more important and wider role
especially in the management of macular disorders.
 Identifying subclinical neovascular lesions in the other eye of patients with
AMD. There are several reports that mention that 10% of such eyes with no
clinical or fluorescein angiographic evidence of an exudative process
harbor plaques of neovascularization evident on ICGA.
 ICG-guided feeder vessel photocoagulation: SLO high-speed ICGA can
adequately image the feeding vessels of the CNVM which are 0.5 to 3 mm
in length and are believed to lie in the Sattler’s layer of the choroid.

80. HEIDELBERG RETINAL
ANGIOGRAPH
• HRA2 a product of Heidelberg
Engineering GmbH, Germany.
• Preferred imaging device of retinal
specialist in research centers and
apex institutes.
• Unique feature is dynamic high
speed angiography and higher
resolution.

81.  16 frames per second motion images
 Also called as Confocal scanning laser ophthalmoscope
 It is used in the following basic modes like
• Fluorescein angiography (FA mode) 488nm
• ICGA mode 790nm
• Red free reflection 488nm
• Infrared reflection 820n

82. SCHEMATIC STRUCTURE OF CSLO

83. SALIENT FEATURES OF HRA
• Spherical refractive error of –12 to +30D can be compensated by setting
the control dial.
• In addition, internal myopic lens of –6 or –12D spherical correction can be
set without using any external lenses.
• HRA2 field of view are 30, 20 and 15 degrees
• Simultaneous mode – e.g. both FA and ICG images of identical areas can
be captured and stored.
• Composite mode – the software of HRA2 automatically evaluate the
images and connects them to one another, creating large composite image
( 100 or 80 degrees) .

84. • Fixation mode – ensure the patient’s visual fixation is stable there are both
internal and external fixation lights.
• Wide angle objective – width of field is broadened to 57 degrees for examining
the peripheral fundus. Can be used in composite mode also.
• Automatic real time module (ART) – software detects and corrects for eye
movements. Helpful in imaging autofluorescenes, cloudy media or high
astigmatism.
• Examining the anterior segment – to perform iris angiography by setting optics
control to +40D and adjust the distance between camera and eye to optimize
the focus.
• Stereoscopic viewing – helpful in examining the 3 dimensional images.
• Components of analytical software – converted into other image modes.
Biometric functions also available

85. ADVANTAGES
 Higher resolution and contrast
 Used in imaging FFA, ICG and autofluorescene

88. THANK YOU