A brief comparison of FFA and ICG

1. FFA and ICG
Dr. Paresh Nichlani
PG Dept. Of Ophthalmology
MGMCRI
Moderated by -:
Prof. Dr. K Srikanth
Dr. N Swathi

2. Introduction - FFA
 Novotny and Alvis – introduced dye circulation in
human eye.
 Maumenee – FFA in choroidal hemangioma.
 Fluorescence is the emission of light by a substance
that has absorbed light or other electromagnetic
radiation.

3. Pharmacology
 Sodium fluorescein (NaFl) - xanthene derivative.
 Molecular weight of 376.27 kD.
 Does not cross outer and inner blood retinal barrier.
 Rapidly diffuses through the fluid compartments and
the choriocapillaris.
 Kidney excretes the majority of the dye.

4. Characteristics and Uses
 It shows the flow characteristic of blood vessels.
 It records fine details of the pigment epithelium and
retinal circulation that may not be otherwise visible.
 Provides a clear picture of the retinal vessels and an
assessment of their functional integrity. ( Normally
impermeable)

5.  Choriocapillaris normally leak
fluorescein dye.
 Normal pigment epithelium is
a barrier.

7. Fluorescein Solution
 Following solutions of 500 mg
 10 ml of 5 percent NaFl
 5 ml of 10 percent NaFl
 3 ml of 25 percent NaFl
 Greater the volume-longer is the time taken
 Smaller volume - remain within the venous dead space

8.  Oral administration also possible.
 Used for assessment of blood retinal barrier.
 Inadequate in determining blood flow velocity or
anatomic detail.
 10% NaFl is mixed with orange juice and given
30mg/Kg
 Picture taken after 20-60 mins.

9. Indications
 Chorioretinal vascular diseases (Diabetic retinopathy, Wet
ARMD)
 Assessment of intermediate or posterior uveitis.
 Macular diseases (Central serous chorioretinopathy)
 Planning of retinal laser procedures.
 Unexplained visual loss
 Choroidal melanoma
 Hereditary retinal dystrophies

10. Side effects
 Extravasations and local tissue necrosis
 Inadvertent arterial injection
 Nausea and vomiting
 Vasovagal reaction (circulatory shock, myocardial
infarction)
 Allergic reaction, anaphylaxis
 Neurologic problems (seizures)
 Thrombophlebitis, pyrexia
 Temporary discoloration of skin and urine.

11. Contraindications
 Fluorescein allergy in past. – Absolute
contraindication
 H/O sevear allergic reaction to other allergen in past.
 Renal failure.
 Pregnancy
 Asthma
 Cardiac disease

12. Injecting procedure
 23G scalp vein needle.
 Ante cubital vein.
 Rapid injection in 2-3 seconds
 Followed by 5ml NS

14. Arm to Retina Time (dye delay
time)
 First true fluorescence
appear in the choroids
about 10 to 12 seconds after
injection.

15. Pre arterial phase or choroidal flush
 Choroid fluoresces - 1 to 2
seconds before.
 Early choroidal
fluorescences are faint,
patchy and irregularly
scattered throughout the
posterior fundus.
 Interspersed with scattered
islands of delayed
fluorescein filling.

16. Arterial phase
 Central retinal artery start
fluorescing within 1 to 3
seconds of choroidal phase.
 Approximately 10 to 15
seconds after the injection of
the dye.
 Time delay depends upon
concentration of retinal
pigment epithelium.

17. Arteriovenous phase central retinal artery
retinal arterioles
precapillary arterioles
capillaris
post capillaris venules
retinal venules

18. Venous phase
 Next 5 to 10 seconds.
 Dye enters the veins.
 Flow is laminar, because
the vascular flow is faster
in the center of the lumen,
the fluorescein seems to
stick to the sides, creating
a laminar pattern.

19. Venous phase
Early
Lamellar venous flow
Mid
Veins are nearly filled
and the intensity of
venous fluorescence
becomes more than the
arteries.
Late
veins are completely
filled and arteries are
starting to empty.

21. Late (recirculation) phase
 Residual background
fluorescences in the
extravascular spaces, in
the deeper choroid, the
sclera and the optic nerve.
 Shows abnormal dye
accumulation indicative of
leakage or staining.

22.  Dark appearance of fovia is
due to -:
 Absence of blood vessels in
FAZ.
 Blockage of background
fluorescence by RPE cells-
contain more melanin and
lipofuscine.
 High dencity of
xanthophylls.

24. Interpretation of Fluorescein Angiography
 The first step in the
interpretation is to recognize
areas of abnormal
fluorescence and to
determine whether they are
hyperfluorescent or
hypofluorescent.

25. Autofluorescence
 Area of hyperfluorescence in the fundus seen in the pre-
injection photographs.
 optic disk drusen
 astrocytic hamartomas
 large deposits of highly reflectile material such as
lipofuscin
and exudates

26. Pseudofluorescence Seen when blue light is reflected from highly reflective
fundus lesions.
 Myelinated nervefibres
 Chorioretinal scars.

27. Transmission or Window Defect
 Area of hyperfluorescence
that occurs in early transit
and decreases
progressively in intensity
throughout the transit as
the choroidal
fluorescences decreases.

28.  Caused by atrophy of the RPE cells which produces
increased visibility of the underlying choroidal
fluorescence.
 Corresponds to choroidal phase.
 Do not increase in intensity of shape
 No widening
 No diffusion

32. Leakage

33. Leakage
 Defined as increase in size and intensity of
hyperfluorescence from the early to late phase of
angiogram.
 Produced when there is a disruption of inner (retinal
capillaris) or outer blood retinal barrier (retinal pigment
epithelium).
 Pooling – When leakage occurs in anatomical space.
 Initial small spot.
 Increases in intensity and shape in following phase
 Edge are ill defined
 Persistance in late phase

34.  Causes-:
 At macula-:
 Cystoid macular edema, ect
 At Disc-:
 Papilledema, NVD
 Ischemic optic neuropathy
 Inflammation
 Elsewhere -:
 NVE
 CNV
 Vasculitis
 PED

38. Staining
 Fluorescein leaks into tissues
 Hyperfluorescence increases in intensity, from early to
late phase.
 Sharp edges in the late phase

41. Filling Defects
 Areas of decreased fluorescence due to occlusion in
the normal circulation or to tissue defects.
 Produced by retinal arterial, venous and capillary
occlusions
 Physiologic filling defects a- patchy filling of
choriocapillaris in the early choroidal phase.

43. Blocked Fluorescence
 Masking effect of normal
fluorescence produced by
barriers that are situated
between areas of
fluorescence and the film
plane.
 Pigments
 Exudates
 Hemorrhage

45. Retrofluorescence
 Negative contrast of non-fluorescent structures
against background fluorescence.
 During late phase retinal and choroidal vessels that are
free of fluorescein are seen as black shadows against
the scleral fluorescence.

48. ICG
 FFA has limited applications for
choroidal imaging due to-:
 Masking of choroidal
circulation by ocular pigments
and blood.
 Rapid leakage from
choriocapillaris masking the
choroidal vasculature.

49. Properties
 Water soluble tricarbocyanine dye.
 Contain 5% sodium Iodide.
 Absorption – 805nm
 Emission – 835nm
 98% protein – binding
 excreted exclusively by the liver
 Dosage 25mg/2ml followed by 5ml bolus saline

50. Adverse Reactions
 Mild
 Nausia,Vomiting,Pruritis
 Moderate
 Urticaria, syncope, skin eruptions, pyrexia, local tissue
necrosis, nerve palsy.
 Severe
 RS - Bronchospasm, Laryngospasm and anaphylaxis
 CVS - Circulatory shock, myocardial infarction and arrest.
 CNS - Tonic-clonic seizure

51. Instrumentation
Fundus Camera
with infrared
filter
Field -50º,30º,20º 1 FPS
SLO
Reflected light
blocked by filter
Field 10º-30º
Real time dual
Videography

52. Early phase (Upto 20 seconds)
 Hyperfluorescence of the optic disc
 Poor perfusion of the vertical zone
near the optic disc (watershed
zone)
 Prominent filling of choroidal
arteries and early filling of
choroidal veins.
 Early filling of retinal arteries

53. Early middle phase (20 sec. – 3 minutes)
 Filling of watershed zone.
 Fading of choroidal arterial
 Prominent filling of choroidal
veins.
 Retinal arteries and veins are
visible

54. Late middle phase (3-6 minutes)
 Fading of choroidal vessels.
 Diffuse hyperfluorescence-
from chorio-capillaris.
 Retinal vessels still visible

55. Late Phase (6-21 minutes)
 Virtually black optic disc
 Retinal vessels are no
more visible.

56. Clinical Interpretation
 Hypofluorescence
 Blockage : (Blocked Fluorescence)
 Pigment
 Hemorrhage
 Exudation, Myelination and Scarring
 Vascular Filling Defect
 Physiological
 Vascular occlusion
 Tissue atrophy.

57.  Hyperfluorescence-:
 Pseudofluorescence
 Transmitted fluorescence – Window defect
 Abnormal vessels
 Leakage
 Pooling
 Staining

58. Clinical applications.
 Age Related Macular Degeneration
 Focal CNV (Hot Spot):Solitary area of well delineated
focal neovascularization,less than 1 disc diameter.
 Plaque:area of occult CNV larger than 1 disc diameter in
size.Can be well defined or ill defined.
 Identifty feeder vessels to CNV

60.  Idiopathic Polypoidal
Choroidal Vasculopathy (IPCV)
 vascular network overlying the
large normal choroidal vessels.
 Small hyperfluorescent polyps
are visible within the choroid.

61.  Choroidal Tumors
 Choridal hemangioma- Demonstrate intrinsic vascular
pattern
 Choroidal Nevus – diffusely hypofluroscence
 Choroidal Melanoma

62.  Central Serous Chorio-Retinopathy
 Reveals more leaking sites along with more number of
PEDs

63.  Inflammatory Chorio-
Retinal Diseases
 Bird shot Chorio-
retinopathy
 Serpiginous
Choroidopathy
 Multiple Evanescent
White Dot Syndrome

64. Advantage over FA
 ICG had better penetration.
 98% protein binding.
 Infrared light scatter less.
 More useful in choroidal diseases.