Introduction To Fundus Fluorescein Angiography (FFA)And Indocyanine Green(ICG)
- Dr HITESH SHARMA, JR1 , DEPT OF OPHTHALMOLOGY, IMS B.H.U.
FUNDUS ANGIOGRAPHY
1. Fluorescein (FA)
Characteristics of Fluorescein & General principles Excitation and emission Filters Photographic technique Phases of normal angiogram Causes of dark appearance of fovea Causes of hyperfluorescence Causes of hypofluorescence
2. Indocyanine green (ICG)
General principles Phases of normal angiogram
Characteristics of Fluorescein
Nontoxic, inexpensive, safe Alkaline solution Highly fluorescent Absorbs blue light (480-500 nm) Emits yellow-green (500-600 nm [525 nm]) Effective at pH 7.37-7.45 Removal from blood by kidneys and liver within 24 hrs.
General principles of FA
Fluorescein
85% bound to serum proteins 15% unbound free fluorescein
Inner blood-retinal barrier (retinal capillaries)
Impermeable to fluorescein
Outer blood-retinal barrier (zonula occludens)
Impermeable to fluorescein
Choriocapillaris
Permeable only to free fluorescein
Excitation and emission
Filters
Photographic technique
1. Take red-free photograph 2. Inject rapidly 5 ml of 10% solution 3. Take photographs at 1 sec intervals between 5-25 sec after injection 4. Take photographs after 10 min and 20 min, if appropriate
Normal FFA
Arm-to-retina circulation time is 12-15 sec. Five angiographic phases:
Pre arterial Arterial Arteriovenous Venous Recirculation
Phases of normal FA
Arterial
Arterial filling
Arteriovenous (capillary)
Early venous
Very early lamellar venous flow
Marked lamellar venous flow
Mid-venous
Late venous
Almost complete venous filling
Complete venous filling
Progressively weaker fluorescence Staining of disc
Late
Leak
Hyperfluorescence
Transmission increase
Abnormal vessels
Pooling (in a space) Leak Staining (in a tissue). Transmission increase Pigment epithelial window defect Retinal Abnormal Vessels Subretinal Tumors
Retinal Pooling (in a space) Subretinal Hyperfluorescence Leak Retinal Staining (in a tissue). Subretinal
Cystoid edema Sensory retina detachment Retinal pigment epithelium Noncystoid edema Perivascular staining Drusen Scars Sclera Lamina cribrosa
Pigment Hyperfluorescence Transmission Increase Epithelial Window Defect Atrophy Drusen
Retinal
Tortuosity and Dilation Neovascularization Microaneurysms Aneurysms Macroaneurysms Telangiectasias Shunts and collaterals Neovascularization Vessels in scar Angioma Retinal Retinoblastoma Hemangioma Melanoma Metastases
Hyperfluorescence
Abnormal Vessels Subretinal
Tumors Subretinal
Transmission Decrease (blocking effect) Hypofluorescence
Filling defect (delay and occlusion)
Pigment
Melanin Hemoglobin Xanthophyll Lipofuscin Hard Soft
Hypofluorescence
Transmission Decrease (blocked)
Exudates Edema and transudate
Other abnormal materials
Best`s disease Foreign body Fundus flavimaculatus
H y p o f l u o r e s c e n c e
Artery Retinal Vein Capillary bed
Filling defect (delay and occlusion)
Dystrophies Loss of tissue
Choroideremia Choroidal atrophy etc. Myopia Central areolar atrophy
Subretinal
Degeneration Nonperfusion
Causes of dark appearance of fovea
Avascularity Blockage of background choroidal fluorescence by:
Increased density of xanthophyll Large RPE cells with more melanin
Causes of hyperfluorescence ( 1 )
RPE window defect Pooling of dye
RPE atrophy
(bulls eye maculopathy
Under RPE
(pigment epithelial detachment)
(central serous retinopathy)
Under sensory retina
Causes of hyperfluorescence (2)
Leakage of dye Prolonged dye retention ( staining )
(cystoid macular oedema)
Into sensory retina
(choroidal neovascularization
From new vessels
Associated with drusen
Causes of hypofluorescence (1)
Blocked retinal or choroidal fluorescence
Blood under retinal pigment epithelium
Abnormal material Increased pigment
Preretinal or intraretinal blood
Causes of hypofluorescence (2)
Vascular occlusion Loss of vascular tissue
Capillary non-perfusion (venous occlusion)
Choroideremia or high myopia
Side Effects
Minimal relatively safe drug Use of dilating drops Red after images from the photoflash Temporary tan skin color Fl. Urine discoloration Interfere with serological tests 2-4% Transient nausea and occ. VOMITING Hives, asthmatic symptoms Laryngeal edema Rarely Syncope, anaphylactic rxn, MI, resp. or Cardiac arrest Rx oral or I.V. Benadryl or Cortisone A physician in the 1st few minutes
During Pregnancy and Lactation
Controversial Fl. Crosses the placenta Has been done in pregnancy with no adverse effect Do it when necessary
General Principles of ICG Angiography
1. Binding
98% bound to proteins Less leakage from choriocapillaris Much less than fluorescein Excitation peak 800 nm Emission at 835 nm Infrared barrier and excitation
2. Fluorescence
3. Filters
4. Safer than fluorescein
Phases of normal ICG angiogram (1)
Early (20 sec) Early middle (3 min)
Disc hypofluorescence Poor perfusion of vertical (watershed) zone near disc Prominent filling of choroidal arteries Early filling of choroidal veins Filling of retinal arteries but not veins
Filling of watershed zone Fading of choroidal arterial filling Prominent filling of choroidal veins Filling of retinal arteries and veins
Phases of normal ICG angiogram (2)
Late middle (6 min) Late (21 min)
Reduced filling of choroidal vessels Diffuse hyperfluorescence due to diffusion of dye from choriocapillaris Persistent filling of retinal vessels
Large choroidal and retinal vessels are empty Diffuse background hyperfluorescence
FFA
Things to remember Not all abnormal conditions of the ocular fundus will produce abnormal fluorescein angiograms.
