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Fundus Fluorescein Angiography
Dr Md Afzal Mahfuzullah
MCPS,FCPS,Felow Vitreo-Retina
Retina Specialist & Surgeon
Bangabandhu Sheikh Mujib Medical University
WHY FFA
To confirms the elements already revealed by clinicalexamination.
Flow characteristics in the blood vessels as the dyereaches and circulates through the retina and choroid.
Gives a clear picture of the retinal vessels and assessmentof their functional integrity.
To monitor the disease intensity and impact of therapy.
Provides guidance for application of focal laser inphotocoagulation therapy.
To detect the leakages without clinical manifestation ofedema
What are the informations we get from FFA
FFA reveals:
Inflammatory status of retinal and choroidal blood vessels.
Localization of intra retinal lesions e.g. depth of pathological involvement in DR.
CNV
Neovascularisation in disc or retina
FFA reveals: Cont
Subretinal fluid status
Cystoid macular edema
Intraretinal/ preretinal haemorrhages
Optic nerve disorders
RPE integrity and disorders
Choroidal neovessels and chorioretinal atrophy
BASIC PRINCIPLES:
BASIC PRINCIPLES:
Based on luminescence and fluorescence.
Luminescence – is the emission of light from any source
other than high temperature.
Fluorescence is luminescence that is maintained only by
continuous excitation. Excitation occurs at one wave length
and immediate emission occurs through a longer wave
length.
FLUORESCENCE
Refers to fluorescein sodium (C20H10Na2O5)
A brown or orange red crystalline substance, alkaline innature.
MW- 376 dalton
Readily diffuses through body fluids and choriocapillariesbut does not diffuse through vascular endothelial cellsand RPE (Blood retina barriers)
OPTICAL PRINCIPLE
Absorbs blue light (465-490nm ) and Emits yellow-green light (520-530nm)
Metabolized by liver and exerted by kidney
FILTERS
1.Blue excitation filter
2.Yellow-green filter
Blood supply to retina
Layers & blood supply
GENERAL PRINICIPLES OF FFA
Fluorescein• 85% bound to serum proteins• 15% unbound ‘free’ fluorescein
• Impermeable to fluorescein
Outer blood-retinal barrier (zonula occludens)
• Impermeable to fluorescein
Choriocapillaris
Permeable only to ‘free’ fluorescein
Inner blood-retinal barrier(retinal capillaries)
Circulation of NaFDye injected from peripheral vein
Venous circulation
Heart
Arterial system
INTERNAL CAROTID ARTERY
Ophthalmic artery
Short posterior ciliary artery) Central retinal artery
(choroidal circulation.) ( retinal circulation)
N.B. The choroidal filling is 1 second prior to the retinal filling.
ANGIOGRAPHIC PHASES
Five angiographic phases:
• Pre arterial (Choroidal 9-15 seconds)
• Arterial
• Arteriovenous(capillary)
• Venous
• Recirculation
Basic anatomy :
The inner retina contains the retinal blood vessels.
The larger vessels in the Nerve fiber layer.
The retinal capillaries in the Inner nuclear layer.
Both are impermeable to dye.
The outer retina is primarily interstitial space of the retina, where hemorrhages, edematous fluid and hard exudates accumulate.
In normal conditions this layer does contain NaF as because of RPE tight junctions(Outer BRB)
Large choroidal vessels do not leake NaF but choriocapillaris does leak.
BASIC ANATOMY
PRE-ARTERIAL/ CHOROIDAL PHASE
Choroidal flush
Patchy Choroidal filling because of lobular arrangements of choriocapillaris
10-12 sec in young
12-15 sec in old
Cilioretinal artery fills at the same time with choroid circulation
Macula remains dark due to tall RPE and more pigments.
ARTERIAL PHASE
ARTERIAL PHASE Cont…
ARTERIOVENOUS PHASE
VENOUS PHASE
Recirculation phase
ABNORMAL ANGIOGRAPHIC FINDINGS
Hypofluorescence:
Filling defect
Blocking defect
Hyperfluorescence :
Window defect
Leakage
Pooling
Staining
Hypofluorescence
Blocked fluorescence (Transmission defects- blood, pigment, hard exudates etc)
Vascular filling defects (Circulation abnormality)
Blocked Retinal fluorescence
1. Arterial segment material
2. Vitreous material
3. Inner retinal material
Blocked choroidal fluorescence
1. Deep retinal material
2. Subretinal material
3. Sub RPE material
4. Choroidal material
Hypofluorescence.Cont
Hyperfluorescence
Anomalous vessels
Choroid
Retina
Optic nervehead
Subretinal neovasculari-zation
Tumor vesselsChorioretinal anastomosis
Vascular tortuosities
Dilation and shuntsAnastomosisNeovascularization
Aneurysms
TeleangiectasiaTumor vesselsHamatoma
NeovascularizationTortuosity
DilationHamatomaTumor vessels
Hyper-
fluorescence
In a preformedspace (pooling)
Into tissue(staining)
Retinal
Subretinal
Retina
Subretinal
Cystoid edema
Detachment ofthe pigmentepithelium
Detachment ofthe sensoryretina
noncystoidedema
e.g.dursen
Leakage
Fluorescencewithout theadministration of fluorescein
Autofluorescence
Pseudofluorescence
Drusen of the optic nerve head
Hamatoma
Scleral exudate
Myelinate nerve Fibers, optic nerve drusen
Scar tissue
Foreign body
Causes of dark appearance of fovea
-Avascularity
• Increased density of
xanthophyll
• Large RPE cells with more melanin
-Blockage of background choroidal fluorescence by:
Causes of Hyperfluorescence
RPE ‘ window’ defect
RPE atrophy
(bull’s eye maculopathy
Pooling of dye
Under RPE
(pigment epithelial detachment)Under sensory retina
(central serous retinopathy)
Causes of Hyperfluorescence
Leakage of dye Prolonged dye retention ( staining )
Into sensory retina (cystoid macular oedema)
From new vessels(choroidal neovascularization
Associated with drusen
Vascular occlusion
Capillary non-perfusion(venous occlusion)
Loss of vascular tissue
Choroideremia or high myopia
Causes of Hypofluorescence
BRVO- HYPO F- BLOCKED F
BRVO
SUB HYLOID. Hge/ PRERETINAL Hge HYPO F- BLOCKED
STARGARDT'S DISEASE
Fundusflavimaculatus: (Stargardt disease (STGD) is the most
common childhood recessively inherited macular dystrophy.
Blocked the choroidal fluorescence, so fundus background looks
black.
AION – HYPO F OF DISC
Red-free Fundus photos
Normal appearance Autofluorescence
Macular Hole
ARMD - HYPER- STAINING
CHOROIDAL NAEVUS
DIABETIC RETINOPATHY
Diabetic retinopathy gives a combination of both hyper/ hypofluorescence. Several pathologies are seen in this frame:
DIABETIC RETINOPATHY
Hypofluorescence:
Retinal haemorrhage (1)
Ischaemia (2).
Hyperfluorescence:microaneurysms (3) and neovascularization (4)In addition, there are IRMA (5) between the retinal artery and vein and venous beading (6)
DIABETIC MACULOPATHY TREATED WITH
LASER
PDR- HYPER F
BACKGROUND DIABETIC RETINOPATHY
CENTRAL SEROUS RETINOPATHYPOOLING/ HYPER F
Late phase of FFA shows a spot of pigment epithelium leakage has enlarged & fuzzy,in this case there is pooling of fluorescein under the detched retina
HYPER F- WINDOW/ POOLING EFFECT
Fundus photography shows PED & late phase of angiogram showing the corresponding well defined hyperfluorescent lesion
HYPERTENSIVE RETINOPATHY
Limitations of FFA
1) Does not permit study of choroidal circulation details due to
a) melanin in RPE
b) low mol wt of fluorescein
2) More adverse reaction
3) Inability to obtain angiogram in patient with excesshemoglobin or serum protein.
Thank you