D R . G . N A G E S W AR R A O ; M D
A S S O . P R O F. O P H T H A L M O L O G Y, K I M S
V I T R E O - R E T I N A L S U R G E O N
Fundus fluorescein angiography
What is fluorescence ???
LUMINESCENCE & fluorescence
 Luminescence:- Emission of light from any source
other than high temperature
 It occurs when energy in the form of electromagnetic
radiation is absorbed and then re-emitted at another
frequency
 Fluorescence:- luminescence that is maintained
only by continuous excitation
Understanding fluorescence
Fluorescent
chemical
absorbs
Radiant
energy
release
Free
electron
Jump
to
higher
level
Becomes
unstable
Returns
To
Lower
level
Emit
energy
Luminescence
/fluorescence
Purpose of ffa
 studying the normal physiology of the retinal
and choroidal circulation,as well as disease
process affecting the macula.
 Evaluation of the vascular integrity of the
retinal and choroidal vessels
 Check the integrity of the blood ocular barrier.
- outer blood retinal barrier breaks in CSR
- inner blood retinal barrier breaks in NVD,NVE
Therefore ,
it helps :
 In clinical diagnosis
 to determine extent of damage
 To formulate treatment strategy for choroidal and
retinal disease
 To monitor result of treatment
Indications
of FFA
Macular
disorders
Retinal diseases
1) Diabetic retinopathy
2) Retinal vein occlusions
3) Retinal artery occlusion
4) Retinal vasculitis
5) Coats disease
6) Familial exudative
vitreoretinopathy
Macular diseases
1) Central serous
retinopathy
2) RPE detachment
3) Cystoid macular edema
4) Macular hole
5) ARMD
6) Cone rod dystrophy
7) Epiretinal membrane
8) Vitiliform dystrophies
9) Stargardts dystrophy
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) Pregnancy ( especially 1st trimester)
Adverse effects
MILD MODERATE SEVERE
Staining of skin,
sclera and
mucous
membrane
Nausea and
vomiting
Respiratory-
laryngeal edema
,bhroncospasm
Stained secretion
Tear, saliva
Vasovagal
response
Circulatory
shock, MI,
cardiac arrest
Vision tinged
with yellow
urticaria Generalized
convulsion
Orange-yellow
urine
fainting Skin necrosis
Skin flushing,
tingling lips
pruritus
PROCEDURE
Patient is informed of the normal procedures, the side effects and
the adverse reactions.
Dilating the pupil
Made to sit comfortable.
3-4 red free photographs taken.
(control photographs)
5ml of 10% or 3ml of 25% NAF injected through the anticubital
vein
wait for 10 – 12 seconds( normal arm-retina time)
Photos are taken at 1 second interval for 10 seconds
Then every 2 seconds interval for 30 seconds
Late photographs are usually taken after 3 ,5 and 10
minutes.
CIRCULATION OF DYE
Dye injected from peripheral vein
venous circulation
heart
arterial system
INTERNAL CAROTID ARTERY
Ophthalmic artery
Short posterior ciliary artery) Central retinal
(choroidal circulation.) ( retinal circulation)
N.B. The choroidal filling is 1 second prior to the retinal filling.
what is normal angiography?
Two types of circulation in fundus
A.Choroidal
circulation
-choriocapillaries are
fenestrated
-so allows dye to diffuse
freely
BUT,
-outer blood-retinal barrier
in RPE don’t let dye to
reach retina
B.Retinal circulation
-endothelial cells of retinal
blood vessels joined by
tight junctions (inner
blood retinal barrier)
-prevents leakage of dye
from vessels
Phases of angiogram
A) Choroidal (pre-arterial)
B) Arterial
C)
iovenous(capillary)
D) Venous and
E) Late(elimination)
Patchy filling
No leakage
No complication
WHY
???
Prearterial/choroidal phase
 8-12 seconds after dye
injection
 Initial patchy filling
followed by diffuse filling
 No dye has entered
retinal circulation
Arterial phase
 Shows arterial filling
 Continuation of
choroidal filling
 1 second after choridal
phase
Arterio-venous phase(capillary phase)
 Complete filling of
arteries and capillaries
 Early laminar flow to
veins
 Dye seen along lateral
wall of veins
Early venous phase
 Arteries and capillaries
completely filled
 Marked lamellar venous
flow
Mid-venous phase
 Some veins completely
filled
 Some shows marked
laminar flow
Late venous phase
 All veins completely
filled
 Arteries begin to empty
Late/elimination phase
 Elimination of dye from
choroidal and retinal
circulation
 Staining of disc – normal
 In 5-10 minutes
fluorescein absent from
angiogram
 And from body in several
hours
Fovea in FFA
 Appears dark
AVASCULARI
TY IN FAZ
BLOCKAGE OF
CHOROIDAL
FLUORESCENCE
INCREASED
XANTHOPHYL
L PIGMENTS
LARGER RPE
CELLS WITH
MORE
MELANIN
Hypofluorescenc
e (black) patch
Hyperfluorescen
ce (white) patch
FFA interpretation flow chart
Fluorescein angiogram
Normal Abnormal Artifact
Hyperfluorescence Hypofluorescence
Leakage Pooling Staining Window Blocked Nonfilling
defect filling
hyperflourescence
 Greater level of fluorescence than would be found in
normal angiogram
 Occur due to:
-window defect
-increased accumulation of dye
leakage
pooling
staining
examples
 Papilledema
 Abnormal choroidal vasculature(CNV)
 Breaking of inner blood retinal barrier(cystoid macular
oedema)
 Abnormal retinal or disc vasculature(retinal
neovascularization)
 Proliferative Diabetic Retinopathy(NVD,NVE)
Flower petal appearance
CME
papilloedema
Neovascularization at disc(NVD)
Neovascularization elsewhere (NVE)
pooling
 Accumulation of fluorescein in anatomical space
 Due to breakdown of outer blood retinal barrier
CENTRAL SEROUS
RETINOPATHY
PED
staining
 Accumulation of fluorescence within a tissue
 Due to prolonged dye retention
 Minimum hyperfluorescence in early and midphase
which increases in late phase
 Can be seen in normal as well as pathologically
altered tissue
examples
RETINAL
a. non-cystoid macular
oedema
b. Perivascular staining
SUB RETINAL
a. Drusens
b. Sclera
c. Lamina cribrosa
d. scars
Drusens in ARMD
hypofluorescence
 Reduction or absence of fluorescein
 Two causes
BLOCKED
FLUORESCENCE
VASCULAR
FILLING
DEFECTS
BLOCKED FLUORESCENCE
 Optical obstruction (masking) of normal density of
fluorescein
 Caused by lesions anterior to retina
examples
 Pre-retinal lesions eg.vitreous opacity,preretinal
haemorrhage block all fluorescence
 Deep retinal lesions eg.intraretinal haemorrhage and
hard exudates block only capillary fluorescence
 Increased density of RPE eg.congenital hypertrophy
 Choroidal lesions eg.naevus
RPE
hypertrophy
Retrohyaloid haemorrhage
Filling defects
 Inadequate perfusion of tissue with resultant low
fluorescein content
examples
 vascular occlusion of choroidal circulation or
retinal arteries,veins and capillaries
 Loss of vascular bed eg.severe myopic degeneration
– choroideremia
 Emboli
 arteriosclerosis
CRAO
CRVO
Zonula occludents open up
normal
Endothelial cell is lost
Pores in endothelial cells
PERIVASCULITIS
DIABETIC
MICROANEURYSM
PROLIFERATED
RETINAL VESSELS
RETINAL PIGMENT EPITHELIUM
 Normal RPE is tight
 zonula occludens seal portion of all the
intercellular spaces of the pigment epithelial
monolayer.
Cental serous
chorioretinopathy Type I
Haemorrhagic PED
in wet ARMD
summary
 Even today FFA, has its position in the diagnosis of
retinal diseases
 Normal retinal vessels will not leak dye
 Hypofluorescence –
blocked/filling defect
always match with red free fundus photo
 Hyperfluorescence – leakage of dye from
abnormal vasculature/collection of the dye into an
extracellular space
 Wide field angiogram – recent advancement
THANK YOU

FFA ppt.pptx