FUNDUS FLUORESCEIN ANGIOGRAPHY TECHNIQUE AND INTERPRETATION

FUNDUS FLUORESCEIN
ANGIOGRAPHYDr Shruti laddha

BASIC PRINCIPLE
– To understand fluorescein angiography, knowledge of
fluorescence is essential.
– To understand fluorescence, knowledge of luminescence is
essential.

Luminescence-emission of light by any source other than high temperature .
• When light energy is absorbed into a luminescent material, free electrons
are elevated into higher energy states.
• This energy is then reemitted by spontaneous decay of the electrons into
their lower energy states.
• When this decay occurs in the visible spectrum, it is called luminescence.
• Luminescence therefore always entails a shift from a shorter wavelength to
a longer wavelength

FLUORESCENCE
– Fluorescence is luminescence that is maintained only by continuous
excitation.
– Emission stops when excitation stops.
– Excitation at one wavelength occurs and isemitted immediately
through alonger wavelength.

PSEUDOFLUORESCENCE
– Occurs when non-fluorescent light passesthrough entire filter system
– It causesnon-fluorescent structures to appearfluorescent
– Thus excitation (blue) and barrier (green-yellow) filters should be
matched to avoid overlap of light between them

• To avoid pseudofluorescence filter combination to be sure that
no significant overlap exists
• Over the time filter alter the range of light transmission so
should be change in certain time.

Equipment for Fluorescein Angiography
• Fundus Camera (20° – 35° – 50°) with Digital Imaging System Matched
fluorescein filters (Barrier andExciter)
• 23-G scalp vein needle 5ml syringe
• 5ml of 10 %fluoresceinsolution
• Tourniquet
• Alcohol swab / bandage Standard emergency equipment

Sodium fluorescein
• Anorganic vegetable dye.
• Orange– red, crystalline hydrocarbon (C20-H12-O5-Na)
• Molecular weight - 376Dalton
• Excitedbetween 465-490 nm & fluoresces at520-530 nm.
• Doesnot diffuses out through outer and inner blood retinal barrier
• Itdiffuses through chorio-capillaries and Bruchsmembrane
• Eliminated by liver and kidneys within 24hours

• Non expensive, non toxic , highly fluorescent thatcan be used safely
with mostpeople.
• It fluoresces effectively at normal blood ph level(7.37-7.45)
• 80%bound to plasmaprotein and also with RBC
• High solubility in water.
 Advantage- can’t passthrough tight retinal barriersso
allows study of retinalcirculation
 Disadvantage- can’t study choroidalcirculation

 FluoresceinSolutions :
- 10ml of 5% (500mg)
- 5ml of 10% (500mg)
- 3 ml of 25% (750mg)

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
• Checkthe integrity of the bloodocularbarrier.
• Outer blood retinal barrier breaksin CSR
• Inner blood retinal barrier breaks in NVD, NVE

INDICATIONS
• Retinal vascular disorders
• Macular disorders
• Retinal vascular malformation
andtumors
• Choroidal disease
• Optic nerve disease

CONTRAINDICATIONS
ABSOLUTE:
• known allergy to iodine containingcompounds.
• H/O adverse reaction to FFAin the past.
RELATIVE:
• Asthma
• Hay fever
• Renal failure
• Hepatic failure
• Pregnancy ( especially 1sttrimester)

TECHNIQUE
- Informed consent
- Dilate pupils
- Prepare fluorescein solution, scalp vein cannula & syringe
- Prepare the fundus camera i.e. clean the front lens, focusing
of eyepiece crosshairs
- Position patient for comfort, alignment and focus
- Align and focus camera

- Take colour photographs
- Take red-free photographs
- Insert scalp vein cannula
- Inject dye as bolus and start timer
- Shoot exactly at start and exactly at finish of injection
- Again start shooting at 8 sec. in young and 12 sec. in adults after
injection, at interval of 1-2 sec.
- Shoot late pictures at 5 min. and 10 min.

Circulation of NAF
venous circulation
heart
arterial system
INTERNAL CAROTID
ARTERY
Ophthalmic artery
Short posterior ciliaryartery)
(choroidal circulation.)
Central retinal artery
( retinal circulation)
- The choroidal filling is 1 second prior to the retinal filling.
Dyeinjected from peripheral vein

INTERPRETATION
Normal Fluorescein Angiogram:
• Consists of the following overlapping phases
1. Choroidal phase
2. Arterial phase
3. Arterial venous (capillary) phase
4. Venous phase
• Early phase
• Mid phase
• Late phase
5. Late elimination phase

Outer blood–retinal barrier
• The major choroidal vessels are impermeable to both bound and
free fluorescein.
• However, the walls of the choriocapillaris contain fenestrations
through which unbound molecules escape into the extravascular
space, crossing Bruch membrane
• but on reaching the RPE are blocked by intercellular complexes
termed tight junctions or zonula occludentes

Inner blood–retinal barrier
• is 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 inner blood–retinal barrier permits leakage of both
bound and free fluorescein into the extravascular space

Choroidal Phase
• 10-12 seconds after dye
injected
• Initially patchy filling followed by
the diffuse filling as the dye
leaks from the choriocapillaries.
• No dye has reached the retinal
arteries.
• Cilioretinal artery if present fills
in this phase

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.

Arteriovenous phase
(capillary phase)
• Complete filling of the retinal
arteries and capillaries.
• Early laminar flow of the veins so
dyes seen along lateral wall

Arteries and capillaries are completely filled and marked lamellar venous flow
EARLY VENOUS PHASE

MID VENOUS PHASE
• Some veins are completely filled
• Some shows marked laminar flow

LATE VENOUS PHASE
• All veins are completely filled
and the arteries beginning to
empty

LATE PHASE
• After 10-15 minutes little dye remains in
the blood stream
• This phase demonstrate gradual
elimination of the dye from the retinal and
choroidal vasculature staining of optic disc
, sclera is normal finding
• Any other hyperfluorescence suggest the
presence of abnormality

FLUORESCENCE IN
FOVEAL REGION
 Dark appearance :
• Avascularity in the FAZ
• Blockage of the choroidal
flourescein because of
increased amount of
xanthophyll pigments at
fovea ,melanin in RPE

Autofluorescence
• Innate property of fluorescence in
certain ocular tissue Fluorescein
without dye
• It is exhibited by drusen, astrocytic
hamartoma, crystalline lens,
basement membrane, myelinated
nerve fibers, melanin granules.

Hyperfluorescence
Window defect-
• focal RPE atrophy, RPE tear.
• Unmasking of normal background of
choroidal fluorescence characterized by
early hyperfluorescence which
increases in intensity then fade without
changing shape and size.
e.g. Geographic atrophy.

Leakage
• Increase in size and intensity of hyperfluorescence
from the early to late phase of angiogram.
• Produced when there is a disruption of inner
(retinal capillaries) or outer blood retinal barrier
(retinal pigment epithelium).
e.g. Abnormal choroidal vasculature(CNVM),
Breaking of inner blood retinal barrier(cystoid
macular oedema), Abnormal retinal or disc
vasculature (NVE, NVD)

Pooling
• When leakage occurs in
anatomical space.
• Initial small spot.
• Increases in intensity in
following phase
• Persistence in late phase
• CSR, PED

STAINING
• Accumulation of fluorescence within a tissue
• Due to prolonged dye retention
• Minimum hyperfluorescence in early and mid
phase which increases in late phase
• Can be seen in normal as well as pathologically
altered tissue
Example
a. Drusens
b. Sclera
c. Lamina cribrosa
d. scars

Hypofluorescence
Blockage
• Optical obstruction (masking) of normal density
of fluorescein caused by lesions anterior to
retina
• Pre-retinal lesions e.g. vitreous opacity,
preretinal haemorrhage block all fluorescence
• Deep retinal lesions e.g. intraretinal
haemorrhage and hard exudates block only
capillary fluorescence
• Increased density of RPE e.g. congenital
hypertrophy

FILING DEFECTS
• Inadequate perfusion of tissue with
resultant low fluorescein content
• Avascular occlusion of choroidal
circulation or retinal arteries, veins and
capillaries
• Loss of vascular bed e.g. severe myopic
degeneration – choroideremia

Hard Drusen
• Fundus photograph of the right
eye showing multiple discrete
drusen at the fovea
• Arteriovenous phase showing
discrete early hyperfluorescence
• The hyperfluorescence at the
drusen has increased in the mid
arteriovenous phase
• Fading of the hyperfluorescence
is seen in the late phase
• The RPE atrophy overlying the
drusen allows the background
choroidal fluorescence to be
seen as transmitted
hyperfluorescence

Soft Drusen
• Fundus photograph of the RE
showing large soft Drusen
• Faint hyperfluorescence is seen at
the drusen in early AV phase
• Further increase in the
hyperfluorescence is noted
• Maximum hyperfluorescence is
seen in the late phase due to
staining of the soft drusen.
• Due to the hydrophobic nature of
the soft drusen material, the entry
of the dye into the drusen is
delayed. Hence, the soft drusen do
not show hyperfluorescence until
the late stages.

• Fundus photograph showing large
atrophic patches arranged in an annular
fashion around the fovea. RPE alteration
is noted in the foveal region
• Arteriovenous phase shows relative
hypo-fluorescence in the region of
atrophy. Irregular hyper-fluorescence is
seen at the rest of the macula
• Normal scleral staining is seen through
the atrophic areas making them appear
hyperfluorescent in the late phase
• Early hypofluorescence within an atropic
lesion indicates non filling of the
underlying atrophic choriocapillaris along
with atrophy of the RPE

• Fundus photograph of the left eye
showing multiple discrete atrophic
patches around the foveal center
• The atrophic patches appear
hyperfluorescent in the arteriovenous
phase due to transmission window
defect indicating preservation of the
underlying choriocapillaris
• Some fading of the hyper-fluorescence
in the atrophic area is seen in the late
phase
• Early hyperfluorescence in the region
of RPE atrophy indicates the filling of
the underlying choriocapillaris which
has not atrophied along with the RPE.

Pigment Epithelial Detachment
• PED at the fovea
• Early AV phase
hyperfluorescence at the PED.
The margins of the PED are well
defined
• Increase in intensity of
hyperfluorescence is seen in the
arteriovenous phase. The extent
of the lesion remains the Same
• Marked increase in the intensity of
the hyperfluorescence is seen
within the PED. The margins of
the PED remain well defined

CLASSIC CNVM
• CNVM, blood, drusen.
• Early arteriovenous phase - early, well-
defined and demarcated
hyperfluorescence. It also features
several small areas of hypofluorescence
(blockage due to hemorrhage and hard
drusen.)
• Late arteriovenous phase-marked
increase in hyperfluorescence
• Late phase. Leakage from the CNV
Fluorescein is flowing out of the vessels,
and the area of increasing
leakage extends beyond the vessel
network that was visible in
the early phase.

CLASSIC CNVM
• Juxtafoveal membrane with
surrounding rim of subretinal
haemorrhage. Subretinal fluid
and hard exudates
• Arteriovenous phase- filling up
of the juxtafoveal classic
CNVM. blocked choroidal
fluorescence due to the
subretinal blood
• Leakage of dye from the new
vessels obscures the details
of the CNVM
• Intense hyperfluorescence of
the CNVM in the late phase

OCCULT CNVM
• PED at the fovea. Haemorrhage
is seen at the foveal center.
• Mid arteriovenous phase- filling
of the upper part of the PED.
Faint irregular hyperfluorescence
is seen in the rest of the area of
PED
• Stippled hyperfluorescence in
the lower part of the PED has
increased. Increased filling of the
superior part of the PED
• Late phase shows increased
stippled hyperfluorescence
around the fovea suggestive of
an occult CNVM. Pooling of the
dye is noted superiorly

MINIMALLY CLASSIC CNVM
• CNVM
• Early phase. A well-defined area of bright
hyperfluorescence, consistent with a CNV
• Arteriovenous phase. Leakage in the area
of the classic CNV. An increasing
inhomogeneous area of
hyperfluorescence below and above it.
• Late phase. classic CNVM ,occult CNVM
(type 1; fibrovascular pigment epithelial
detachment).
The subfoveal neovascular lesion
with classic and occult components. The
classic choroidal neovascularization
represents less than 50% of the neovascular
lesion (minimally classic choroidal
neovascularization).

• A hypopigmented area, ill-defined oval
pigmented lesion .
• Early arteriovenous phase. Choroidal
vessels are visible temporal to fovea
(window defect), blockage caused by the
curled RPE.
• Arteriovenous phase - increase in the
hyperfluorescence - leakage of the
choriocapillaris. In the middle of the
blockage, punctate hyperfluorescent spots
are seen suggesting a CNV.
• Late phase. There is an increase in the
intensity of the hyperfluorescence,
consistent with detachment of the
neurosensory retina.
The fluorescein angiogram findings in this
eye are consistent with an acute pigment
epithelial tear, caused by an occult CNV on
the inferonasal edge of the lesion.

SCARRED CNVM
• Large scarred CNVM at the
macula.
• Early AV phase- the large
network of vessels of the
choroidal neovascular
membrane
• Late AV phase - leakage of
the dye from the edge of the
CVNM
• Intense hyperfluorescence is
seen in the late phase due to
staining of the tissue and due
to leakage and pooling of the
dye in the subretinal space

CYSTOID MACULAR EDEMA
• Cystoid changes are seen in the
foveal region
• The arteriovenous phase shows
dilation and early leakage of the
dye from the perifoveal
capillaries
• Increased leakage of the dye is
noted in the perifoveal region
• Late leakage and accumulation
of the dye in cystoid spaces in
seen. Increased staining of the
disc is seen

CSCR
a. Color photograph- central serous
chorioretinopathy,
b Early arteriovenous phase. Blocked
fluorescence caused by the exudate
inside the detachment; irregular
hyperfluorescent surface with three
hyperfluorescent points .
c Late arteriovenous phase-
smokestack appearance.
d Late phase. The leakage continues
expanding upward and starts to
occupy the hollow space in the
neurosensory detachment

• Serous elevation of the retina at the
macula
• The arteriovenous phase shows a
point hyperfluorescence superior to
the fovea
• The hyperfluorescence has increased
in intensity and extent due to leakage
in fovea
• Typical ink blot appearance of the
leak is seen in the late film. The
extent of the detachment is well
made out

FLUORESCEIN ANGIOGRAPHY
OF
RETINAL VASCULAR DISEASES

NPDR
• Color photograph. Moderate
NPDR.
• Early arteriovenous phase.
Blockage of the background
fluorescence caused by retinal
hemorrhages.
• Arteriovenous phase. Dot-like
hyperfluorescence of the
microaneurysms.
• Late phase. Areas of mild
hyperfluorescence in a region with
permeable capillaries and
microaneurysms, reflecting
localized retinal edema.

Diabetic maculopathy
• Color photograph. DME, Hard exudates .
• Early arteriovenous phase. Ectatic capillaries and microaneurysms, as well as localized
areas with closed capillaries temporal and superior to the fovea, can be seen.
• Late phase. There is diffuse hyperfluorescence temporal and superior to the fovea in the
area of the permeable capillaries.

• Color photograph. Two years later, new hard exudates have appeared, extending from
the temporal retina to the fovea.
• early arteriovenous phase. Laser scars seen, ectatic changes of retinal capillaries seen
temporal to the fovea. The parafoveal capillary arcades show discontinuity, a sign of
initial central ischemia.
• Late phase. There is distinct hyperfluorescence with a cystoid component temporal to
the fovea.

Different patient
• Middle arteriovenous phase –preretinal proliferation ,areas with marked capillary
occlusion.
• Late phase. Fluorescein has leaked into the area due to the permeable walls in the
proliferative vessel, creating the appearance of a diffuse hyperfluorescent “cloud.”
• Late phase. After scatter laser coagulation, the new vessel has regressed and undergone
fibrosis. The fibrosis shows weak, diffuse staining in the late phase, but there is no
evidence of any further
active neovascularization

• Markedly delayed filling of the veins is seen
• Late phase shows the washout of the dye

BRANCH RETINAL ARTERY OCCLUSION
• Retinal whitening in the inferior part of the fovea
• Red free photograph showing the retinal whitening inferior to the fovea
• Arterial phase - delayed filling of the arteriole exiting from the inferotemporal part of the disc
(arrows). The arterioles superior to the fovea have filled up

• Early arteriovenous phase - normal filling of the arteriole in the upper part of the macula. In
contrast those in the lower half have not filled , absence of capillary details in the lower part of the
macula. There is some progression of the dye column in the inferotemporal macular arteriole
(arrows)
• Arterioles in the lower part of the macula have not filled up completely even in the late phase of
the angiogram

BRVO
• Mid arteriovenous phase.
Hypofluorescence is visible in the
occlusion area due to retinal edema
and capillary dropout or destruction.
Localized areas of hyperfluorescence
caused by telangiectatic vessel
• Late phase. Areas of
hyperfluorescence due to leakages in
the macula and over the occlusion
area, areas of hypofluorescence
resulting from hemorrhage extending
to the fovea can still be seen

CRVO
• Arteriovenous phase-hypofluorescence
due to hemorrhage (blockage) and
extended capillary dropout
(hypoperfusion), areas of
hyperfluorescence due to leakage from
the distended vessels and
accumulation in the vessel walls,
extended arteriovenous passage time.
• Late arteriovenous phase. Increasing
preretinal leakage is evident from the
diffuse fluorescein leakage from the
damaged vessels. Fluorescein staining
is seen in the congested vein walls.

Combined CRVO
With BRAO
• Fundus photograph of CRVO with BRAO Optic disc hyperaemia and edema, dilated and tortuous
veins, intraretinal haemorrhages. Superotemporal to the disc, retinal opacification
• FA shows initial nonperfusion of the branch retinal artery superior to the fovea.

• Marked delay in transit consistent with the occlusive process is seen. The arteriole
occlusion is not complete as the dye eventually does get into the artery.
• In the late phase disc leakage is seen

Ocular Ischemic Syndrome
• Dilated retinal veins and arteriovenous anastomotic channels (inferior to the disc)
• FA (early and midphase) show patchy choroidal filling, delayed A-V transit with classic sign of
leading edge of fluorescein dye in the retinal arterioles and macular ischemia
• Delayed choroidal filling >5 sec
• Delayed AV transit time >15 sec

• FA (late A-V phase) shows multiple pinpoint hyperfluorescent spots suggestive of microaneurysms
• Peripheral fundus shows capillary nonperfusion areas distal to arteriovenous anastomotic
channels

Coats’ Disease
• Hard exudates at the macula and
inferiorly
• Dilated retinal capillaries and
telangiectasias are clearly made
out in the arteriovenous phase.
• Leakage of dye is noted from the
dilated capillaries and the
aneurysmal dilatations.
• Late phase shows leakage of the
dye from the vascular
abnormalities

Retinal Artery Macroaneurysm
• Subretinal dark and altered
haemorrhage, The macroaneurysm is
seen as a white round lesion (arrow)
superior to the fovea, along the retinal
arteriole
• Early AV phase - blocked choroidal
fluorescence caused by the
haemorrhage. The macroaneurysm is
seen as a hyperfluorescent spot along
the retinal arteriole
• Arteriovenous phase shows increased
microaneurysm
• Late phase angiogram shows some
fuzziness around the borders of the
macroaneurysm due to leakage of the
dye through its wall

Eales’ Disease
• Fundus photograph of the
temporal periphery showing
periphlebitis
• Arteriovenous phase-
leakage of the dye from the
vessel walls. Areas of
capillary nonperfusion
• Extensive leakage of the dye
from the walls of the veins
and its draining channels is
seen.
• Late phase shows extensive
staining of the vessel walls
and the adjacent retina

ANGIOD STREAKS
• prominent angioid streaks radiating
from an annular ring around the disc.
A CNVM is noted just superior to this
pigment clump.
• A-V phase - hyperfluorescent
radiating lines. Faint mottled
hyperfluorescence is seen temporally.
• late A-V phase- increase in
hyperfluroscence along angiod
streaks,increase in the
hyperfluorescence in the lesion
superotemporal to the disc s/o CNVM
• Late phase - fading of the
hyperfluorescence . Leakage of dye
in the area of the suspected CNVM

Ocular Ischemic Syndrome
• FA (early and midphase) show patchy choroidal filling, delayed A-V transit with classic sign
of leading edge of fluorescein dye in the retinal arterioles and macular ischemia
• Delayed choroidal filling >5 sec
• Delayed AV transit time >15 sec

• FA (late A-V phase) shows multiple pinpoint hyperfluorescent spots suggestive of
microaneurysms.
• Peripheral fundus shows capillary nonperfusion areas distal to arteriovenous anastomotic
channels.

Retinal Artery Macroaneurysm
• Subretinal dark and altered
haemorrhage, The macroaneurysm
is seen as a white round lesion
(arrow) superior to the fovea, along
the retinal arteriole
• Early AV phase - blocked choroidal
fluorescence - haemorrhage. The
macroaneurysm - hyperfluorescent
spot along the retinal arteriole.
• Arteriovenous phase : increased
microaneurysm.
• Late phase angiogram shows some
fuzziness around the borders of the
macroaneurysm due to leakage of
the dye through its wall

Eales’ Disease
temporal periphery showing
periphlebitis.
capillary nonperfusion.
• Extensive leakage of the dye
from the walls of the veins
and its draining channels is
seen.
• Late phase shows extensive
staining of the vessel walls
and the adjacent retina

OF
OPTIC NERVE DISORDERS

OPTIC PIT
• Optic pit - temporal part of disc
• Arterial phase hypofluorescence
in the region of the optic pit
• The hypofluorescence at the
optic pit is persisting in the mid
arteriovenous phase of the
angiogram
• Hyperfluorescence due to
staining is seen at the optic pit
in the late phase
Early hypofluorescence is seen at
the pit due to absence of vessels
in the optic pit.
Late staining of the tissue in the
optic pit is seen.

PAPPILEDEMA
• Disc edema
• Early AV phase- premature leakage from the
dilated capillaries around disc
• Diffuse leakage from peripapillary capillaries
• Late phase-diffuse hyperfluroscence,optic
disc indistinct margins

ANTERIOR ISCHEMIC OPTIC NEUROPATHY (AION)
• Pallor in the upper half of the disc, microaneurysms and hard exudates
• Filling of the disc capillaries is seen in the lower half. The upper half of the disc shows relative
hypofluorescence
• Increased staining of the disc is seen. Retention of dye is seen in the macula, indicative of macular
edema
• Differential filling of the disc capillaries is seen in AION.

OPTIC NERVE HEAD DRUSEN
• The nodular elevation along the
disc margin
• Mid arteriovenous phase-
Irregularity along the disc margin
• Late arteriovenous phase-
irregularity along the disc margin.
• Late phase showing the increased
staining of the drusen
• Druscen-autofluroscence
(preinjection phase)

Different patient-autofluroscence of several druscen

OPTIC NEURITIS
• Arterial phase-leakage from the capillaries at disc
• Early A-V phase increase in hyperfluroscence
• Mid A-V phase-increase in hyperfluroscence
• Late phase-hyperfluroscence localised to disc

FLUORESCEIN
ANGIOGRAPHY OF
HEREDOMACULAR
DYSTROPHY

RETINITIS PIGMENTOSA
• RPE alteration and pigment
clumping along the arcades
• Early AV phase- large choroidal
vessels in areas of RPE and
choriocapillaris atrophy
• Transmitted fluorescence is
seen in the affected areas
• Late phase- the background
scleral staining as
hyperfluorescence through the
overlying atrophied layers

• Fluorescein angiography is useful to assess the status of the choriocapillaris in RP.
• Early hyperfluorescence through the window defects in the RPE suggests intact
choriocapillaris.
• Delayed hyperfluorescence indicates atrophy of the choriocapillaris.
• Fluorescein angiography can thus be of prognostic value in patients with RP.

OCULAR ALBINISM
• Markedly depigmented fundus
• Arterial phase - increased visibility
of the larger choroidal vessels due
to lack of blockage by RPE.
• A diffuse choroidal fluorescence is
seen due to leakage of dye from
the choriocapillaris
• Late phase - the relatively
hypofluorescent larger choroidal
vessels and the retinal vessels
silhouetted against the background
fluorescence due to scleral staining

• Depigmented fundus
• AV phase- retinal vessels
cant be clearly made out
• Late phase –background
hyperfluroscence due to
staining, foveal
hypofluroscence due to
presence of RPE at macula

STARGARDT’S DISEASE
• RPE alterations at the fovea
• A V phase- stippled
hyperfluorescence in foveal
region due to transmission
defects. Silent choroid.
• No choroidal fluorescence is
seen even in the
midperiphery of the fundus
• Late phase - Fading of the
hyperfluorescence in the
foveal region ( window
defect). Silent choroid .

• Foveal atrophy, mid-periphery
multiple whitish lesions
• Early phase - transmitted
irregular hyperfluroscence,
choroidal hypofluroscence
inferiorly
• Late AV phase-increase in
hyperfluroscence with
persistence of inferior
choroidal hypofluroscence
• Late phase - fading of
hyperfluroscence

BEST DYSTROPHY
• Multiple vitelliform lesions.
• Arteriovenous phase. Blockage of the background fluorescence in all vitelliform lesions.
• Late phase. Persistent blockage caused by the vitelliform lesions.

Depends on the stage of the disease.
• In the vitelliform stage, the early phases of angiogram shows some blocked choroidal
fluorescence in the region of the lesion. In the later phase of the angiogram, the
vitelliform lesion may appear nonfluorescent or may appear to fluoresce slightly.
• In the subsequent stages when the yellow material disrupts, the angiogram shows
areas of hyperfluorescence within the lesion and late staining.
• In the atrophic stage, the large choroidal vessels may be visualized within the atrophic
lesion.
• Angiography in Best’s disease permits the detection of choroidal neovascularization.

• RPE alteration with subretinal
deposits at macula
• Early phase-hyperfluroscence
• Late AV phase – increase in
hyperfluroscence
• Late phase-fading of
hyperfluroscence

• Pseudohypopyon, subretinal scar
• AV phase-transmitted hyperflurocence within the lesion, scar shows intense
hyperfluroscence
• Late phase- scar shows hyperfluroscence

• Vitelliform lesion, greyish
membrane, subretinal and
intraretinal bleed
• Early AV phase- lacy
hyperfluroscence of CNV, blocked
hypofluroscence due to
haemorrhage
• Late AV phase-leakage
hyperfluroscence, blocked
hyperfluroscnec
• Late phase-intense
hyperflurosence

Foveoschisis
• AV phase-no leakage
• Laste phase-no abnormality

OF
INFLAMMATORY DISORDERS

• Vitreous haze
• AV phase- hyperfluroscent disc, increase fluroscence in macular region
• Late phase- CME
Cystoid macular edema and increased disc staining are typical angiographic findings in
intermediate uveitis.
INTERMEDIATE UVEITIS

Vogt-Koyanagi-Harada
Syndrome
• Pockets of SRF
• Mid AV phase-multiple dot
hyperfluroscence
• Late AV phase-increase in
hyperfluroscence
• Late phase-pooling of dye in
subretinal space

• Unlike in CSR, the leaks in VKH are multiple.
• Late pooling of the dye in VKH is extensive .
• In CSR, the entire extent of neurosensory elevation is never filled up with dye
even in the very late phase.
• Late staining of the disc is a common finding in VKH.
• Sympathetic ophthalmia - similar angiographic finding, but is unilateral and has
history of penetrating injury or ocular surgery in the fellow eye.
• Posterior scleritis also has a similar angiographic picture, but is usually unilateral
and has classical T-sign on ultrasonography in majority of cases along with pain
on ocular movements.

SYMPATHETIC OPHTHALMITIS
• Pockets of SRF at the posterior pole
• AV Phase-starry sky appearance with multiple point of hyperfluroscence
• Late phase- pooling of dye, late staining of the disc

POSTERIOR SCLERITIS
• Large, yellowish subretinal mass lesion temporal to the fovea. Prominent choroidal folds at the macula
• Late A-V phase - multiple pinpoint hyperfluorescent spots overlying the subretinal lesion suggestive of
leakage. Alternate hypo- and hyperfluorescent bands in the macula correspond to the choroidal folds
• Late phase angiogram reveals intense, diffuse hyperfluorescence overlying the lesion

BIRDSHOT RETINOCHOROIDOPATHY
• Fundus photograph of the left eye showing multiple flat creamy yellow lesions
• The lesions are not seen in the early arteriovenous phase
• Late phase showing hyperfluorescence of the lesions
• In contrast to APMPPE and GHPC, the lesions in birdshot retinochoroidopathy
do not show hypofluorescence in the early phase.

ACUTE POSTERIOR
MULTIFOCAL PLACOID
PIGMENT EPITHELIOPATHY
• Multiple dull yellow placoid
lesions at the macula
• Early arteriovenous phase
showing hypofluorescence in
the area of the placoid lesions
• Late arteriovenous phase-Faint
hyperfluorescence is seen
within the lesions
• Late phase- Placoid lesions are
hyperfluorescent with fuzzy
margins

GEOGRAPHIC HELICOID
PERIPAPILLARY CHOROIDOPATHY
• Active GHPC. Few skip lesions are
seen temporally
• Early arteriovenous phase- The
lesions appear hypofluorescent.
Few specks of transmitted
hyperfluorescence are seen
superiorly
• Mid arteriovenous phase- lesions
remain hypofluorescent
• Late phase- hyperfluorescence
with fuzzy margins

MULTIPLE EVANESCENT WHITE DOT SYNDROME
• Fundus - few subtle white spots
• A-V phase- multiple hyperfluorescent spots over the posterior pole
• Venous phase -increase in intensity of the hyperfluorescent lesions

BEHÇET’S SYNDROME
• Marked disc pallor, sclerosed vessels, Diffuse RPE atrophy and patches of subretinal scarring
• Arterial phase- thin caliber of vessels and gross RPE window defects along with nonperfusion
areas in the macula
• Late phase shows disc staining with late filling of sclerosed vessels

CHOROIDAL GRANULOMA
• Two discrete, elevated, choroidal granulomas
• Arteriovenous phase - two spots of hyperfluorescence from the lesions due to leakage
• Late phase showing staining of the choroidal mass

OF
TUMORS

CHOROIDAL NEVUS
• Choroidal nevus superotemporal to the fovea. Few RPE alterations are seen just inferonasal to the
foveal center
• Hyperfluorescence due to transmission defects is noted inferonasal to the fovea
• The faint hypofluorescence of the nevus persists in the late phase. The transmission defect has faded

MELANOCYTOMA
• Melanocytoma at the optic nerve
head
• Early arteriovenous phase-
blocked fluorescence due to the
melanocytoma, arteriole is seen
coursing over the tumor
• Arteriovenous phase showing the
blocked fluorescence at the disc
• Hypofluorescence is seen to
persist in the late phase of the
angiogram

CHOROIDAL HEMANGIOMA
• Fundus photograph - a red orange,
minimally elevated mass lesion
temporal to the macula.
• Arterial phase -intense
hyperfluorescence of the tumor
indicating its choroidal origin and
vascularity.
• Mid A-V phase -increase in
hyperfluorescence indicating
leakage of the dye, patches of
blocked fluorescence due to
pigment.
• Late phase - leakage of the dye from
the tumor vessels

RETINAL ANGIOMATOSIS
• Dilated twin feeder vessels with
exudates at the macula
• Arterial phase helps to
differentiate the feeder
arteriole from the venule
• The multiple capillary
haemangiomas are evident in
this montage
• Late phase - Profuse leakage of
the dye from the tumor vessels

OPTIC NERVE HEMANGIOMA
• Orange red well defined lesion at the
disc margin. Hard exudates along the
inferotemporal arcade
• Lesion shows intense
hyperfluorescence in the early
arteriovenous phase indicating the
vascular nature of the lesion
• Late arteriovenous phase- increased
area of hyperfluorescence due to
leakage of the dye
• Late phase- dye leakage from the
tumor and increased intraretinal dye
leakage

COMBINED HAMARTOMA
• Hyperpigmentation at the level of the
RPE. Glial proliferation involving the
retina is seen, causing tortuosity of
retinal vasculature and blurring of disc
Margin
• Mid arteriovenous phase- a well
defined patch of blocked choroidal
fluorescence, Distortion of the retinal
vasculature
• Late arteriovenous phase- increased
hyperfluorescence due to leaking
abnormal vessels in the tumor
• Late phase shows increased staining of
the tumor tissue

RETINOBLASTOMA
superotemporal periphery showing an
elevated pearly white vascularized mass
lesion (arrow) in the area of extensive
chorioretinal atrophy
• Early arteriovenous phase- the intrinsic
vasculature of the tumor vessels and its
connection to the retinal circulation
• Mid arteriovenous phase - increase in
hyperfluorescence due to leakage of the
dye
• Late phase shows leakage of the dye
from the tumor

MALIGNANT MELANOMA
• A dome shaped, pigmented, subretinal mass lesion in the peripapillary region
• AV phase -patchy speckled hyperfluorescence over the mass lesion,tumor vessels
are made out within the mass lesion

USE OF FFA IN VITRITIS
• evaluating the activity of inflammatory lesions,
• evaluating retinal vascular involvement
• Detecting the sequele-neovascularisation, capillary non perfusion,
CNV, CME
• assessing the optic disc involvement

Full venous phase of the fluorescein angiogram
reveals
the characteristic “fern pattern.”
Fluorescein angiogram reveals peripheral venous
leakage.

Widefield fluorescein angiography showing severe
peripheral nonperfusion (short arrows) and an early
neovascular tuft (long arrow).
Advanced peripheral NV (arrow).
A

PHLEBITIS ARTERITIS BOTH
 Tuberculosis
 Sarcoidosis
 Multiple
Sclerosis
 Behcet’s Disease
 HIV
 Eale’s Disease
 Syphilis
 PAN
 ARN/PORN
SLE
 IRVAN
 Toxoplasma
 Wegner’s
granulomatosis
 Crohn’s Disease
 Relapsing
polychondritis

• FFA shows staining of the vessel wall or dye leakage
• phlebitis (or periphlebitis),
• Arteritis
• capillaritis

• FFA allows much better characterization of subclinical capillary
involvement
• Capillaritis in idiopathic retinal vasculitis

STAGE OF ACTIVE VASCULITIS STAGE OF OCCLUSION

STAGE OF NEOVASCULARIZATION STAGE OF COMPLICATIONS

Eales’ Disease
temporal periphery
showing periphlebitis
capillary nonperfusion
• Extensive leakage of the
dye from the walls of the
veins and its draining
channels is seen.
• Late phase shows
extensive staining of the
vessel walls and the
adjacent retina

FUNDUS FLUORESCEIN ANGIOGRAPHY TECHNIQUE AND INTERPRETATION

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