Fundus fluorescein angiography provides 3 key pieces of information: 1) the flow characteristics of blood vessels as fluorescein dye circulates through the retina and choroid, 2) fine details of the retinal pigment epithelium and retinal circulation, and 3) a clear picture of retinal vessels and assessment of their functional integrity. It involves injecting a fluorescent dye and taking rapid photographs under blue light to visualize the retinal and choroidal vasculature. Abnormal patterns include hypofluorescence from blocked fluorescence or vascular defects, and hyperfluorescence from window defects, leakage, pooling, or staining. It is useful for evaluating retinal diseases like epiretinal membranes, myopia, and diabetic retinopathy.

1. FUNDUS FLUORESCEIN
ANGIOGRAPHY
PRESENTER-DR MAHRUKH

2. INTRODUCTION
• The word Angiography - Greek angeion, "vessel" and graphien, "to write or
record".
• it is a fundal photography ,performed in rapid sequence following
intravenous injection of fluorescein dye
• It provides three main information:
• The flow characteristics in the blood vessels as the dye reaches and
circulates through the retina and choroid
• Records fine details of the pigment epithelium and retinalcirculation that
may not otherwise be visible
• Give a clear picture of the retinal vessels and assessment of their
functional integrity.

3. PRINCIPLE
FLUORESCENCE :- Property of the certain
molecules to emit light energy of longer wave
length when stimulated by a shorter
wavelength.
-Absorbs light in the blue range peaking at
465-490 nm
- Emits light of yellow-green range of visible
spectrum peaking at 520-530nm.

4. ABSORPTION AND EMISSION PEAKS OF
FLORESCEIN
• Molecules at the ground state of
energy levels are subjected to
external radiation of a particular
wavelength (excitation -490nm
in blue spectrum )
• Transition to a higher energy
state
• Remain in excited energy state
for a certain period and then
transit back to ground state of
energy .
• This transitions requires less
energy and emits light of
wavelength 530 nm in green
/yellow spectrum

5. • Fluorescein absorbs blue light and emits yellow green light
• Exciter filter (blue) and barrier filter (green)(blocks any reflected bluelight
from th e eye thus allowing only yellow/geeen light to pass )

6. Property of the dye-sodium flurescein
• Yellow Red in color.
• Stable, Highly Water Soluble &
Pharmacologically inert.
• Low Molecular Weight 376.27 D
• Fluoresces at Blood pH
• Peak absorption 465 – 490 nm
• Peak emission 520 – 530 nm
• 80% bound to plasma protein and also with
RBC
• remaining is seen during angiography
DOSAGE :
Solution containing 500 -100mg of fluorescien
available as :
• 5ml of 10% fluorescein
• 3ml of 25% fluorescien (preferred in opaque
media )

7. • Fluorescein cannot diffuse through
tight cellular junctions
• present at two sites within the
fundus:
– retinal blood vessel endothelium (inner
blood retinal barrier )
– retinal pigment epithelium (outer
blood retinal barrier )
ANGIOGRAPHY IS COMPOSED OF THE
SUPERIMPOSITION OF TWO SEPARATE
CIRCULATIONS
– Choroidal circulation -
the fluorescein freely leaks out of the
fenestrated choroidal capillaries, and
from there through Bruch's membrane.
– Retinal circulation -
the retinal blood vessel endothelial cells
are joined by tight junctions which
prevent leakage of fluorescein into the
retina.

8. OUTER BLOOD–RETINAL BARRIER
• The major choroidal vessels
are impermeable to both
bound and free fluorescein.
• The walls of the
choriocapillaries contain
fenestrations through which
unbound molecules escape
into the extravascular space.
• It crosses Bruch membrane
but on reaching the RPE are
blocked by intercellular
complexes termed tight
junctions or zonula occludens.

9. INNER BLOOD–RETINAL BARRIER
• It 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 blood–retinal
barrier permits leakage of both
bound and free fluorescein into
the extravascular space.

10. REQUIREMENTS

11. PROCEDURE
• Patient is informed of the normal
procedures, the side effects and the adverse
reactions.
• pupil dilated
• Made to sit comfortable.
• 3-4 red free photographs taken.(control
photographs)
• 5ml of 10% or 3ml of 25% NAF injected
through the antecubital 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
• Start fluorescein photograph 8 seconds after
start of injection in young and after 10
seconds in older patients

12. CIRCULATION
Peripheral vein
venous circulation
heart
arterial system
INTERNAL CAROTID ARTERY
Ophthalmic artery
Short posterior ciliary artery Central retinal Artery
(choroidal circulation) (retinal circulation)

13. FLUORESCEIN PATHWAY
• Arm-to-retina circulation time is 8-10
sec.
• Normally 10-15 seconds elapse between
dye injection and arrival of dye in the
short ciliary arteries.
• Choroidal circulation precedes retinal
circulation by 1 second.
• Transit of dye through the retinal
circulation takes approximately 15 to 20
seconds.

14. SEQUENCE OF PHOTOGRAPH
• Color photograph of Each eye.
• Red free photograph of each eye
• Room light to be kept dim
• Activate Barrier and exciter filter
change the flash intensity and
take control photographs.
• Once dye is being injected set
the machine at fluorescein mode
and start the timer.

15. 1. PREARTERIAL [ CHOROIDAL FLUSH ] – 10 sec
2. ARTERIAL – 12sec
3. ARTERIO-VENOUS [ CAPILLARY ]
4. VENOUS – 30sec
-EARLY VENOUS
- MID VENOUS
- LATE VENOUS
5. LATE ( ELIMINATION ) – after 10 min
PHASES OF ANGIOGRAM

16. • CHOROIDAL PHASE -- initial patching filing of lobules followed by a diffuse (flush) as dye
leaks out of the choroidocapillaris. Visualisation of choroid depends on retinal
pigmentation. Cilioretinal vessels and prelaminar optic disc capillaries fill during
this phase.
• ARTERIAL PHASE : the central retinal artery fills about 1 second later than
choroidal filling

17. ARTERIO-VENOUS
• The arteriovenous (capillary)
phase shows complete filling of
the arteries and capillaries with
early laminar flow in the veins
in which the dye appears to
line the venous wall leaving an
axial hypofluorescent strip.
• This phenomenon (laminar
flow) reflects initial drainage
from posterior pole capillaries
filling the venous margins, as
well as the small vessel velocity
profile, with faster plasma flow
adjacent to vessel walls where
cellular concentration is lower.

18. VENOUS PHASE
EARLY VENOUS PHASE: filling of the
veins is from tributaries joining their
margins, resulting in a tramline effect
(lamellar flow)
MID VENOUS PHASE: veins are
nearly filled
LATE VENOUS PHASE: veins are filled
and arteries start to empty.

19. Late phase (elimination phase )
• after 10 to 15 minutes little dye remains within the blood circulation.
• Dye which has left the blood to ocular structures is particularly visible.
• it shows abnormal dye accumulations indicative of leakage or staining

20. PHASE TIME ( IN Secs)
Injection 0
Choroidal phase 10
Arterial 10-12
Arterio venous 13
Early venous 14-15
Mid venous 16-17
Late venous 18-20
Late ( elimination) 5 mins

22. ABNORMAL FLUORESCEIN PATTERN
• HYPOFLUORESCENCE
Dark area on the positive print of
any angiogram
Two major patterns :-
• blocked fluorescence
• vascular filling defects
• HYPER FLUORESCENCE
Appearance of areas that are more
fluorescent either due to enhanced
visualization of a normal density of
fluorescein in the fundus or an
absolute increase in the fluorescein
content of the tissues . Seen in several
major patterns
• Window defect
• Pooling of dye
• Leakage
• Staining of tissues

23. Hypofluorescene
Blocked fluorescence:
• Optical obstruction (masking)of normal density of fluorescein.
a. Pigments eg rpe hypertrophy ,hemoglobin
b. Exudates
c. Edema and transudates
d. Hemorhages eg , choroidal ,retinal , subhyloid
Fundus fluorescein image of the congenital hypertrophy
of retinal pigment epithelium lesion showing blocked
fluorescence from pigment epithelial hypertrophy,
segmented filling within a small retinal vein suggestive of
sluggish flow (arrow) and areas of capillary dropout with
leakage from smaller venules (arrowheads)

24. • pre-retinal opaque structures superficial to the retinal circulation will mask both the retina
andchoroidal circulation eg. -Preretinal hemorrhage, -myelinated nerve fibres.
• prechoroidal opaque structures deep to the retinal circulation but superficial to the choroidal
circulation will mask only the choroidal circulational eg Sub retinal hemorhage , Increased RPE
density , Choroidal naevi

25. Focal rpe atrophy Chroidal nevie
Hemorhage under RPE

26. Vascular filling 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 eg.severe myopic
degeneration –
• choroideremia
• Emboli
• arteriosclerosis

28. HYPERFLUORESCENE
A. PREINJECTION PHASE :
Autofluorescence :- innate property
of fluorescence in certain ocular
tissue i.e. fluorescence without dye
eg Optic nerve head drusen &
astrocytic hamartoma
Pseudofluorescene :- Non fluorescent
light passes through entire filter
system.
- Decreased contrast and resolution
Conditions: Any light colored fundus
change
e.g.Sclera ,Scar tissue ,Myelinated
nerve fibre ,Foreign Body

29. INCREASED TRANSMISSION
(WINDOW DEFECT )
• It refers to a view of normal
choroidal flurosence through a
defect in in the pigment or
loss of pigment in the RPE .
• This results in unmasking of
normal background choroidal
fluorescence, characterized by
very early hyperfluorescence
that increases in intensity and
then fades without changing
size or shape.
• It is caused by atrophy or
absence of the RPE as in :
• Atrophic ARMD
• A full-thickness macular hole.
• RPE tears.

30. • LEAKAGE
It refers to the gradual , marked increase in
fluorescence throughout the angiogram when
-fluroscien molecules seep through the pigment
epithelium into sub reitnal space or
neurosensory retina
-out of retinal blood vessels into the retinal
intersitium
-from retinal neovascularization into the viterous
• The border of hyper fluorescence become
increasingly blurred and the greatest intensity
of hyperfluroscene is appreciated in the late
phase of the study , when only significant
fluorescein dye remaining in the eye is extra
vascular eg
• Papilledema
• Microaneurysms
• Breaking of inner blood retinal barrier(CME)
• Retinal neovascularization
• Proliferative Diabetic Retinopathy (NVD,NVE)
-

31. • POOLING
Refers to accumulation
of fluorescein in a
fluid filed space in
retina or choroid .
The margins of the
space trapping the
fluorescein are
usually distinct as
seen in RPE
detachment in csr

32. STAINING
• Accumulation of fluorescence within a
tissue
• Due to prolonged dye retention
• Can be seen in normal as well as
pathologically altered tissue
• It is seen in the later phases of the
angiogram, particularly after the dye has
left the choroidal and retinal circulations
• RETINAL
– a. Non-cystoid macular oedema
– b. Perivascular staining
• SUB RETINAL
– A. Drusens
– B. Sclera
– C. Lamina cribrosa
– D. Scars

33. uses
• Evaluation of vascular integrity of retinal & choroidal vessels
• Disease process affecting macula
• Integrity of the Blood Ocular Barrier.
- outer blood retinal barrier breaks in :- CSR
- inner blood retinal barrier breaks in:-NVD ,NVE
• Determining the extent of damage
• Formulating the treatment strategy for retinal & choroidal disease.
• Monitoring the result of treatment.

34. Use in pregnancy and lactation
• Controversial
• Avoid angiography on patients who are pregnant,
especially those in first trimester.
• Fluorescein Crosses the placenta
• Fluorescein is secreted in milk.
• Has been done in pregnancy with no adverse
effect
• There have been no reports of fetal complications
for fluorescein injection during pregnancy.

35. Complications
MILD MODERATE SEVERE
Staining of skin, sclera
and mucous membrane
Nausea ,vomiting laryngeal edema
bronchospasm
Stained secretion-
Tear, saliva
Vasovagal response Circulatory shock, MI,
cardiac arrest
Orange-yellow urine urticaria Generalized convulsion
Skin flushing, tingling
lips, pruritus
fainting Skin necrosis
periphlebitis

36. CONTRA INDICATIONS
• 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) Cardiac disease – cardiac failure, Myocardial infarction
– 6) Previous mild reaction to dye.
– 7) Tonic-clonic seizures
– 6) Pregnancy ( especially 1st trimester)

37. LIMITATIONS
• 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
excess hemoglobin or serum protein.e.g.
– - polycythemia
– -weldenstrom macroglobulenaemia
• because binding of fluorescein with excess Hb or
protein so ,Lack of freely circulating molecule

38. FFA IN COMMON RETINAL
PATHOLOGIES

39. EPIRETINAL MEMBERANE
• The vascular tortuosity caused by the epiretinal
membranes is very well seen on the fluorescein
angiogram.
• The fovea may be displaced and the perifoveal capillary
network distorted.
• Varying degree of leakage from the retinal capillaries
can be seen in the area of traction.
• Late cystoid changes may be evident.
• In cases of epiretinal membranes secondary to
vascular occlusion, the diagnosis is quite evident on the
angiogram due to the presence of areas ofcapillary
non-perfusion, microaneurysms or collateral vessels.

40. Fundus photograph of the left eye showing a thick epiretinal membrane at the macula . b. Marked
distortion of the retinal vessels is seen. Few hyperfluorescent dots caused by microaneurysms are seen. Areas
of capillary non-perfusion are noted in the superior part of the macula.
.C. Increased leakage of the dye is seen in the late phase
D. The red free photograph shows the distortion of the vessels in the macula
E. Leakage of dye from the microaneurysms and the tortuous retinal vessels at the fovea is seen

41. MYOPIA
Fundus photograph of the right eye showing a lacquer crack (Break in bruck’s membrane) inferior
and temporal to the foveal center. Peripapillary atrophy is seen . B. Arteriovenous phase shows
hyperfluorescence due to transmission defect in the area of lacquer cracks (arrows). C. Late phase
angiogram shows persistence of the hyperfluorescence at the lacquer cracks .d. Increased
hyperfluorescence is seen at these lesions in the late arteriovenous phase
Degenerative myopia is
associated with increased
axial length and progressive
choroidal degeneration at
the posterior pole.
■ Tesselated fundus, tilted
and oblique optic disc,
temporal crescent or myopic
conus, breaks in Bruch’s
membrane (lacquer cracks),
atrophy of the
RPE and choroid at the
posterior pole, and posterior
staphyloma are common
changes in degenerative
myopia.
■ Choroidal
neovascularization can
occur.

42. COAT’S DISEASE
Fundus photograph of the left eye showing hard exudates at the macula and inferiorly.
.B. Dilated retinal capillaries and telangiectasias are clearly made out in the arteriovenous phase. Vascular
abnormalities are also noted close to the fovea. Aneurysmal dilations are seen inferior .C. Late phase shows leakage
of the dye from the vascular abnormalities .D. Leakage of dye is noted from the dilated capillaries and the aneurysmal
dilatations. Areas of capillary non-perfusion are also seen
Fluorescein angiogram
shows numerous localized
anomalies of the retinal
vasculature.
■ Telangiectasia, aneurysms,
beading of vessel walls, and
vascular communicating
channels are seen.
■ These are very well made
out in the early and mid
arteriovenous phases of the
angiogram.
■ The retinal capillary bed
shows marked dilation and
tortuosity with multiple
saccular and aneurysmal
outpouchings.
■ Leakage from the vascular
abnormalities is seen in the
late films.
■ Areas of diffuse capillary
non-perfusion may be seen
in the midperiphery

43. EALE’S DISEASE
Fundus photograph of the left eye showing a sheathed superotemporal vessel. Hard exudates are seen in
the macula .B. Arteriovenous phase showing leakage of the dye from the vessel walls. Areas of capillary
non-perfusion are seen.C. Extensive leakage of the dye from the walls of the veins and its draining
channels is seen. The arterioles are unaffected .D. Late phase shows extensive staining of the vessel walls
and the adjacent retina
Narrowing of the
lumen may be seen
in the areas of active
periphlebitis.
■ The wall of the vein
in the affected part
stains and leaks dye
in the late phase of
the angiogram.
■ Areas of capillary
non-perfusion are
seen in the
periphery. Associated
vascular
abnormalities like
collaterals are also
common.
■ Neovascularization
is commonly seen in
the periphery.

44. STARGART’S DISEASE
The characteristic feature of
Stargardt’s disease on a
fluorescein angiogram is the
absence of choroidal
fluorescence or the ‘silent
choroid’. This is
considered almost
pathognomonic of Stargardt’s
disease.
■ Lipofuscin like material
deposition in the retinal
pigment epithelium is probably
responsible for blockage of the
underlying choroidal
fluorescence.
■ The retinal vessels especially
the retinal capillary network
are seen more prominently
against the dark background.
■ The atrophic macular lesion
shows up as a hyperfluorescent
area due to window defect.
■ Multiple irregular
hyperfluorescent spots that do
not precisely correspond to the
flecks are seen in the
midperipheral retina
Fundus photograph of the right eye showing RPE alterations at the fovea .B. Arteriovenous phase of the
angiogram showing stippled hyperfluorescence in foveal region due to transmission defects. Choroidal
fluorescence is not seen in the rest of the areas .C. Fading of the hyperfluorescence is seen in the foveal region in
the late phase . Silent choroid can still be appreciated .D. No choroidalfluorescence is seen even in the mid-
periphery of the fundus

45. OCULAR ALBINISM
Increased visibility of
the choroidal vessels
is noted due to lack of
masking by the
overlying pigment.
■ Foveal hypoplasia
may be evident by
absence of a well
formed foveal
avascular zone.
■ Late phase shows
the choroidal and
retinal vessels
silhouetted against
the background
fluorescence from
scleral staining
Fundus photograph of the right eye showing a markedly depigmented fundus. Few patches of pigmented RPE are seen
in the macula .B. Arterial phase of the angiogram shows increased visibility of the larger choroidal vessels due to lack
of blockage by the normally pigmented RPE. The choroidal details are blurred in the few areas of preserved RPE in the
macula .C. Late phase shows the relatively hypofluorescent larger choroidal vessels and the retinal vessels silhouetted
against the background fluorescence due to scleral staining .D. A diffuse choroidal fluorescence is seen due to leakage
of dye from the choriocapillaris. Note the retinal vessels are not clearly visualized due to ack of contrast

46. PAPILLOEDEMA
Fundus photograph of the right eye showing
the swollen hyperemic disc .B. Mid
arteriovenous phase of the angiogram
showing dilation of the disc capillaries. The
margins of the disc are blurred .C. Late
phase of the angiogram showing increased
staining of the disc

47. ANTERIOR ISCHEMIC OPTIC NEUROPATHY (AION)
Fundus photograph of the left eye showing
pallor in the upper half of the disc..B.
Filling of the disc capillaries is seen in the
lower half. The upper half of the disc
shows relative hypofluorescence.
Microvascular abnormalities
are seen in the macula .C. Increased
staining of the disc is seen. Retention of
dye is seen in the macula, indicative of
macular edema
ISCHEMIC DAMAGE
TO OPTIC NERVE
HEAD FROM
OCCLUSION OF
SHORT POSTERIOR
CILLIARY ARTERY
-early av phase –
hypofluorescene of
the disc
-midavphase –
capillary leak and
edema
-areas of capillary
nonperfusion

48. CHOROIDAL NEVUS
Fundus photograph of the right eye showing
a choroidal nevus superotemporal to the
fovea. Few RPE alterations are seen just
inferonasal to the foveal center .B. Mid
arteriovenous phase of the angiogram
showing faint hypofluorescence at the site
of the nevus. Hyperfluorescence due to
transmission defects is noted inferonasal to
the fovea .C. he faint hypofluorescence at
the nevus persists in the late phase. The
transmission defect has faded
Angiographic
appearance depends
on the degree of
pigmentation of the
nevus, its exact
location in the choroid
and changes in the
overlying retinal
pigment epithelium.
■ If the nevus is
confined to the outer
choroid, sparing the
choriocapillaris, the
fluorescein angiogram
may be relatively
normal.
■ If the
choriocapillaris is
partially involved, it
may show up as a
relatively
hypofluorescent
lesion.
■ If changes in the
overlying retinal
pigment epithelium
are present, it may
show up as
hyperfluorescent
transmission defects
within the
hypofluorescent lesion

49. DIABETIC RETINOPATHY
Microaneurysms—appear as hyperfluorescent dots which leak dye in the later phases.
■ Dilation of the retinal capillaries may occur.
■ Capillary closure appears as areas of hypofluorescence due to non-filling; they are
usually bordered by dilated capillaries and microaneurysms.
■ Intraretinal microvascular abnormalities (IRMA)—irregular segmental dilatation of the
retinal capillary bed. They usually occur in areas of
capillary non-perfusion and usually appear to originate and drain into the venous side of
the circulation. They remain within the confines of the
retina and do not leak fluorescein except minimally at their growing tips. They probably
represent intraretinal neovascularization or dilatation of
existing retinal channels.
■ Superficial and deep retinal hemorrhages cause blocked choroidal fluorescence.
■ Venous abnormalities in the form of venous dilation, beading, loops and reduplication
may be seen.
■ Neovascularization on the disc or the retinal surface appears as irregularly branching
vessels which freely leaks the dye.

50. NPDR
the fundus photograph at first blush looks almost normal. The changes clinically apparent are
microaneurysms, some red spots of hemorrhage, and hard yellow exudates, and on close inspection
early signs of ischemia. The damage to the retina in DR is most clearly seen in the angiographs where
the damage to the retinal vessels and arterioles are more obvious than in the fundus photos. The
fluorescein angiogram (right) shows the hemorrhages as dark spots. This photograph was taken as the
dye began to fill the vessels, and a few bright spots indicate the presence of microaneurysms.

51. Proliferative diabetic retinopathy
A large neovascular frond is seen at the disc. Hard exudates are seen in the upper
and lower part of the macula while the foveal area has a dull
washed out appearance (b) Marked leakage of the dye is seen from the NVD. A
large area of capillary non-perfusion is seen in the upper part of the macula
involving the fovea; dilated capillaries are seen around this.

52. Focal Maculopathy
Fundus photograph of the left eye showing
hard exudates arranged in a lose circinate
pattern in the superior part of the macula
(b) Arteriovenous phase showing the multiple
hyperfluorescent points caused by
microaneurysms. These are seen boarding the
areas of capillary nonperfusion (c) Increased
fuzziness is seen around the microaneurysms
due to leakage of the dye in the late phase. The
area of capillary non-perfusion remain
hyperfluorescent

53. Diffuse diabetic maculopathy
Fundus photograph of the left eye. Retinal thickening was noted in the macular region. There is absence of hard exudates
or retinal Hemorrhages (b) Mid arteriovenous phase shows leakage of dye from the dilated capillaries throughout the
macula. A fuzzy hyperfluorescence is seen along the inferotemporal arcade indicative of a small neovascular frond. Few
microaneurysms are noted superiorly .(c ) Late film shows accumulation of the dye in cystoid spaces around the fovea.
Non-cystoid collection of the dye is also noted in the other parts ofthe macula. The leakage from the neovascular frond
has also increased . (d) The leakage from the capillaries has increased and the dye is seen to be collecting in cystoid
spaces around the fovea
A
B
C
D

54. CYSTOID MACULAR EDEMA
• In the late phase of FA,
leakage into the cystoid
spaces is distributed radially
in Henle’s layer forming the
classic petaloid leakage
pattern or expansile dot
appearance
• Less common but
pathognomonic for CME is a
smokestack pattern. FA can
also show late staining of the
optic disc

55. CENTRAL SEROUS RETINOPAHY
• 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
DEFINES THE LOCATION
Ink-blot (85%):
– Even spread in all directions
• Smoke-stack (10%):
Rises superiorly Expands
laterally
• Mushroom-like
• Umbrella-like

56. PED
• serous PED classically
shows an early uniform
hyperfluorescence of
the entire lesion,
slightly delayed
compared to the
background
fluorescence, that
progressively increases
in brightness as the
examination progresses
(pooling).

57. MACULAR HOLE
A-Fundus photograph of the right eye showing a
full thickness macular hole at the fovea
surrounded by a broad cuff of subretianal fluid
B-Magnified view of the macular hole showing
the hyperfluorescence due to transmission defect
at the base of the macular hole
C-The hyperfluorescence at the macular hole has
increased in the arteriovenous phase. The
surrounding cuff of subretinal fluid shows a
relative
hyperfluorescence
A B
C

58. ARMD
DRY ARMD
• Several types of drusen can be identified. Hard drusen are small (<63 µm), round, well-
defined, yellowish deposits that correspond to accumulation of hyaline material in the
inner and outer collagenous zones of Bruch’s membrane.
• On FA, they appear hyperfluorescent as transmission defects due to overlying RPE
thinning(6).
• On occasion there may be a myriad of small drusen, termed cuticular or basal laminar
drusen, which appear as a “starry sky” on FA
Figure 1 - Cuticular drusen with the typical pattern of “starry sky

59. • Soft drusen are larger (>63
µm) with poorly defined
borders and they tend to
coalesce and become
confluent.
• They are hyperfluorescent
with phospholipid
accumulation and in
younger patients(7).
• Soft drusen represent
localized detachments of
the RPE.
Geographic atrophy-
severest form of the dry
AMD, RPE atrophy >175
microns with exposure of
the underlying choroidal
vessels
ATROPHIC ARMD
f hard and soft drusen

60. THE HALLMARK OF WET ARMD IS CNV
-CLASSIC CNV
Classic CNV is characterized by well-demarcated
hyperfluorescence in early phases on FA and late leakage
that obscures the boundaries of the lesion
-

61. • OCCULT- obscuration of the fibrovascular ingrowth by
intervening tissue alters the appearance of lesion on FA.
we can observe the fluorescence characteristic of the
vessel indirectly.

62. CRVO
reveal a mild increase in retinal circulation time. In non-ischemic CRVO, FA
shows marked delay in arteriovenous transit time, which is longer than 20
seconds, masking by retinal haemorrhages, and vessel wall staining. Late
staining along the large retinal veins is a characteristic finding in moderate and
severe degrees of central retinal vein obstruction. The ischemic form has
extensive areas of capillary non- perfusion

63. BRVO
The characteristic FA for BRVO is delayed filling of the occluded retinal
vein with varying degrees of capillary nonperfusion. Intraretinal
hemorrhages will result in blockage, and macular edema or retinal
neovascularization will results in dye extravasation