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BASIC PRINCIPLES AND INTERPRETATION OF FLUORESCEIN ANGIOGRAPHY
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FLUORESCEIN ANGIOGRAPHYBASIC PRINCIPLES AND INTERPRETATION
Mr A Abumattar
MRCOphth
FLUORESCEIN ANGIOGRAPHY
Irvine Gass
American ophthalmologist (b. Aug. 2, 1928, Prince
Edward Island—d. Feb. 26, 2005, Nashville, Tenn.),
Gass was among the leading developers of
fluorescein angiography
Gass was a key figure in the discovery of the cause of
macular holes.
He was also among the first researchers to identify
the macular swelling that sometimes occurs after
cataract surgery, a condition called Irvine-Gass
syndrome.
2
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FLUORESCEIN ANGIOGRAPHY
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
retinal circulation that may not otherwise be visible
Give a clear picture of the retinal vessels and
assessment of their functional integrity.
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SODIUM FLUORESCEIN Ja
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Sodium fluorescein (C20H10O5Na2) is an organic water soluble dye.
Molecular weight is 376 daltons, and is 80% bound to plasma albumin. The remaining 20% is seen during angiography.
The dye absorbs light in the blue range of the visible spectrum, with absorption peaking at 490nm (blue). It emits light at 530nm (yellow).
ADVANTAGES OF DIFFERENT TYPES OF
ANGIOGRAPHY Ja
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Visible spectrum of
light 490nm 520nm
Shows fine retinal
vascular architecture
Does not pass through
RPE or pigment
Does not explore
choroidal lesions well
Infrared range.
805nm 835nm
Poor definition of
vascular tree
Bypass RPE and light
pigment including
blood
Improved view of
choroidal vessels
Fluorescein Indocyanine Green
FLUORESCEIN ANGIOGRAPHY Ja
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Confirm clinical
diagnosis
Plan management
Predict prognosis
Assist in follow up (↑↓)
Review outcome of
treatment
Following clinical
examination
Before discussing
diagnosis with patient
Remember to ask
patient if allergic to
any particular drug
Why do it? When to do it?
PHARMACOLOGICAL PROPERTIES OF
FLUORESCEIN Ja
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Safe (?)
Dose is 5ml of 20% of Sodium fluorescein
Warn diabetics not to adjust dosage based on Benedict’s test of urine
Give test dose in suspected cases (0.1 ml) 1/200,000 anaphylaxis, of
which 1/3000 death rate
Caution Pregnant / breast feeding
women Can be used in pregnancy
but not 1st trimester
Renal / hepatic failure patients
In Peritoneal dialysis patients the Dye takes weeks to clear
Previous allergy to fluorescein, iodine or contrast media
H/O Bronchospasm, Asthma, or chronic bronchitis
Recent MI
Congestive heart failure
Hay fever / Atopy
CHEMICAL PROPERTIES OF SODIUM FLUORESCEIN Ja
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Water soluble
Detectable at 1:100,000 dilution
Optimum fluorescence at 7.5 pH
Optimum absorption at 485-490nm and emission at 525nm
In circulation it binds to albumin
Coats RBCs but does not get inside
Metabolized by the liver and excreted by the kidneys.
Most dye is cleared within 24 hours
The skin stains yellow
Patient will urinate
bright yellow
fluorescent urine for
several hours after
administration.
ADVERSE EFFECTS Ja
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Nausea 4.6%
Vomiting 1.3%
Sneezing
Pruritus
Photosensitivity
Colour vision changes Last about 20 minutes
Inadvertent extravasation Warm sponges qds / 30 minutes each.
Review patient 1-2 days and be generous with pain killers
Mild
5-10% Transient, full recovery without medical treatment is
most likely.
ADVERSE EFFECTS Ja
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Urticaria skin rashes
Necrosis, abscess formation and, even
thrombophlebitis.
Pyrexia
Moderate
Transient, but some form of medical treatment is needed
ADVERSE EFFECTS Ja
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Anaphylaxis
Bronchospasm
Micro-embolisation Not dye particle
Plaques dislodge from carotid system
Cardiac arrest
Syncope
Death 1:222,000
Severe
Prolonged effects needs intensive medical treatment. Life
may be at risk
ADVERSE EFFECTS/ SYNCOPE Ja
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Keep IV line in situ
Head down or lay patient flat on floor
Maintain clear airway
Monitor BP and pulse
? IV steroids
IV or IM atropine if pulse rate is low
If in any doubt surely contact the crash team
Syncope is a transient loss of consciousness T-LOC due to
transient global cerebral hypoperfusion characterized by
rapid onset, short duration, and spontaneous complete
recovery.*
PHYSIOLOGICAL PRINCIPLES Ja
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Two Circulations within the fundus:
1. Choroidal circulation:The fluorescein
freely leaks out of the fenestrated Choriocapillaris, and from there through Bruch's membrane. however, tight junctions between (RPE) cells prevents dye reaching the retina
CHOROIDAL CAPILLARY
PHYSIOLOGICAL PRINCIPLES Ja
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2. Retinal circulation :
The retinal blood
vessel endothelial
cells are joined by
tight junctions which
prevent leakage of
fluorescein into the
retina. This
constitutes the blood
retina barrier.RETINAL CAPILLARY
OCULAR TISSUE RESPONSE TO FLUORESCEIN Ja
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Larger choroidal vessels are
impermeable to fluorescein
Choriocapillaris is very leaky
Extra-vascular fluorescein
stain the choroid and
connective tissues
Fluorescein permeates
through Bruch’s membrane
and binds to collagen and
drusen
Choroid Bruch’s membrane
Retinal pigment
epithelium
The tight junctions provided by zonulae occludentes prevents the dye getting into the retina except in pathological states
Retina
Retinal vessels prevent dye
escaping through the vascular
walls
OCULAR TISSUE RESPONSE TO FLUORESCEIN Ja
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Blood vessels of the ciliary body are freely permeable to the dye
Allows free flow between the posterior and anterior chamber
The superficial retinal vessels are impermeable
The deeper posterior ciliary vessels are permeable thus the optic nerve head shows mild staining during the late phase of the angiography
Ciliary body Optic nerve head
Vitreous
Takes several days for the
dye to be completely removed
from the vitreous
The anterior vitreous clears
through the forward diffusion
into the aqueous
Sclera
The inner surface of the
sclera stains from the leaked
dye from the Choriocapillaris.
This is seen in late phases
through window defects
NO STANDARD NOMENCLATURE FOR THE
VARIOUS PHASES
The time from when an injection of fluorescein is administered into an antecubital vein until the time that the dye first appears in the central retinal artery is called the arm-retina-time and it can vary significantly (between circa 7 to 15 seconds). It depends on a number of factors, including the size of the cubital vein, the speed of the injection, the blood pressure and cardiac output. It is shorter in young people and longer in the elderly. The dye appears first in the choroid and then shortly thereafter in the central retinal artery. There is no standard nomenclature for the various phases. Generally, though, an early phase is identified as the time to filling of the retinal arterioles (arterial phase), an intermediate phase (“arteriovenous phase”) that lasts up to the first appearance of the dye in retinal veins (and often subdivided into early, intermediate and late arteriovenous phases), and finally a late phase during which the fluorescence gradually fades away.
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PHASES OF A NORMAL FLUORESCEIN
ANGIOGRAPHY Ja
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Choroidal phase
10-15 seconds
choroidal filling via the
short ciliary arteries
results in initial patchy
filing of lobules, very
quickly followed by a
diffuse (blush) as dye
leaks out of the
Choriocapillaris.
Cilioretinal vessels and
prelaminar optic disc
capillaries fill during
this phase
PHASES OF A NORMAL FLUORESCEIN
ANGIOGRAPHY Ja
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Arterial phase
The central retinal
artery fills about 1
second later than
choroidal filling
PHASES OF A NORMAL FLUORESCEIN
ANGIOGRAPHY Ja
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Early arteriovenous phase
The fluorescein dye from the smaller venules enters the vein along their walls resulting in a laminar flow of the dye in the vein.
As the vascular flow is faster in the centre of the vessel than on its side ,the fluorescein dye sticks to the walls of the vein another contributing factor for laminar flow
PHASES OF A NORMAL FLUORESCEIN
ANGIOGRAPHY Ja
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Arteriovenous phase
The dye completely fills the lumen of the vein.
Perifoveal capillary network is best visualized at 20 to 25 seconds after the injection when the concentration of the dye is maximum.
The fovea appears hypofluorescent because of: Absence of the blood vessels
in the foveal avascular zone (FAZ)
Blockage of the background choroidal fluorescence by the increased pigment in the tall RPE cells at the fovea
PHASES OF A NORMAL FLUORESCEIN
ANGIOGRAPHY Ja
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Venous phase
The whole diameter of
the veins is filled
PHASES OF A NORMAL FLUORESCEIN
ANGIOGRAPHY Ja
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Late 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
during this phase
MAIN INDICATIONS FOR FLUORESCEIN ANGIOGRAPHY Ja
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Detecting any significant macular oedema which is not clinically obvious.
Locating the area of oedema for laser treatment
Differentiating ischemic from exudative diabetic maculopathy.
Differentiating between IRMA and new blood vessels if clinical differentiation is difficult
Determining the integrity of the foveal capillary bed and the extent of macular oedema following branch retinal vein occlusion
Differentiating collaterals from neovascularization
Less commonly it is used purely to determine the extent of retinal ischaemia (as this can be done clinically)
Diabetic patients: Retinal vein occlusion:
MAIN INDICATIONS FOR FLUORESCEIN ANGIOGRAPHY Ja
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Locate the subretinal
neovascularization
and determine its
suitability for
treatment
Locating subretinal neovascularmembrane in various conditions (high myopia, angioid streaks, choroidal rupture and chorioretinitis)
Locating abnormal blood vessels (for example idiopathic retinal telangietasia, retinal retinopathy etc)
Looking for break down of RPE tight junctions (central serous retinal retinopathy) or the blood retinal barrier (cystoid macular oedema)
Help with diagnosis of retinal conditions (for example Stargardt's disease gives a characteristic dark choroid).
Age-related macular
degenerationOther indications:
FLUORESCEIN ANGIOGRAPHY
INTERPRETATION
A systematic approach to angiogram will ensure that maximum information is gained.
Colour fundus photograph and relevant clinical information is essential for meaningful interpretation.
Follow an abnormal feature through a sequence of angiogram photographs, then analyse each photograph separately.
Start with any striking abnormality and describe this in detail:
Hypo/hyper fluorescent components
Intensity of fluorescence and changes with time
Area of fluorescence and changes with time
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FL
UO
RE
SC
EIN
AN
GIO
GR
AP
HY
INT
ER
PR
ET
AT
ION
Color (A) and
red-free (B)
photographs
of a fundus
with soft
drusen and
hyper-
pigmentation.
Soft drusen
hyper-
fluoresce
during the
early phase of
angiography
(C) and stain
in the late
phase (D)
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FLUORESCEIN ANGIOGRAPHY INTERPRETATION
CAUSES OF HYPOFLUORESCENCE
1. Decreased transmission
Blockage may be caused by:
Pre-retinal opaque structures superficial to the retinal
circulation will mask both the retina and choroidal
circulation e.g. Preretinal haemorrhage or Myelinated
nerve fibres.
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FLUORESCEIN ANGIOGRAPHY INTERPRETATION
CAUSES OF HYPOFLUORESCENCE
Opaque structures deep to the retinal circulation but
superficial to the choroidal circulation will mask only the
choroidal circulation for example:
1. Retinal haemorrhages in diabetic retinopathy
2. Retinal vein occlusion
3. Subretinal blood from choroidal new vessels
4. Hard exudates
5. Cotton wool spots
6. Melanin in choroidal naevus
7. Xanthophyll pigment - in the area of the macula
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FLUORESCEIN ANGIOGRAPHY INTERPRETATION
CAUSES OF HYPOFLUORESCENCE Ja
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2. Filling defect due to
abnormal circulation
Arterial non-perfusion is
seen in occlusion of the
central retinal artery and
its branches
Capillary non-perfusion is
an important signs of
retinal ischaemia.
Diabetic retinopathy and
Retinal vein occlusion.
FLUORESCEIN ANGIOGRAPHY INTERPRETATION
CAUSES OF HYPERFLUORESENCE Ja
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1. Window defects
of the RPE
Like in RPE
atrophy or
Macular hole
Hyperfluoresence
in the macula due
to RPE window
defect allowing
choroidal
fluorescein to
show through
brightly.
FLUORESCEIN ANGIOGRAPHY INTERPRETATION
CAUSES OF HYPERFLUORESENCE Ja
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2. Leakage of dye
Neovessels with
leakage
Microaneurysms
Note the
Hypofluorescence
from dot and blot
haemorrhages
FLUORESCEIN ANGIOGRAPHY INTERPRETATION
CAUSES OF HYPERFLUORESENCE Ja
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3. Leakage with
pooling
1) RPE detachment
2) Central serous
retinopathy CSR
3) Cystoid macular
oedema CMO
Cystoid macular
oedema with petalloid
pattern in late phase
FLUORESCEIN ANGIOGRAPHY INTERPRETATION
CAUSES OF HYPERFLUORESENCE Ja
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4. Leakage with
staining
Collagen absorbs
fluorescein dye causing
staining which persists
after dye has been
cleared from the
choroidal and the
retinal circulations.
Profound ischaemia
and vasculitis both
lead to incompetence of
retinal endothelium
tight junction.
Par planitis showing
staining of the
blood vessels
and dye leakage at the
optic disc
FLUORESCEIN ANGIOGRAPHY INTERPRETATION
CAUSES OF HYPERFLUORESENCE Ja
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5. Drusen present in
age-related
maculopathy
becomes stained by
absorbing dye from the
choroidal circulation
6. Leakage from
abnormal vessels
Fundal tumours such
as choroidal malignant
melanoma, have their
own blood supply
which may leak.
Late phase.
Leaking subretinal
neovascularization and
staining of the drusen.
FLUORESCEIN ANGIOGRAPHY INTERPRETATION
CAUSES OF HYPERFLUORESENCE Ja
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7. Autofluorescence of optic nerve head drusen.
(A) Pre-injection photograph of the optic nerve in a patient with optic nerve head drusen. Both barrier and exciter filters are in place.
(B) Same patient after filling of retinal vessels
FLUORESCEIN ANGIOGRAPHY INTERPRETATION
ABNORMAL DYE DISTRIBUTION SUMMARY Ja
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Decreased fluorescence
Decreased
transmission
Filling defect due
to abnormal
circulation
Increased fluorescence Window defects of
the RPE
Leakage with pooling
Leakage with staining
Drusen present in age-related maculopathy
Leakage from abnormal vessels
Autofluorescence of optic nerve head drusen
Hypofluorescence Hyperfluoresence
FLUORESCEIN ANGIOGRAPHYBASIC PRINCIPLES AND INTERPRETATION
Quiz
Ja
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Flu
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An
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DIABETIC MACULOPATHY
RIGHT FFA, VENOUS PHASE, HYPO, HYPER Ja
nu
ary
20
10
40
Flu
ore
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An
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A A
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Ja
nu
ary
20
10
41
Flu
ore
scein
An
gio
gra
ph
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asic P
rincip
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A A
bu
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NPDR RIGHT FFA, VENOUS PHASE, HYPO, HYPER, MA, DOTS, BLOTS
Ja
nu
ary
20
10
42
Flu
ore
scein
An
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A A
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Ja
nu
ary
20
10
43
Flu
ore
scein
An
gio
gra
ph
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asic P
rincip
les
A A
bu
ma
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CSRLEFT FFA, LATE PHASE, HYPER, POOLING, SMOKE STALK J
an
ua
ry 2
01
0
44
Flu
ore
scein
An
gio
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rincip
les
A A
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Ja
nu
ary
20
10
45
Flu
ore
scein
An
gio
gra
ph
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asic P
rincip
les
A A
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ma
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BRVORIGHT FFA, VENOUS PHASE, HYPO, HYPER, LASER SCARS, NON PERFUSION
Ja
nu
ary
20
10
46
Flu
ore
scein
An
gio
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rincip
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A A
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Ja
nu
ary
20
10
47
Flu
ore
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An
gio
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ph
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NVDLEFT FFA, EARLY VENOUS PHASE, HYPER WITH BRANCHING FINE
VESSELS, MASKING Ja
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ary
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10
48
Flu
ore
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An
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A A
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Ja
nu
ary
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10
49
Flu
ore
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An
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STARGARDT’SRIGHT FFA, VENOUS PHASE, CHOROID FLUORESCEIN ABSENT, DARK CHOROID
Ja
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Ja
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20
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51
Flu
ore
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ANGIOID STREAKS
RIGHT FFA, VENOUS, HYPER, RADIATES OUT FROM DISC
IF CNV DEVELOP VISION WELL BE SEVERELY AFFECTED
Ja
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Ja
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10
53
Flu
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WET AMD
RIGHT FFA, EARLY VENOUS, HYPO, HYPER, EARLY LACY PATTERN
CONSISTENT WITH SRNVM, SUBRETINAL HGE
Ja
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bu
ma
ttar
Ja
nu
ary
20
10
Flu
ore
scein
An
gio
gra
ph
y B
asic P
rincip
les
A A
bu
ma
ttar
55
CHOROIDAL MELANOMA Ja
nu
ary
20
10
Flu
ore
scein
An
gio
gra
ph
y B
asic P
rincip
les
A A
bu
ma
ttar
56
Early FFA of choroidal melanoma showing
intrinsic vascularity
Late FFA showing early diffuse staining
Colour photograph of a dome-shaped choroidal
melanoma.
CHOROIDAL MELANOMA Ja
nu
ary
20
10
Flu
ore
scein
An
gio
gra
ph
y B
asic P
rincip
les
A A
bu
ma
ttar
57
Early FFA of choroidal melanoma showing
intrinsic vascularity
Late FFA showing early diffuse staining
Colour photograph of a dome-shaped choroidal
melanoma.
B-scan ultrasound showing acoustic
hollowing and uveal excavation
Ja
nu
ary
20
10
Flu
ore
scein
An
gio
gra
ph
y B
asic P
rincip
les
A A
bu
ma
ttar
58