Fluorescein Angiography Basic Principles and Interpretation

FLUORESCEIN ANGIOGRAPHY
BASIC PRINCIPLES AND INTERPRETATION

Mr A Abumattar
MRCOphth
January 2010
 Irvine Gass
 American ophthalmologist (b. Aug. 2, 1928, Prince
Edward Island—d. Feb. 26, 2005, Nashville, Tenn.),
A Abumattar
Fluorescein Angiography Basic Principles
 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
January 2010
 Fundal photography, performed in rapid
sequence following intravenous injection of
fluorescein dye.
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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.
3
SODIUM FLUORESCEIN
January 2010
 Sodium fluorescein
(C20H10O5Na2) is an
organic water soluble
dye.
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 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). 4
ADVANTAGES OF DIFFERENT TYPES OF
ANGIOGRAPHY
January 2010
Fluorescein Indocyanine Green
Visible spectrum of Infrared range.
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 
light 490nm  520nm 805nm  835nm
 Shows fine retinal  Poor definition of
vascular architecture vascular tree
 Does not pass through  Bypass RPE and light
RPE or pigment pigment including
blood
 Does not explore  Improved view of
choroidal lesions well choroidal vessels

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January 2010
Why do it? When to do it?
Confirm clinical Following clinical
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 
diagnosis examination
 Plan management  Before discussing
 Predict prognosis diagnosis with patient

 Assist in follow up (↑↓)
 Review outcome of Remember to ask

treatment patient if allergic to
any particular drug
6
PHARMACOLOGICAL PROPERTIES OF
FLUORESCEIN
January 2010
 Safe (?)  Caution
 Dose is 5ml of 20% of  Pregnant / breast feeding
Sodium fluorescein women
 Can be used in pregnancy
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 Warn diabetics not to adjust but not 1st trimester
dosage based on Benedict’s  Renal / hepatic failure
test of urine patients
In Peritoneal dialysis
Give test dose in suspected

 patients the Dye takes
cases (0.1 ml) weeks to clear
 1/200,000  anaphylaxis, of  Previous allergy to
which 1/3000 death rate fluorescein, iodine or contrast
media
 H/O Bronchospasm, Asthma,
or chronic bronchitis
 Recent MI
 Congestive heart failure
 Hay fever / Atopy
7
CHEMICAL PROPERTIES OF SODIUM FLUORESCEIN
January 2010
 Water soluble
 Detectable at 1:100,000 dilution
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 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 Patient will urinate
inside
bright yellow
 Metabolized by the liver and
excreted by the kidneys. fluorescent urine for
 Most dye is cleared within 24 several hours after
hours administration.
 The skin stains yellow
8
ADVERSE EFFECTS
January 2010
Mild
5-10% Transient, full recovery without medical treatment is
most likely.
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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 9
ADVERSE EFFECTS
January 2010
Moderate
Transient, but some form of medical treatment is needed
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 Urticaria skin rashes
 Necrosis, abscess formation and, even
thrombophlebitis.
 Pyrexia
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ADVERSE EFFECTS
January 2010
Severe
Prolonged effects needs intensive medical treatment. Life
may be at risk
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 Anaphylaxis
 Bronchospasm
 Micro-embolisation
 Not dye particle
 Plaques dislodge from carotid system
 Cardiac arrest
 Syncope
 Death 1:222,000
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ADVERSE EFFECTS/ SYNCOPE
January 2010
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.*
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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

12
PHYSIOLOGICAL PRINCIPLES
January 2010
 Two Circulations
within the fundus:
1. Choroidal circulation:
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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 13
CHOROIDAL CAPILLARY
PHYSIOLOGICAL PRINCIPLES
January 2010
2. Retinal circulation :
The retinal blood
vessel endothelial
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cells are joined by
tight junctions which
prevent leakage of
fluorescein into the
retina. This
constitutes the blood
retina barrier.
RETINAL CAPILLARY
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OCULAR TISSUE RESPONSE TO FLUORESCEIN
January 2010
Choroid Bruch’s membrane
Larger choroidal vessels are Fluorescein permeates
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 
impermeable to fluorescein through Bruch’s membrane
 Choriocapillaris is very leaky and binds to collagen and
drusen
 Extra-vascular fluorescein
stain the choroid and Retinal pigment
connective tissues epithelium
Retina  The tight junctions provided
by zonulae occludentes
 Retinal vessels prevent dye prevents the dye getting
escaping through the vascular into the retina except in
walls pathological states
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OCULAR TISSUE RESPONSE TO FLUORESCEIN
January 2010
Ciliary body Optic nerve head
Blood vessels of the ciliary The superficial retinal vessels
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 
body are freely permeable to are impermeable
the dye  The deeper posterior ciliary
 Allows free flow between the vessels are permeable thus
posterior and anterior the optic nerve head shows
chamber mild staining during the late
phase of the angiography
Vitreous
Sclera
 Takes several days for the
dye to be completely removed  The inner surface of the
from the vitreous sclera stains from the leaked
dye from the Choriocapillaris.
 The anterior vitreous clears
This is seen in late phases
through the forward diffusion 16
through window defects
into the aqueous
NO STANDARD NOMENCLATURE FOR THE
VARIOUS PHASES
January 2010
 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
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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. 17
PHASES OF A NORMAL FLUORESCEIN
ANGIOGRAPHY
January 2010
 Choroidal phase
 10-15 seconds
 choroidal filling via the
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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
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ANGIOGRAPHY
January 2010
 Arterial phase
 The central retinal
artery fills about 1
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second later than
choroidal filling
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ANGIOGRAPHY
January 2010
 Early arteriovenous
phase
 The fluorescein dye from
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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 20
ANGIOGRAPHY
January 2010
 Arteriovenous phase
 The dye completely fills
the lumen of the vein.
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 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 21
RPE cells at the fovea
ANGIOGRAPHY
January 2010
 Venous phase
 The whole diameter of
the veins is filled
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ANGIOGRAPHY
January 2010
 Late phase
 After 10 to 15 minutes
little dye remains
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within the blood
circulation. Dye which
has left the blood to
ocular structures is
particularly visible
during this phase
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MAIN INDICATIONS FOR FLUORESCEIN ANGIOGRAPHY
January 2010
Diabetic patients: Retinal vein occlusion:
Detecting any significant Determining the integrity
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 
macular oedema which is of the foveal capillary bed
not clinically obvious. and the extent of macular
 Locating the area of oedema following branch
oedema for laser treatment retinal vein occlusion
 Differentiating ischemic  Differentiating collaterals
from exudative diabetic from neovascularization
maculopathy.  Less commonly it is used
 Differentiating between purely to determine the
IRMA and new blood extent of retinal ischaemia
vessels if clinical (as this can be done
differentiation is difficult clinically)
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MAIN INDICATIONS FOR FLUORESCEIN ANGIOGRAPHY
January 2010
Age-related macular
Other indications:
degeneration
Locating subretinal neovascular
Locate the subretinal
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
 membrane in various conditions
(high myopia, angioid streaks,
neovascularization choroidal rupture and
chorioretinitis)
and determine its  Locating abnormal blood vessels
suitability for (for example idiopathic retinal
telangietasia, retinal retinopathy
treatment 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).
25
INTERPRETATION
January 2010
 A systematic approach to angiogram will ensure
that maximum information is gained.
 Colour fundus photograph and relevant clinical
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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
26
 Area of fluorescence and changes with time
Color (A) and
red-free (B)
photographs
of a fundus
January 2010
with soft
drusen and
hyper-
pigmentation.
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Soft drusen
hyper-
fluoresce
during the
early phase of
angiography
(C) and stain
INTERPRETATION
in the late
phase (D)
27
FLUORESCEIN ANGIOGRAPHY INTERPRETATION
CAUSES OF HYPOFLUORESCENCE
January 2010
1. Decreased transmission
 Blockage may be caused by:
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 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.
28
January 2010
 Opaque structures deep to the retinal circulation but
superficial to the choroidal circulation will mask only the
choroidal circulation for example:
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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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January 2010
2. Filling defect due to
abnormal circulation
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 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.
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CAUSES OF HYPERFLUORESENCE
January 2010
1. Window defects
of the RPE
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 Like in RPE
atrophy or
Macular hole
 Hyperfluoresence
in the macula due
to RPE window
defect allowing
choroidal
fluorescein to
show through
brightly. 31
January 2010
2. Leakage of dye
 Neovessels with
leakage
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 Microaneurysms
Note the
Hypofluorescence
from dot and blot
haemorrhages
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January 2010
3. Leakage with
pooling
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1) RPE detachment
2) Central serous
retinopathy CSR
3) Cystoid macular
oedema CMO
Cystoid macular
oedema with petalloid
pattern in late phase
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January 2010
4. Leakage with
staining
Collagen absorbs
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
fluorescein dye causing
staining which persists
after dye has been
cleared from the
choroidal and the
retinal circulations. Par planitis showing
staining of the
 Profound ischaemia blood vessels
and vasculitis both and dye leakage at the
lead to incompetence of optic disc
retinal endothelium
tight junction.
34
January 2010
5. Drusen present in
age-related
maculopathy
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becomes stained by
absorbing dye from the
choroidal circulation
6. Leakage from
abnormal vessels
Fundal tumours such Late phase.
as choroidal malignant Leaking subretinal
neovascularization and
melanoma, have their staining of the drusen.
own blood supply
which may leak. 35
January 2010
7. Autofluorescence
of optic nerve head
drusen.
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 (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
36
ABNORMAL DYE DISTRIBUTION SUMMARY
January 2010
Hypofluorescence Hyperfluoresence
Decreased fluorescence Increased fluorescence
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 
 Window defects of
 Decreased the RPE
transmission  Leakage with
 Filling defect due pooling
to abnormal  Leakage with
staining
circulation  Drusen present in age-
related maculopathy
 Leakage from
abnormal vessels
 Autofluorescence of
optic nerve head
drusen 37
BASIC PRINCIPLES AND INTERPRETATION
Quiz
January 2010
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39
January 2010
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40
RIGHT FFA, VENOUS PHASE, HYPO, HYPER
DIABETIC MACULOPATHY
January 2010
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41
January 2010
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RIGHT FFA, VENOUS PHASE, HYPO, HYPER, MA, DOTS, BLOTS
NPDR
January 2010
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43
January 2010
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44
LEFT FFA, LATE PHASE, HYPER, POOLING, SMOKE STALK
CSR
January 2010
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45
BRVO
RIGHT FFA, VENOUS PHASE, HYPO, HYPER, LASER SCARS, NON PERFUSION
January 2010
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46
January 2010
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47
NVD
LEFT FFA, EARLY VENOUS PHASE, HYPER WITH BRANCHING FINE
VESSELS, MASKING
January 2010
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48
January 2010
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49
STARGARDT’S
RIGHT FFA, VENOUS PHASE, CHOROID FLUORESCEIN ABSENT, DARK CHOROID
January 2010
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50
January 2010
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51
ANGIOID STREAKS
RIGHT FFA, VENOUS, HYPER, RADIATES OUT FROM DISC
IF CNV DEVELOP VISION WELL BE SEVERELY AFFECTED
January 2010
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52
January 2010
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53
WET AMD
RIGHT FFA, EARLY VENOUS, HYPO, HYPER, EARLY LACY PATTERN
CONSISTENT WITH SRNVM, SUBRETINAL HGE
January 2010
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January 2010
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CHOROIDAL MELANOMA
January 2010
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Early FFA of choroidal melanoma showing
intrinsic vascularity
Colour photograph of a dome-shaped choroidal

melanoma.
56
Late FFA showing early diffuse staining

CHOROIDAL MELANOMA
January 2010
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Early FFA of choroidal melanoma showing
intrinsic vascularity
B-scan ultrasound showing acoustic

hollowing and uveal excavation
Colour photograph of a dome-shaped choroidal

melanoma.
57
Late FFA showing early diffuse staining

January 2010
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58

Fluorescein Angiography Basic Principles and Interpretation

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FLUORESCEIN ANGIOGRAPHY

BASIC PRINCIPLES AND INTERPRETATION

Visible spectrum of Infrared range.

choroidal lesions well choroidal vessels

Confirm clinical Following clinical

 Predict prognosis diagnosis with patient

 Review outcome of Remember to ask

 Maintain clear airway

 Monitor BP and pulse

 IV or IM atropine if pulse rate is low

 If in any doubt surely contact the crash team

Larger choroidal vessels are Fluorescein permeates

Blood vessels of the ciliary The superficial retinal vessels

Detecting any significant Determining the integrity

Decreased fluorescence Increased fluorescence

Colour photograph of a dome-shaped choroidal

Late FFA showing early diffuse staining

B-scan ultrasound showing acoustic

Colour photograph of a dome-shaped choroidal

Late FFA showing early diffuse staining

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