This document discusses fluorescent angiography (FFA). It provides information on: 1. How fluorescent dyes like sodium fluorescein work by absorbing radiant energy and emitting light energy during fluorescence. 2. The uses and indications of FFA in evaluating retinal and choroidal diseases. It is used to assess vascular integrity and the blood-ocular barriers. 3. The phases seen during a normal FFA including the choroidal, arterial, arteriovenous, venous, and late phases. 4. Common abnormalities seen on FFA including leakage, pooling, staining, hyperfluorescence, hypofluorescence, and filling defects. These provide information on disease diagnosis and monitoring.

1. Kopila kafle
Bachelor of optometry
3rd year

4. Fluorescent
chemical
absorbs
Radiant
energy
release
Free
electron
Jump
to
higher
level
Becomes
unstable
Returns
To
Lower
level
Emit
energy
fluorescence

5. Absorbed radiant energy > emitted energy
AND
As energy – inversely proportional to –
wavelength
SO,
λ of emitted wave > λ of absorbed wave

7.  Depending on the chemical to be excited,
the electromagnetic energy (excitation
light) must lie within a particular range of
wavelengths absorption spectrum
 The wavelengths of fluorescent light
emitted by a particular chemical substance
lie within a characteristic range called
emission spectrum.

8.  What is fluorescent material ? ?
 What is the range of absorption spectrum ? ?
 What is the range of emission spectrum ? ?

9. Sodium Fluorescein
C20 H10 O5 Na 2
Properties
-non-expensive
-non-toxic
-Flouresces at blood pH
level (7.37-7.45)
-rapid diffusion

10.  Is an orange water-soluble dye
 Fluorescein is the product of reaction of
phthalic acid anhydride and resorcinol in which
Zinc Chloride is the catalyst.

11.  Lies between 465-490 nm
 Excitation peak = 490nm(blue part of
spectrum)
represents maximal absorption of light
energy by fluorescein.

12.  Lies between 520 – 530 nm
 Emission peak = 530 nm
 Represents green part of spectrum

14.  studying the normal physiology of the
retinal and choroidal circulation,as well as
disease process affecting the macula.
 Evaluation of the vascular integrity of the
retinal and choroidal vessels
 Check the integrity of the blood ocular
barrier.
- outer blood retinal barrier breaks in CSR
- inner blood retinal barrier breaks in
NVD,NVE

15.  In clinical diagnosis
 to determine extent of damage
 To formulate treatment strategy for
choroidal and retinal disease
 To monitor result of treatment

16. Indications
of FFA
Macular
disorders

17. Retinal diseases
1) Diabetic retinopathy
2) Retinal vein
occlusions
3) Retinal artery
occlusion
4) Retinal vasculitis
5) Coats disease
6) Familial exudative
vitreoretinopathy
Macular diseases
1) Central serous
retinopathy
2) RPE detachment
3) Cystoid macular
edema
4) Macular hole
5) ARMD
6) Cone rod dystrophy
7) Epiretinal membrane
8) Vitiliform
dystrophies
9) Stargardts dystrophy

18. Retinal vascular malformations and
tumors
1) Capillary hemangioma of retina
2) Cavernous hemangioma of retina
3) Retinal AV malformation
4) Congenital tortuosity of retinal
vasculature
5) Congenital hypertrophy of RPE
6) Angioid streaks
7) Astrocytic hamartoma

19. Choroidal lesions
1) Choroidal
neovascular
membrane (CNV)
2) Hemangioma
3) Nevus
4) Melanoma
5) Choroiditis
6) Metastasis
7) MEWDS
8) APMPPE
9) Choroidal folds
Optic nerve disorders
1) Optic atrophy
2) Papilloedema
3) Ischemic optic
neuropathy
4) Optic disc pit
5) Optic disc drusen
6) Optic disc
hemangioma
7) Melanocytoma
8) Myelinated nerve
fibers

20. ABSOLUTE
1) known allergy to iodine containing compounds.
2) H/O adverse reaction to FFA in the past.
RELATIVE
1) Asthma
2) Hay fever
3) Renal failure
4) Hepatic failure
5) Pregnancy ( especially 1st trimester)

21. MILD MODERATE SEVERE
Staining of skin,
sclera and
mucous
membrane
Nausea and
vomiting
Respiratory-
laryngeal edema
,bhroncospasm
Stained secretion
Tear, saliva
Vasovagal
response
Circulatory
shock, MI,
cardiac arrest
Vision tinged
with yellow
utricaria Generalized
convulsion
Orange-yellow
urine
fainting Skin necrosis
Skin flushing,
tingling lips
pruritis
periphlebitis

22. Patient is informed of the normal procedures, the
side effects and the adverse reactions.
Dilating the pupil
Made to sit comfortable.
3-4 red free photographs taken.
(control photographs)
5ml of 10% or 3ml of 25% NAF injected through
the anticubital vein

23. 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.

24. Dye injected from peripheral vein
venous circulation
heart
arterial system
INTERNAL CAROTID ARTERY
Ophthalmic artery
Short posterior ciliary artery) Central retinal
(choroidal circulation.) ( retinal circulation)
N.B. The choroidal filling is 1 second prior to the retinal filling.

27. A.Choroidal
circulation
-choriocapillaries are
fenestrated
-so allows dye to
diffuse freely
BUT,
-outer blood-retinal
barrier in RPE don’t
let dye to reach
retina
B.Retinal circulation
-endothelial cells of
retinal blood vessels
joined by tight
junctions (inner
blood retinal
barrier)
-prevents leakage of
dye from vessels

30. A) Choroidal (pre-arterial)
B) Arterial
C) Arteriovenous(capillary)
D) Venous and
E) Late(elimination)
Patchy filling
No leakage
No complication
WHY ???

32.  Choriocapillaries has number of lobules
 The lobules fill independently from one
another,
 giving a transiently patched or blotched
appearance

33.  8-12 seconds after
dye injection
 Initial patchy
filling followed by
diffuse filling
 No dye has
entered retinal
circulation

34.  Shows arterial
filling
 Continuation of
choroidal filling
 1 second after
choridal phase

35.  Complete filling of
arteries and
capillaries
 Early laminar flow
to veins
 Dye seen along
lateral wall of
veins

36.  Arteries and
capillaries
completely filled
 Marked lamellar
venous flow

37.  Some veins
completely filled
 Some shows
marked laminar
flow

38.  All veins
completely filled
 Arteries begin to
empty

39.  Elimination of dye
from choroidal and
retinal circulation
 Staining of disc –
normal
 In 5-10 minutes
fluorescein absent
from angiogram
 And from body in
several hours

40.  Appears dark
AVASCULARITY
IN FAZ
BLOCKAGE OF
CHOROIDAL
FLUORESCENCE
INCREASED
XANTHOPHYLL
PIGMENTS
LARGER RPE
CELLS WITH
MORE MELANIN

41.  Patchy filling of choroid
 Retinal blood vessels filling
 Dark area of foveal avascular zone
BUT,
No hyperdense(white) or hypodense (black)
patch in retina Outer blood retinal barrier
Inner blood retinal barrier

42. Hypodense
(black) patch
Hyperdense
(white) patch

43. Fluorescein angiogram
Normal Abnormal Artifact
Hyperfluorescence Hypofluorescence
Leakage Pooling Staining Window Blocked Non
filling defect filling

44.  Hyperfluorescence and hypofluorescence can
alternate in same location
 Especially in inflammatory disorder
 1st hypofluorescence due to retinal oedema
 Later hyperfluorescence due to increased
vascular permeability

45.  Greater level of fluorescence than would be
found in normal angiogram
 Occur due to:
-window defect
-increased accumulation of dye
leakage
pooling
staining

46.  Defect in RPE – increased transmission of
choroidal fluorescence
 Sharply defined hyperfluorescence - does not
change in shape and size

48. LEAKAGE
POOLING
STAINING

49.  Escape of fluorescein from vessels with
pathologically increased permeability
 Progressive increase in size and intensity

50.  Papilledema
 Abnormal choroidal vasculature(CNV)
 Breaking of inner blood retinal
barrier(cystoid macular oedema)
 Abnormal retinal or disc vasculature(retinal
neovascularization)
 Proliferative Diabetic Retinopathy(NVD,NVE)

51. Flower petal appearance
CME
papilloedema

52. Neovascularization at disc(NVD)
Neovascularization elsewhere (NVE)

53.  Accumulation of fluorescein in anatomical
space
 Due to breakdown of outer blood retinal
barrier

54. A . In subretinal space
As in CSR
Early hyperfluorescence
Increase in size and intensity
B . In sub RPE space
As in PED
Early hyperfluorescence
Increase in intensity but
not in size

55. CENTRAL SEROUS
RETINOPATHY
PED

56.  Accumulation of fluorescence within a tissue
 Due to prolonged dye retention
 Minimum hyperfluorescence in early and
midphase which increases in late phase
 Can be seen in normal as well as
pathologically altered tissue

57. RETINAL
a. non-cystoid macular
oedema
b. Perivascular staining
SUB RETINAL
a. Drusens
b. Sclera
c. Lamina cribrosa
d. scars

58. Drusens in ARMD

59.  Reduction or absence of fluorescein
 Two causes
BLOCKED
FLUORESCENCE
VASCULAR
FILLING
DEFECTS

60.  Optical obstruction (masking) of normal
density of fluorescein
 Caused by lesions anterior to retina

61.  Pre-retinal lesions eg.vitreous
opacity,preretinal haemorrhage block all
fluorescence
 Deep retinal lesions eg.intraretinal
haemorrhage and hard exudates block only
capillary fluorescence
 Increased density of RPE eg.congenital
hypertrophy
 Choroidal lesions eg.naevus

62. RPE hypertrophy Retrohyaloid haemorrhage

63.  Inadequate perfusion of tissue with resultant
low fluorescein content

64.  Avascular occlusion of choroidal circulation
or retinal arteries,veins and capillaries
 Loss of vascular bed eg.severe myopic
degeneration – choroideremia
 Emboli
 arteriosclerosis

65. CRAO
CRVO

66.  All the process of occurrence of hyper or
hypo-fluorescence can be described under
following 3 phenomenons
A. OPTICAL PHENOMENON
B .MECHANICAL PHENOMENON
C. DYNAMIC PHENOMENON

67.  Normal neurosensory retina is transparent
 Normal RPE and Bruch’s Membrane are
semitransparent
 Hence, we can see choroidal fluorescence
 BUT, this transparency can be pathologically
increased or decreased

68.  In case of blocked fluorescence ,
transparency is lost
 SO, WE DO NOT SEE CHOROIDAL
FLUORESCENCE

69. Accumulation of blood haemorrhage

70. RPE hypertrophy
Choroidal naevus

71.  In case of staining due to drusens,angioid
streaks ,scars and degenerative processes

72. Accumulation of drusens under RPE

73. Angioid streaks
Areolar degeneration

74.  Related to adhesion of RPE to Bruch’s
Membrane
 RPE firmly attached to Bruch’s membrane by
hemidesmosomes

76. Absence of hemidesmosomes
RPE splits away from Bruch’s membrane
Fluorescein stained fluid accumulate in
between them eg.CSR TYPE II

78.  Related to diffusion of fluorescein in ocular
tissue
 Determined by inner and outer blood retinal
barrier I.E DIFFUSION BARRIER

79.  Normal retinal vessels do not leak fluorescein
- due to zonula occludents in between
endothelial cells
 These zonula occludents open up during
inflammatory process

80. Zonula occludents open up
normal
Endothelial cell is lost
Pores in endothelial cells

81. PERIVASCULITIS

82. DIABETIC
MICROANEURYSM

83. PROLIFERATED
RETINAL VESSELS

84.  Normal RPE is tight
 zonula occludens seal portion of all the
intercellular spaces of the pigment epithelial
monolayer.

86. Cental serous
chorioretinopathy Type I

87. Haemorrhagic PED
in wet ARMD