5. Absorbed radiant energy > emitted energy
AND
As energy – inversely proportional to –
wavelength
SO,
λ of emitted wave > λ of absorbed wave
6.
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
13.
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
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.
25.
26.
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
28.
29.
30. A) Choroidal (pre-arterial)
B) Arterial
C) Arteriovenous(capillary)
D) Venous and
E) Late(elimination)
Patchy filling
No leakage
No complication
WHY ???
31.
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
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
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
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
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
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
64. Avascular occlusion of choroidal circulation
or retinal arteries,veins and capillaries
Loss of vascular bed eg.severe myopic
degeneration – choroideremia
Emboli
arteriosclerosis
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
74. Related to adhesion of RPE to Bruch’s
Membrane
RPE firmly attached to Bruch’s membrane by
hemidesmosomes
75.
76. Absence of hemidesmosomes
RPE splits away from Bruch’s membrane
Fluorescein stained fluid accumulate in
between them eg.CSR TYPE II
77.
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