Kopila kafle

Bachelor of optometry

3rd year

Fluorescent

chemical

absorbsRadiant

energy

release

Free

electron

Jump

to

higher

level

Becomes

unstable

Returns

To

Lower

level

Emit

energy

fluorescence

Absorbed radiant energy > emitted energy

AND

As energy – inversely proportional to –

wavelength

SO,

λ of emitted wave > λ of absorbed wave

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.

What is fluorescent material ? ?

What is the range of absorption spectrum ? ?

What is the range of emission spectrum ? ?

Sodium Fluorescein

C20 H10 O5 Na 2

Properties

-non-expensive

-non-toxic

-Flouresces at blood pH

level (7.37-7.45)

-rapid diffusion

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.

Lies between 465-490 nm

Excitation peak = 490nm(blue part of spectrum)

represents maximal absorption of light energy by fluorescein.

Lies between 520 – 530 nm

Emission peak = 530 nm

Represents green part of spectrum

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

In clinical diagnosis

to determine extent of damage

To formulate treatment strategy for

choroidal and retinal disease

To monitor result of treatment

Indications

of FFA

Macular

disorders

Retinal diseases

1) Diabetic retinopathy

2) Retinal vein occlusions

3) Retinal artery occlusion

4) Retinal vasculitis

5) Coats disease

6) Familial exudativevitreoretinopathy

Macular diseases1) Central serous

retinopathy2) RPE detachment3) Cystoid macular

edema4) Macular hole5) ARMD6) Cone rod dystrophy7) Epiretinal membrane8) Vitiliform

dystrophies9) Stargardts dystrophy

Retinal vascular malformations and tumors

1) Capillary hemangioma of retina2) Cavernous hemangioma of retina3) Retinal AV malformation 4) Congenital tortuosity of retinal

vasculature5) Congenital hypertrophy of RPE6) Angioid streaks7) Astrocytic hamartoma

Choroidal lesions1) Choroidal

neovascularmembrane (CNV)

2) Hemangioma3) Nevus4) Melanoma5) Choroiditis6) Metastasis7) MEWDS8) APMPPE9) 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

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)

MILD MODERATE SEVERE

Staining of skin, sclera and mucous membrane

Nausea and vomiting

Respiratory-laryngeal edema

,bhroncospasm

Stained secretion

Tear, saliva

Vasovagalresponse

Circulatory shock, MI, cardiac arrest

Vision tinged with yellow

utricaria Generalized convulsion

Orange-yellow urine

fainting Skin necrosis

Skin flushing, tingling lips pruritis

periphlebitis

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

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.

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.

A.Choroidalcirculation

-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

A) Choroidal (pre-arterial)

B) Arterial

C) Arteriovenous(capillary)

D) Venous and

E) Late(elimination)

Patchy filling

No leakage

No complication

WHY ???

Choriocapillaries has number of lobules

The lobules fill independently from one

another,

giving a transiently patched or blotched

appearance

8-12 seconds after

dye injection

Initial patchy

filling followed by

diffuse filling

No dye has

entered retinal

circulation

Shows arterial

filling

Continuation of

choroidal filling

1 second after

choridal phase

Complete filling of

arteries and

capillaries

Early laminar flow

to veins

Dye seen along

lateral wall of

veins

Arteries and

capillaries

completely filled

Marked lamellar

venous flow

Some veins

completely filled

Some shows

marked laminar

flow

All veins

completely filled

Arteries begin to

empty

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

Appears dark

AVASCULARITY

IN FAZ

BLOCKAGE OF

CHOROIDAL

FLUORESCENCE

INCREASED

XANTHOPHYLL

PIGMENTS

LARGER RPE

CELLS WITH

MORE MELANIN

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

Hypodense

(black) patch

Hyperdense

(white) patch

Fluorescein angiogram

Normal Abnormal Artifact

Hyperfluorescence Hypofluorescence

Leakage Pooling Staining Window Blocked Non filling defect filling

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

Greater level of fluorescence than would be

found in normal angiogram

Occur due to:

-window defect

-increased accumulation of dye

leakage

pooling

staining

Defect in RPE – increased transmission of

choroidal fluorescence

Sharply defined hyperfluorescence - does not

change in shape and size

LEAKAGE

POOLING

STAINING

Escape of fluorescein from vessels with

pathologically increased permeability

Progressive increase in size and intensity

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)

Flower petal appearance

CME

papilloedema

Neovascularization at disc(NVD)

Neovascularization elsewhere (NVE)

Accumulation of fluorescein in anatomical

space

Due to breakdown of outer blood retinal

barrier

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

CENTRAL SEROUS

RETINOPATHY

PED

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

RETINAL

a. non-cystoid macular

oedema

b. Perivascular staining

SUB RETINAL

a. Drusens

b. Sclera

c. Lamina cribrosa

d. scars

Drusens in ARMD

Reduction or absence of fluorescein

Two causes

BLOCKED

FLUORESCENCE

VASCULAR

FILLING

DEFECTS

Optical obstruction (masking) of normal

density of fluorescein

Caused by lesions anterior to retina

Pre-retinal lesions eg.vitreousopacity,preretinal haemorrhage block all fluorescence

Deep retinal lesions eg.intraretinalhaemorrhage and hard exudates block only capillary fluorescence

Increased density of RPE eg.congenitalhypertrophy

Choroidal lesions eg.naevus

RPE hypertrophy Retrohyaloid haemorrhage

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

CRAOCRVO

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

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

In case of blocked fluorescence ,

transparency is lost

SO, WE DO NOT SEE CHOROIDAL

FLUORESCENCE

Accumulation of blood haemorrhage

RPE hypertrophyChoroidal naevus

In case of staining due to drusens,angioid

streaks ,scars and degenerative processes

Accumulation of drusens under RPE

Angioid streaksAreolar degeneration

Related to adhesion of RPE to Bruch’s

Membrane

RPE firmly attached to Bruch’s membrane by

hemidesmosomes

Absence of hemidesmosomes

RPE splits away from Bruch’s membrane

Fluorescein stained fluid accumulate in

between them eg.CSR TYPE II

Related to diffusion of fluorescein in ocular

tissue

Determined by inner and outer blood retinal

barrier I.E DIFFUSION BARRIER

Normal retinal vessels do not leak fluorescein

- due to zonula occludents in between

endothelial cells

These zonula occludents open up during

inflammatory process

Zonula occludents open up

normal

Endothelial cell is lost

Pores in endothelial cells

PERIVASCULITIS

DIABETIC

MICROANEURYSM

PROLIFERATED

RETINAL VESSELS

Normal RPE is tight

zonula occludens seal portion of all the

intercellular spaces of the pigment epithelial

monolayer.

Cental serous

chorioretinopathy Type I

Haemorrhagic PED

in wet ARMD