Fundus Fluorescein Angiography

Dr Md Afzal Mahfuzullah

MCPS,FCPS,Felow Vitreo-Retina

Retina Specialist & Surgeon

Bangabandhu Sheikh Mujib Medical University

WHY FFA

To confirms the elements already revealed by clinicalexamination.

Flow characteristics in the blood vessels as the dyereaches and circulates through the retina and choroid.

Gives a clear picture of the retinal vessels and assessmentof their functional integrity.

To monitor the disease intensity and impact of therapy.

Provides guidance for application of focal laser inphotocoagulation therapy.

To detect the leakages without clinical manifestation ofedema

What are the informations we get from FFA

FFA reveals:

Inflammatory status of retinal and choroidal blood vessels.

Localization of intra retinal lesions e.g. depth of pathological involvement in DR.

CNV

Neovascularisation in disc or retina

FFA reveals: Cont

Subretinal fluid status

Cystoid macular edema

Intraretinal/ preretinal haemorrhages

Optic nerve disorders

RPE integrity and disorders

Choroidal neovessels and chorioretinal atrophy

BASIC PRINCIPLES:

BASIC PRINCIPLES:

Based on luminescence and fluorescence.

Luminescence – is the emission of light from any source

other than high temperature.

Fluorescence is luminescence that is maintained only by

continuous excitation. Excitation occurs at one wave length

and immediate emission occurs through a longer wave

length.

FLUORESCENCE

Refers to fluorescein sodium (C20H10Na2O5)

A brown or orange red crystalline substance, alkaline innature.

MW- 376 dalton

Readily diffuses through body fluids and choriocapillariesbut does not diffuse through vascular endothelial cellsand RPE (Blood retina barriers)

OPTICAL PRINCIPLE

Absorbs blue light (465-490nm ) and Emits yellow-green light (520-530nm)

Metabolized by liver and exerted by kidney

FILTERS

1.Blue excitation filter

2.Yellow-green filter

Blood supply to retina

Layers & blood supply

GENERAL PRINICIPLES OF FFA

Fluorescein• 85% bound to serum proteins• 15% unbound ‘free’ fluorescein

• Impermeable to fluorescein

Outer blood-retinal barrier (zonula occludens)

• Impermeable to fluorescein

Choriocapillaris

Permeable only to ‘free’ fluorescein

Inner blood-retinal barrier(retinal capillaries)

Circulation of NaFDye injected from peripheral vein

Venous circulation

Heart

Arterial system

INTERNAL CAROTID ARTERY

Ophthalmic artery

Short posterior ciliary artery) Central retinal artery

(choroidal circulation.) ( retinal circulation)

N.B. The choroidal filling is 1 second prior to the retinal filling.

ANGIOGRAPHIC PHASES

Five angiographic phases:

• Pre arterial (Choroidal 9-15 seconds)

• Arterial

• Arteriovenous(capillary)

• Venous

• Recirculation

Basic anatomy :

The inner retina contains the retinal blood vessels.

The larger vessels in the Nerve fiber layer.

The retinal capillaries in the Inner nuclear layer.

Both are impermeable to dye.

The outer retina is primarily interstitial space of the retina, where hemorrhages, edematous fluid and hard exudates accumulate.

In normal conditions this layer does contain NaF as because of RPE tight junctions(Outer BRB)

Large choroidal vessels do not leake NaF but choriocapillaris does leak.

BASIC ANATOMY

PRE-ARTERIAL/ CHOROIDAL PHASE

Choroidal flush

Patchy Choroidal filling because of lobular arrangements of choriocapillaris

10-12 sec in young

12-15 sec in old

Cilioretinal artery fills at the same time with choroid circulation

Macula remains dark due to tall RPE and more pigments.

ARTERIAL PHASE

ARTERIAL PHASE Cont…

ARTERIOVENOUS PHASE

VENOUS PHASE

Recirculation phase

ABNORMAL ANGIOGRAPHIC FINDINGS

Hypofluorescence:

Filling defect

Blocking defect

Hyperfluorescence :

Window defect

Leakage

Pooling

Staining

Hypofluorescence

Blocked fluorescence (Transmission defects- blood, pigment, hard exudates etc)

Vascular filling defects (Circulation abnormality)

Blocked Retinal fluorescence

1. Arterial segment material

2. Vitreous material

3. Inner retinal material

Blocked choroidal fluorescence

1. Deep retinal material

2. Subretinal material

3. Sub RPE material

4. Choroidal material

Hypofluorescence.Cont

Hyperfluorescence

Anomalous vessels

Choroid

Retina

Optic nervehead

Subretinal neovasculari-zation

Tumor vesselsChorioretinal anastomosis

Vascular tortuosities

Dilation and shuntsAnastomosisNeovascularization

Aneurysms

TeleangiectasiaTumor vesselsHamatoma

NeovascularizationTortuosity

DilationHamatomaTumor vessels

Hyper-

fluorescence

In a preformedspace (pooling)

Into tissue(staining)

Retinal

Subretinal

Retina

Subretinal

Cystoid edema

Detachment ofthe pigmentepithelium

Detachment ofthe sensoryretina

noncystoidedema

e.g.dursen

Leakage

Fluorescencewithout theadministration of fluorescein

Autofluorescence

Pseudofluorescence

Drusen of the optic nerve head

Hamatoma

Scleral exudate

Myelinate nerve Fibers, optic nerve drusen

Scar tissue

Foreign body

Causes of dark appearance of fovea

-Avascularity

• Increased density of

xanthophyll

• Large RPE cells with more melanin

-Blockage of background choroidal fluorescence by:

Causes of Hyperfluorescence

RPE ‘ window’ defect

RPE atrophy

(bull’s eye maculopathy

Pooling of dye

Under RPE

(pigment epithelial detachment)Under sensory retina

(central serous retinopathy)

Causes of Hyperfluorescence

Leakage of dye Prolonged dye retention ( staining )

Into sensory retina (cystoid macular oedema)

From new vessels(choroidal neovascularization

Associated with drusen

Vascular occlusion

Capillary non-perfusion(venous occlusion)

Loss of vascular tissue

Choroideremia or high myopia

Causes of Hypofluorescence

BRVO- HYPO F- BLOCKED F

BRVO

SUB HYLOID. Hge/ PRERETINAL Hge HYPO F- BLOCKED

STARGARDT'S DISEASE

Fundusflavimaculatus: (Stargardt disease (STGD) is the most

common childhood recessively inherited macular dystrophy.

Blocked the choroidal fluorescence, so fundus background looks

black.

AION – HYPO F OF DISC

Red-free Fundus photos

Normal appearance Autofluorescence

Macular Hole

ARMD - HYPER- STAINING

CHOROIDAL NAEVUS

DIABETIC RETINOPATHY

Diabetic retinopathy gives a combination of both hyper/ hypofluorescence. Several pathologies are seen in this frame:

DIABETIC RETINOPATHY

Hypofluorescence:

Retinal haemorrhage (1)

Ischaemia (2).

Hyperfluorescence:microaneurysms (3) and neovascularization (4)In addition, there are IRMA (5) between the retinal artery and vein and venous beading (6)

DIABETIC MACULOPATHY TREATED WITH

LASER

PDR- HYPER F

BACKGROUND DIABETIC RETINOPATHY

CENTRAL SEROUS RETINOPATHYPOOLING/ HYPER F

Late phase of FFA shows a spot of pigment epithelium leakage has enlarged & fuzzy,in this case there is pooling of fluorescein under the detched retina

HYPER F- WINDOW/ POOLING EFFECT

Fundus photography shows PED & late phase of angiogram showing the corresponding well defined hyperfluorescent lesion

HYPERTENSIVE RETINOPATHY

Limitations of FFA

1) Does not permit study of choroidal circulation details due to

a) melanin in RPE

b) low mol wt of fluorescein

2) More adverse reaction

3) Inability to obtain angiogram in patient with excesshemoglobin or serum protein.

Thank you