FUNDUS FLUORESCEIN ANGIOGRAPHY

Prasanta Kumar Sahoo

WHY FFA?

• To confirms the elements already revealed by clinical examination.

• Flow characteristics in the blood vessels as the dye reaches and circulates through the retina and choroid.

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

• To monitor the disease intensity and impact of therapy.• Provides guidance for application of focal laser in

photocoagulation therapy.• To detect the leakages without clinical manifestation of

edema

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• Subretinal fluid status• Cystoid macular edema• Intraretinal/ preretinal haemorrhages• Optic nerve disorders• RPE integrity and disorders• Choroidal neovessels and chorioretinal atrophy

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 in nature.

• MW- 376 dalton• Readily diffuses through body fluids

and choriocapillaries but does not diffuse through vascular endothelial cells and 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

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 NaF Dye 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

CONTI…..• 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.

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

Conti …

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 fluorescence1. Arterial segment material2. Vitreous material3. Inner retinal material• Blocked choroidal fluorescence1. Deep retinal material2. Subretinal material3. Sub RPE material4. Choroidal material

HyperfluorescenceAnomalous vessels

Choroid

Retina

Optic nerve head

Subretinal neovasculari-zationTumor vesselsChorioretinal anastomosis

Vascular tortuositiesDilation and shuntsAnastomosisNeovascularizationAneurysmsTeleangiectasiaTumor vesselsHamatoma

NeovascularizationTortuosityDilationHamatomaTumor 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. H/ PRERETINAL H HYPO F- BLOCKED

STARGARDT'S DISEASE

• Fundus flavimaculatus (Stargardt disease (STGD) is the most common childhood recessively inherited macular dystrophy.

• The condition has a genetic basis due to mutations in the ABCA4 gene, and results from the accumulation of visual cycle kinetics-derived byproducts in the retinal pigmented epithelium (RPE) with secondary photoreceptor dysfunction and death.

• 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

GHPC- HYPER- STAINING

CHOROIDAL NAEVUS

DIABETIC MACULOPATHY TREATED WITH LASER

DIABETIC RETINOPATHY

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

• 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)

PDR- HYPER F

BACKGROUND DIABETIC RETINOPATHY

CENTRAL SEROUS RETINOPATHY

CSR – POOLING/ HYPER F

HYPER F- WINDOW/ POOLING EFFECT

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 excess hemoglobin or serum protein.

THANK YOU