9.8  Fundus Angiography - Fluorescein

Fundus fluorescein angiography (FFA) provides valuable information regarding fundus pathology. Intravenous fluorescein is injected, which remains in the retinal vasculature and is freely permeable to the choriocapillaris. It is impermeable to an intact blood-retinal barrier (retinal vessel walls and the retinal pigment epithelium (RPE)). Fluorescein absorbs blue light (wavelength 490nm) and emits yellow-green light (wavelength 530nm). A yellow-green barrier filter removes un-fluoresced reflected light wavelengths. A fundus camera is therefore able to detect the location of the fluorescein dye. Colour and red free photographs are usually taken prior to commencing FFA. All FFA’s should be read in conjunction with the clinical history and examination. It is important to recognise that this is a dynamic test.

The phases of FFA are as follows:

1. Choroidal Filling (10 - 15s)

  • This provides a background flush that may be patchy in appearance. The time for choroidal filling can be highly variable, depending on the nature of the vein and cannula that the intravenous fluorescein is injected

2. Arterial Filling (1 - 3s Later)

3. Arteriovenous Phase

  • Laminar flow is observed along venous walls

4. Venous Phase

  • The arterio-venous (AV) transit time is calculated from the time it takes for fluorescein to first appear in the temporal retinal arteries, to the time that the corresponding temporal retinal veins are completely filled. This is usually under 12s

5. Late Phase

  • Fluorescein recirculates back into the retinal arterial system after ~60s. By ~10 minutes fluorescein is no longer evident
Figure 9.8.1 Phases of a Normal Fundus Fluorescein Angiogram

Figure 9.8.1
Phases of a Normal Fundus Fluorescein Angiogram

Top left (14s): Arterial filling (note normal patchy choroidal filling)
Top right (17s): Arteriovenous phase (note laminar flow along the walls of the retinal veins
Bottom left (24s): Venous phase
Bottom right (6 minutes): Late phase

Hyperfluorescence

1. Leakage

  • Vessels that leak demonstrate hyperfluorescence that increases with time. This occurs with breakdown of the blood-retinal barrier such as in: retinal neovascularisation (pre-retinal), “choroidal” neovascularisation (sub-RPE/Type1, sub-retinal/Type 2, intra-retinal/Type 3) and macular oedema

2. Staining

  • Some structures (drusen, fibrosis) absorb fluorescein and slowly increase in hyperfluorescence. These structures retain some fluorescence even after it has been eliminated from the retinal and choroidal circulations

3. Window Defect

  • Window (transmission) defects typically occur when there is absence of the RPE, as occurs with geographic atrophy in atrophic age-related macular degeneration or following retinal laser scars. Background choroidal hyperfluorescence is clearly seen without the interference of RPE melanin and lipofuscin. Fluorescence increases then fades, without extending beyond the boundaries of the window defect

4. Pooling

  • Pooling occurs when fluorescein accumulates in an empty space. Examples include central serous chorioretinopathy (hyperfluorescence increases in intensity and size until the borders of the serous retinal detachment are reached) and serous pigment epithelial detachments (hyperfluorescence increases in intensity but due to rapid early filling of the PED with fluorescein, it does not increase in size)

Hypofluorescence

1. Avascular Zones

  • The foveal avascular zone (usually 500m) is hypofluorescent because it does not contain retinal capillaries. In addition, choroidal fluorescence is blocked by retinal xanthophyll and RPE melanin and lipofuscin. Lack of choroidal hyperfluorescence is also seen with capillary nonperfusion (such as in proliferative diabetic retinopathy or an ischaemic central retinal vein occlusion). Retinal artery occlusions are characterised by hypofluorescence in the vessel distal to the occlusion

2. Blocked Fluorescence

  • Fluorescence can be blocked by structures that do not fluoresce. The degree of blocked fluorescence depends on the depth of blocking structure in relation to the retina. Pre-retinal haemorrhage will block all fluorescence; retinal and RPE lesions (deep haemorrhages, exudate, pigment) will block choroidal fluorescence

Contents

Figure 9.8.2 Acute Posterior Multifocal Placoid Pigment Epitheliopathy (APMPPE)

Figure 9.8.2
Acute Posterior Multifocal Placoid Pigment Epitheliopathy (APMPPE)

Early hypofluorescence from blocking of choroidal blush. (30s)

Figure 9.8.3 Adult Vitelliform Macular Degeneration

Figure 9.8.3
Adult Vitelliform Macular Degeneration

The hyperfluorescent subretinal material at the macula represent degenerate photoreceptor outer segments and retinal pigment epithelium mixed with lipofuscin.

Figure 9.8.4 Branch Retinal Vein Occlusion

Figure 9.8.4
Branch Retinal Vein Occlusion

Blocked fluorescence from retinal haemorrhage and collaterals.

Figure 9.8.5 Branch Retinal Vein Occlusion

Figure 9.8.5
Branch Retinal Vein Occlusion

Dilated, hyperfluorescent veins with leakage and hypofluorescence from blocking by haemorrhage, exudate and retinal oedema. (Late)

Figure 9.8.6 Central Serous Chorioretinopathy

Figure 9.8.6
Central Serous Chorioretinopathy

Early image demonstrating pinpoint hyperfluorescence which will pool into the area of serous retinal detachment on subsequent images. (5 mins)

Figure 9.8.7 (Classic Subfoveal) Choroidal New Vessel

Figure 9.8.7
(Classic Subfoveal) Choroidal New Vessel

Early hyperfluorescence with late leak.

Figure 9.8.8 Coats Disease

Figure 9.8.8 Coats Disease
Telangiectatic vessels hyperfluoresce

Figure 9.8.9 Cystoid Macular Oedema

Figure 9.8.9
Cystoid Macular Oedema

Figure 9.8.10 Fundus Flavimaculatus (ABCA4 Gene Mutation)

Figure 9.8.10
Fundus Flavimaculatus (ABCA4 Gene Mutation)

Silent choroid (hypofuorescence) with hyperfluorescent pisciform flecks.

Figure 9.8.11 Hemi-retinal Artery Occlusion

Figure 9.8.11 Hemi-retinal Artery Occlusion
Hypofluorescent arteries and veins inferiorly with loss of retinal capillary architecture. The choroidal fluorescence is unaffected.

Figure 9.8.12 Hypertensive Retinopathy

Figure 9.8.12
Hypertensive Retinopathy

Figure 9.8.13 Neovascularisation of the Optic Disc (NVD)

Figure 9.8.13
Neovascularisation of the Optic Disc (NVD)

An extensive fan of new vessels are seen at the disc due to proliferative diabetic retinopathy. Other features include early inferior retinal arcade neovascularisation, laser burns, capillary drop out, subhyaloid haemorrhage, an enlarged foveal avascular zone, and retinal microaneurysms. (55s)

Figure 9.8.14 Proliferative Diabetic Retinopathy

Figure 9.8.14
Proliferative Diabetic Retinopathy

Hyperfluoresence from leakage from new vessels elsewhere (NVE).

Figure 9.8.15 Proliferative Diabetic Retinopathy (Optos®)

Figure 9.8.15
Proliferative Diabetic Retinopathy (Optos®)

An Optos® wide-field FFA showing the extent of changes in proliferative diabetic retinopathy.

Figure 9.8.16 Retinal Macroaneurysm

Figure 9.8.16
Retinal Macroaneurysm

Hyperfluorescent retinal macroaneurysm with blocked fluorescence from retinal haemorrhage.

Figure 9.8.17 Retinal Arteriolar Macroaneurysm

Figure 9.8.17
Retinal Arteriolar Macroaneurysm

Pinpoint hyperfluorescence along the inferior retinal artery arcade (34s). Subretinal blood is blocking fluorescence in a C-shaped configuration around the posterior pole.

Figure 9.8.18 Retinal Macroaneurysm (Ruptured)

Figure 9.8.18
Retinal Macroaneurysm (Ruptured)

Subretinal and subhyaoid haemorrhage is demonstrated as blocked fluorescence at difference levels. (48s)

Figure 9.8.19 Retinopathy of Prematurity

Figure 9.8.19
Retinopathy of Prematurity

An elevated ridge of new vessels is seen in the periphery with non-perfusion of the retinal peripheral to the ridge (3min18s).

Figure 9.8.20 RPE Rip

Figure 9.8.20
RPE Rip

Hypofluorescence from blocking of the choroidal blush is demonstrated where the ripped RPE has heaped up. The area of choriocapillaris exposed by the rip is hyperfluorescent (1 min).

Figure 9.8.21 Sarcoid Periphlebitis

Figure 9.8.21
Sarcoid Periphlebitis

Late hyperfluorescence of retinal vein walls with minimal associated leakage (5 mins).

Figure 9.8.22 Serous PED

Figure 9.8.22
Serous PED

Pooling hyperfluorescence is demonstrated (3 mins).

Figure 9.8.23 Sickle Cell Disease

Figure 9.8.23
Sickle Cell Disease

Figure 9.8.24 Stargardt Disease

Figure 9.8.24
Stargardt Disease

The “dark choroid” sign is demonstrated due to increased blocking of choroidal blush due to accumulation of lipofuscin.

Figure 9.8.25 Susac Syndrome

Figure 9.8.25
Susac Syndrome

Multifocal retinal arteritis is shown with multiple branch retinal artery occlusions.

Figure 9.8.26 Vasoproliferative Tumour

Figure 9.8.26
Vasoproliferative Tumour

(18s)

Figure 9.8.27 Vogt-Koyanagi-Harada Disease

Figure 9.8.27
Vogt-Koyanagi-Harada Disease

Pinpoint hyperfluorescence and multifocal serous retinal detachments.

          

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