9.7 Fundus Autofluorescence Imaging

Fundus Autofluorescence (FAF) Imaging is an easy, non-invasive modality for diagnosing retinal disease. It is a modality for metabolically mapping the retinal pigment epithelium (RPE) by identifying naturally or pathologically occurring fluorophores in the posterior segment such as A2-E in lipofuscin granules and minor fluorophores like collagen and elastin. When the pathology is centre-involving, the metabolic changes and loss of RPE corresponds to the level of visual function.

Fluorophores are excited in the blue wavelength (488nm) and emits light in the green spectrum (535 - 580nm) which is then recorded in the yellow-orange spectrum (615 - 715nm). Autofluorescence images are acquired without the administration of any intravenous medication. Both fundus camera and confocal scanning laser ophthalmoscope (cSLO) platforms exist.

FAF imaging is useful to identify retinal pathologies which may not be evident on direct fundus examination or digital fundus photography. Dead RPE appears hypoautofluorescent, as seen dramatically in atrophic age-related macular degeneration (AMD). Diseased or dysfunctional RPE appears hyperautofluorescent. Similar to fluorescein angiography, autofluorescence can also be useful in determining the layer of retinal lesions such as haemorrhage- subretinal bleeding will block underlying RPE hyperautofluorescence, whilst sub-RPE bleeding will not. Pathologies which are typically hypo or hyperautofluorescent are outlined below:

Hypoautofluorescent

  1. Reduced RPE lipofuscin
    1. Geographic atrophy
    2. CHRPE
  2. Blockage of RPE lipofuscin
    1. Subretinal haemorrhage

Hyperautofluorescent

  1. Subretinal hyperautofluorescent material
    1. Vitelliform lesions (e.g. Best Disease)
    2. Central serous chorioretinopathy (subretinal fluid)
  2. Increased RPE lipofuscin
    1. Fundus flavimaculatus (ABCA4 mutation) flecks
    2. Pattern dystrophies (RDS/Peripherin mutation)
  3. Window defect- loss of luteal or photopigment
    1. White dot syndromes
    2. Macular telangiectasia type II
  4. Other
    1. Optic disc drusen
    2. Astrocytic hamartoma

Contents

Figure 9.7.1 Astrocytic Retinal Hamartoma

Figure 9.7.1
Astrocytic Retinal Hamartoma

Figure 9.7.2 Central Serous Chorioretinopathy (Chronic)

Figure 9.7.2
Central Serous Chorioretinopathy (Chronic)
Blocking of normal retinal autofluorescence is observed centrally. Patchy RPE damage is noted superiorly. The characteristic “waterfall” sign of gravity-dependant shifting of subretinal fluid is demonstrated arising from the inferiotemporal macula.

Figure 9.7.3 Congenital Hypertrophy of the Retinal Pigment Epithelium (“CHRPE”)

Figure 9.7.3
Congenital Hypertrophy of the Retinal Pigment Epithelium (“CHRPE”)

Figure 9.7.4 Geographic Atrophy

Figure 9.7.4
Geographic Atrophy

Figure 9.7.5 Hydroxychloroquine Maculopathy

Figure 9.7.5
Hydroxychloroquine Maculopathy

Figure 9.7.6 Macular Telangiectasia (Mactel) Type 2

Figure 9.7.6
Macular Telangiectasia (Mactel) Type 2

          

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