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fluorescein angiography : II

The following describe how one would approach a fluorescein angiography in clinical practice. In part II MRCOphth, you will normally be given a frame of fluorescein angiography with characteristic pathology (usually with either hyper or hypofluorescence or a combination).
A methodical approach to angiogram will ensure that maximum information is gained from the investigation.An accompanying colour fundus photograph is essential for meaningful interpretation, along with relevant clinical information. 

Changes in the appearance of abnormal area through the 5 phases of the angiogram add extra information. For this reason it is more meaningful to follow an abnormal feature through a sequence of angiogram photographs, then to analyse each photograph separately.

Start with any striking abnormality and describe this in detail:

    • Hypo/hyperfluorescent components
    • Intensity of lfuorescence and changes with time
    • Area of fluorescence and changes with time
Diabetic retinopathy gives a combination of both hyper/
hypofluorescence. Several pathologies are seen in this frame:
Hypofluorescence: retinal haemorrhage (1) and ischaemia (2).
Hyperfluorescence: microaneurysms (3) and neovascularization (4)
In addition, there are IRMA (5) between the retinal artery and vein and venous beading (6)
Where there are multiple abnormalities, list these systematically. After commenting on all abnormalities, run through an anatomical check list to ensure all feature have been included:
    • macula
    • optic disc
    • large retinal blood vessels
    • retinal capillaries
    The following are common abnormalities seen in fluorescein angiography
    • Timing -

    • arm to eye time and retinal circulation may be prolonged if the cardiac output is low
      or the carotid perfusion is reduced.
    • Abnormal dye distribution

    • area may be present in which fluorescence is abnormally reduced (hypofluorescence)
      or abnormally increased (hypofluorescent).
   Summaries of abnormal dye distribution
  • Transmission defect (blood, pigment, hard exudates etc)
  • Filling defect (circulation abnormality)
  • Window defect (RPE defect)
  • Leakage of dye (SRNVM and new retinal vessels)
  • Pooling of dye (RPE detachment)
  • Staining of dye (damaged blood vessels; drusens)
  • Autofluorescence
    Causes of hypofluorescece:
    It can be caused by either the blockage of light or inadequate circulation in areas of retina or 
      1. Decreased transmission
        - blockage may be caused by the accumulation of pigment, naevi, 
          exudate or abnormal material (eg, the yellow flecks in patient with 
           Stargardt's disease)

        - pre-retinal opaque structures superficial to the retinal circulation 
          will mask both the retina and choroidal circulation eg. preretinal
          haemorrhage, myelinated  nerve fibres.

        - prechoroidal opaque structures deep to the retinal circulation but
          superficial to the choroidal circulation will mask only the choroidal 
          circulation for example:
                     blood - retinal haemorrhages in diabetic retinopathy and retinal vein 

                                - subretinal blood from choroidal new vessels
          exudates -  hard exudates
          cotton wool spots
          melanin- in hyperpigmented areas of RPE; choroidal naevus (see below)
          xanthophyll pigment - in the area of the macula

Choroidal naevus blocking the choroidal fluorescein in the arterial phase.
      2. Filling defect due to abnormal circulation
        - arterial non-perfusion is seen in occlusion of the central retinal artery
          and its branches

        - capillary non-perfusion is an important signs of retinal ischaemia. It is 
           seen in diabetic retinopathy and following retinal vein occlusion.

Central retinal artery occlusion with 
non-perfusion of the retinal vasulature.
Causes of hyperfluorescence
1. Window defects of the RPE (for example in RPE atrophy or macular 
    hole see picture below)
- the RPE behaves as a pigmented filter, reducing 
   transmission of fluorescence. 

- areas of atrophy of RPE act as windows through which the 
   fluorescence may be seen more brightly. In ARMD, 
   fluorescein in the choroidal circulation appears brighter 
   where the overlying RPE is atrophic. These areas of 
   hyperfluorescence are most prominent in the choroidal 
   phase, but persist through out all phases of the angiogram.

Left macular hole. There is left foveal hyperfluorescence due to loss of the marking 
effect of RPE cells.
2. Leakage of dye
- it occurs when there is breakdown of the tight junction of 
  the RPE or the retinal endothelium.
3. Leakage with pooling
-  if fluid is present under the RPE or the sensory retina, 
   fluorescein may collect in these spaces and cause pooling 
   of the dye resulting in the characteristic angiographic 
   picture of serous detachment of the RPE or of the sensory 

-  sometimes, dye may fail to accumulate even in the 
   presence of apparent fluid due to the fact that the fluid is 
   either no longer entering the area or is collecting too slowly 
   for a sufficient concentration fluorescein to be 
   photographed. RPE detachment, central serous retinopathy 
   and cystoid macular oedema are examples of leakage with 

Cystoid macular oedema with
petalloid pattern in late phase.
4. Leakage with staining
- collagen absorbs fluorescein dye causing staining which 
   persists after dye has been cleared from the choroidal and 
   the retinal circulations. For example profound ischaemia 
   and vasculitis both lead to incompetence of retinal 
   endothelium tight junction. Leakage of dye into the 
   connective tissue of the blood vessels result.

- optic disc staining, staining of the sclera, most evident at 
   the optic disc is a normal angiographic feature. The dye is 
   derived from the choroidal circulation, and staining is most 
   evident in the late phase.

Par planitis showing staining of the blood  vessels 
and dye leakage at the optic disc.
5. Drusen present in age-related maculopathy becomes stained by 
     absorbing dye from the choroidal circulation.

Late phase. A leaking subretinal 
neovascularization and staining of 
the drusen.
6. Leakage from abnormal vessels
- choroidal and retinal new vessels are structurally abnormal 
   and do not have intact endothelial tight junctions. Fundal 
   tumours such as choroidal malignant melanoma, have their 
   own blood supply which may leak.
7. Autofluorescence 
- optic disc drusen is the classic example. They are visible
   before dye injection.

Optic disc drusen
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Left superior branch retinal vein occlusion. The fluorescein angiography on the left shows areas of hypofluorescence and hyperfluorescence. 
Hypofluorescence - retina haemorrhages and the hard exudates block the choroidal fluorescein causing dark patches
                                  - pre-retinal haemorrhages, in addition to blocking the choroidal fluorescein also cover the retina
Hyperfluorescence - damaged retina veins have exposed collagen which are stained by fluorescein. Leakage around the
                                     damaged vein occurs due to damage to the endothelium walls
                                  - microaneurysms appear as multiple bright spots.
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This is the right funuds of a patient with dry form of age-related macular degeneration. The macula shows areas of retinal pigment epithelium (RPE) atrophy. 
The fluorescein angiography shows hyperfluorescence in the macula due to RPE window defect allowing choroidal fluorescein to show through brightly.
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Fluorescein angiography of a diabetic patient with peripheral 
Hypofluroescence - dot and block haemorrhages
Hyperfluorescence - new blood vessels with leakage
                                  - microaneurysms
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