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Fluorescein and indocyanine green angiography in arteritic anterior ischaemic optic neuropathy
  1. Department of Ophthalmology and Visual Science, Scientific Institute H San Raffaele, Milano-Roma, Italy
  1. Professer Rosario Brancato, Institute H San Raffaele, Department of Ophthalmology, V le Olgettina 60, 20132 Milan, Italy.

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Editor,—Anterior ischaemic optic neuropathy (AION) is the most common cause of visual loss in giant cell arteritis (GCA). However, other presentations have been described including posterior ischaemic optic neuropathy, choroidal ischaemia, retinal artery occlusion, branch retinal artery occlusion, cilioretinal artery occlusion, and occipital cortex infarction.1 We present the first indocyanine green angiography (ICGA) findings in a case of GCA with simultaneous optic nerve and choroidal ischaemia.


A 65 year old woman was admitted because of bilateral blindness. She had had complete, painless visual loss in her right eye 72 hours before admission followed 48 hours later by visual loss in the left. One week earlier she had noted jaw claudicatio and neck pain. Ophthalmic examination revealed no light perception (NLP) with disc oedema in both eyes. Westergren erythrocyte sedimentation rate (ESR) was 76 mm in the first hour; brain magnetic resonance imaging was normal. She was given 50 mg/day oral prednisone, with no improvement. One week later she was referred to our institution for a neuro-ophthalmological evaluation. Visual acuities were still NLP with mid-dilated, unreactive pupils; funduscopic examination showed pale disc oedema in both eyes. ESR was 30 mm in the first hour. Fluorescein angiography (FA) (Fig 1) showed marked delay in optic nerve and choroidal filling; mild optic nerve leakage, and peripheral hyperfluorescent spots with RPE mottling were seen in the late angiographic phases in the left eye. ICGA (Fig 2) confirmed the severe ischaemia of the choroid especially on the temporal side and highlighted staining of several peripheral choroidal vessels. Temporal artery biopsy was positive for GCA. Prednisone was increased to 100 mg/day but there was no recovery of visual function at follow up.

Figure 1

Fluorescein angiography showed marked delay in optic nerve perfusion (up to 20 seconds) and choroidal filling (up to 10 minutes) in both eyes as well as peripheral hyperfluorescent spots with RPE mottling in the late angiographic phases in the left eye (bottom, right).  

Figure 2

Indocyanine green angiography highlighted severe ischaemia of the choroid especially on the temporal side with staining of several peripheral choroidal vessels (top and bottom, right).  


The association of choroidal ischaemia and AION is particularly suggestive of GCA as indicated by Hayreh.2 Macket al3 and Siatkowski et al4 performed FA in GCA and found significant delay of choroidal filling in comparison with either normal subjects or patients with non-arteritic AION. We report a case of optic nerve and simultaneous choroidal ischaemia in GCA. Choroidal hypoperfusion was more severe on the temporal side suggesting a distinct involvement of the lateral posterior ciliary arteries (PCAs). FA also highlighted areas of RPE atrophy and pigmentary migration in the peripheral retina. Similar abnormalities of the outer retina in GCA were attributed to arteritic involvement of the PCA supply to the choroid.5

This is the first ICGA study of choroidal circulation in GCA. ICGA clearly demonstrated the choroidal ischaemia but also showed staining of some peripheral vessels, probably related to an inflammatory infiltration of their wall not visible with ophthalmoscopy and FA. Even though no conclusions can be drawn from a single case, ICGA may a valuable diagnostic tool for differentiating arteritic from non-arteritic AION and even an interesting way to monitor the disease.


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