Multimodal Retinal Imaging of Intravascular Lipid in Severe/Extreme Hypertriglyceridemia

Figures

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  Figure 1. Composite fundus photograph depicting white vascular retinal lesions both in arteries and veins in the LE with a “cherry red spot” in macula.

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  Figure 2. Serial fundus photography of the LE taken with intervals of 0 seconds (a), 21 seconds (b), 25 seconds (c), and 35 seconds (d) starting from (a) through (d). Red blood cellular aggregates can be traced moving downstream the superior temporal branch of central retinal vein (insert).

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  Figure 3. Fluorescein angiogram of the LE. Delayed choroidal filling at 20 seconds (a) followed by normal arterial phase 2 seconds later (b) and arteriovenous phase 11 seconds later (c). In the venous phase, 31 seconds later (d), arteriolar pruning with capillary dropout (arrowhead) and capillary bed leakage (asterisk) was noted. Microvascular pathology such as microaneurysms and intraretinal microvascular anomalies was ubiquitous.

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  Figure 4. Near infrared image (a) shows hyperinfrared reflection from vascular aggregates in the affected vascular segments (arrowhead). Spectral domain OCT (Spectralis, Heidelberg Engineering™) (b) of the LE with a p-MLM (arrow) and hyperreflective inner retinal layers (asterisk).

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  Figure 5. Fundus autofluorescence (Spectralis, Heidelberg Engineering™) of the LE, demonstrating increased autofluorescence at the observed white retinal vascular lesions (arrowhead).

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  Figure 6. Composite fundus photograph of LE, one day after insulin and statin therapy initiation, showing resolution of the white vascular aggregates and persistence of the “cherry red spot” in macula.

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  Figure 7. Spectral domain OCT (Spectralis, Heidelberg Engineering™) of the LE two years later, presenting atrophy of the inner retinal layers at the macular area.