A better clinical understanding of choroidal damage might be important
Clinical and experimental findings suggested that choroidal vasculopathy in diabetes may play a role in the pathogenesis of diabetic retinopathy.1–3 It has been proposed that the hypofluorescent spots observed in the indocyanine green angiography (ICG) result from ischaemic changes of the choroidal vessels and represent either a dye filling delay or a defect of the choriocapillaris.4
However, hyperfluorescent spots may be secondary to the presence of choroidal neovascularization, intrachoroidal microvasculature abnormalities or nodules at the level of the choriocapillaris or underlying stroma. Additionally, studies assessing the choroidal blood flow beneath the fovea with the use of laser doppler flowmetry indicate a reduction of choroidal blood flow and volume in patients with non-proliferative and proliferative diabetic retinopathy.5
A better clinical understanding of choroidal damage might be important for an accurate assessment of diabetic eye disease. Until recently, the choroid could only be evaluated by ICG, laser doppler flowmetry and ultrasoungraphy. Currently, it is possible to successfully evaluate and measure the choroidal thickness and choroidal morphology in normal and pathologic states using spectral domain-optical coherence tomography (SD-OCT) instruments.
Our group studied the choroidal thickness of 65 patients with different stages of diabetic retinopathy, using a SD-OCT. We showed that eyes with diabetic macular oedema (63.3 μm, 27.2%) and proliferative diabetic retinopathy (69.6 μm, 30.0%) had a significant reduction on the choroidal thickness when compared to age - matched normal subjects. However, eyes with no proliferative diabetic retinopathy did not present a significant thinning of the choroid.
Additionally, Dr Esmaeelpour reported a central choroid thinning in all type 2 diabetic eyes regardless of disease stage.6 Sixty-three eyes were studied and the choroidal thickness mapping of all diabetic patients demonstrated central and inferior thinning compared to healthy eyes. Subfoveal choroidal thickness for healthy eyes was 327 ± 74 μm which was found to be significantly thicker than all diabetic eyes: eyes with microaneurysm 208 ± 49 μm, eyes with exudates 205 ± 54 μm, and eyes with clinically-significant-macula-oedema 211 ± 76 μm (ANOVA P < 0.001, Tukey P < 0.001).
Speculation and conclusions
We can speculate that the thinner choroid may indicate an overall reduction of choroidal blood flow in diabetic patients, as was previously demonstrated with laser doppler flowmetry and ICG angiography. Therefore, it is likely that the decreased choroidal thickness may be related to retinal tissue hypoxia, as the choroid is the major source of nutrition for the retinal pigment epithelium and outer retinal layers.
A structurally and functionally normal choroidal vasculature is essential for the function of the retina: abnormal choroidal blood volume and/or compromised flow can result in photoreceptor dysfunction and death. The diabetic choroidopathy may develop before the diabetic retinopathy in a subset of patients. Using the new OCT technologies we might be able to identify patients with higher risk of developing diabetic retinopathy examining the choroid.
1. A.A. Hidayat and B.S. Fine, Ophthalmology, 1985;92:512–522.
2. D. Weinberger et al., Am. J. Ophthalmol., 1998;126:238–247.
3. C. Shiragami et al., Graefes Arch. Clin. Exp. Ophthalmol., 2002;240:436–442.
4. K. Shiraki et al., Int. Ophthalmol., 1999;23:105–109.
5. L.S. Schocket et al., Int. Ophthalmol., 2004;25:89–94.
6. M. Esmaeelpour et al., Invest. Ophthalmol. Vis. Sci., 2011;52:5311–5316.