Purchase this article with an account.
R. A. Karlsson, S. H. Hardarson, J. M. Beach, T. Eysteinsson, J. A. Benediktsson, E. Stefánsson; Retinal Oxygenation in Patients With Central Retinal Artery Occlusion. Invest. Ophthalmol. Vis. Sci. 2009;50(13):380.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
To measure retinal vessel oxygen saturation in patients, with present or past central retinal artery occlusion (CRAO).
The retinal oximeter (Oxymap ehf., Reykjavik, Iceland) is based on a fundus camera and measures color changes in blood to calculate hemoglobin oxygen saturation in retinal vessels. Oxygen saturation was measured in first and second degree retinal arterioles and venules in 5 patients with a history of CRAO. Thereof, one patient had temporal arteritis and was measured while clear boxcaring was visible, indicating obstructed blood flow. A second measurement was made once blood flow had returned after steroid treatment. One patient had a history of vision loss from the night before oximetry measurements. The remaining 3 patients had a history of vision loss for days up to about 1 month.
The table shows the relative mean oxygen saturation for the patient with temporal arteritis and CRAO (mean±SD for vessels within eye).
The patient, who was measured the day after vision loss, had arteriolar saturation of 82±7% and venular saturation of 34±12% in the affected eye, with lower saturation in the most ischemic areas. In the fellow eye, the corresponding values were 85±3% and 49±17%. In the 3 patients, who had a longer history of vision loss, the arteriolar saturation in the affected eye was 99±6% (mean±SD) and the venular saturation 57±8%. The corresponding numbers for the non-affected fellow eyes were 97±2% and 60±10%.
During acute CRAO, when the blood column is stationary, the arterioles are hypoxic and the oxygen saturation is similar in arterioles and venules. When retinal blood flow resumes and, presumably, the consumption of the tissue has decreased due to atrophy, the oxygen saturation returns to a normal level. This is supported by the normal oxygen saturation seen in the three patients with longer history of CRAO.
This PDF is available to Subscribers Only