Key messages
There was insufficient evidence to support proposed treatments for acute non-arteritic central retinal artery occlusion.
What did we want to find out?
Central retinal artery occlusion occurs when the blood supply to the inner part of the retina (the light-sensitive layer inside the eye) is suddenly blocked. If the blockage is removed in time, and the blood supply returns to the retina, full recovery is possible. However, if the blockage is prolonged, retinal cells die. Various methods have been tried to remove the blockage including massaging the eye, lowering the pressure inside the eye, and dissolving clots with drugs. The best treatment for re-establishing the blood supply is not known, and some treatments can be associated with serious adverse effects.
What did we do?
We searched for studies that examined treatments for acute non-arteritic central retinal artery occlusion. We summarized the results of the studies and rated our confidence in the evidence, based on factors such as study methods and sizes.
What did we find?
It was unclear whether any treatment may improve visual acuity (how clearly your eyes can see and distinguish objects) when compared with observation. Some people treated with tissue plasminogen activator (a protein involved in the breakdown of blood clots) had serious adverse effects such as bleeding into the brain tissue.
What are the limitations of the evidence?
We have little confidence in the evidence because only small number of studies were included.
How up-to-date is this review?
We searched for studies published up to 15 February 2022.
The current research suggests that proposed interventions for acute non-arteritic CRAO may not be better than observation or treatments of any kind such as eyeball massage, oxygen inhalation, tube expansion, and anticoagulation, but the evidence is uncertain. Large, well-designed RCTs are necessary to determine the most effective treatment for acute non-arteritic CRAO.
Acute non-arteritic central retinal artery occlusion (CRAO) occurs as a sudden interruption of the blood supply to the retina and typically results in severe loss of vision in the affected eye. Although many therapeutic interventions have been proposed, there is no generally agreed upon treatment regimen.
To assess the effects of treatments for acute non-arteritic CRAO.
We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (which contains the Cochrane Eyes and Vision Trials Register) (2022, Issue 2); Ovid MEDLINE; Embase.com; PubMed; Latin American and Caribbean Health Sciences Literature Database (LILACS); ClinicalTrials.gov; and the World Health Organization (WHO) International Clinical Trials Registry Platform (ICTRP). We did not use any date or language restrictions in the electronic search for trials. We last searched the electronic databases on 15 February 2022.
We included randomized controlled trials (RCTs) comparing any interventions with another treatment in participants with acute non-arteritic CRAO in one or both eyes.
We used standard Cochrane methodology and graded the certainty of the body of evidence for primary (mean change in best-corrected visual acuity [BCVA]) and secondary (quality of life and adverse events) outcomes using the GRADE classification.
We included six RCTs with 223 total participants with acute non-arteritic CRAO; the studies ranged in size from 10 to 84 participants. The included studies varied geographically: one in Australia, one in Austria and Germany, two in China, one in Germany, and one in Italy.
We were unable to conduct any meta-analyses due to study heterogeneity. None of the included studies compared the same pair of interventions: 1) tissue plasminogen activator (t-PA) versus intravenous saline; 2) t-PA versus isovolemic hemodilution, eyeball massage, intraocular pressure reduction, and anticoagulation; 3) nitroglycerin, methazolamide, mecobalamin tablets, vitamin B1 and B12 injections, puerarin and compound anisodine (also known as 654-2) along with oxygen inhalation, eyeball massage, tube expansion, and anticoagulation compared with and without intravenous recombinant tissue plasminogen activator (rt-PA); 4) transcorneal electrical stimulation (TES) with 0 mA versus with 66% of the participant’s individual electrical phosphene threshold (EPT) at 20 Hz (66%) versus with 150% of the participant’s individual EPT (150%) at 20 Hz; 5) ophthalmic artery branch retrograde thrombolysis versus superselective ophthalmic artery thrombolysis; and 6) pentoxifylline versus placebo.
There was no evidence of an important difference in visual acuity between participants treated with t-PA versus intravenous saline (mean difference [MD] at 1 month −0.15 logMAR, 95% confidence interval [CI] −0.48 to 0.18; 1 study, 16 participants; low certainty evidence); t-PA versus isovolemic hemodilution, eyeball massage, intraocular pressure reduction, and anticoagulation (MD at 1 month −0.00 logMAR, 95% CI −0.24 to 0.23; 1 study, 82 participants; low certainty evidence); and TES with 0 mA versus TES with 66% of EPT at 20 Hz versus TES with 150% of EPT at 20 Hz. Participants treated with t-PA experienced higher rates of serious adverse effects. The other three comparisons did not report statistically significant differences. Other studies reported no data on secondary outcomes (quality of life or adverse events).