Abstract
BackgroundThe critical time from onset of complete occlusion of the central retinal artery (CRA) to functionally significant inner retinal infarction represents a window of opportunity for treatment and also has medical-legal implications, particularly when central retinal artery occlusion (CRAO) complicates therapeutic interventions. Here, we review the evidence for time to infarction from complete CRAO and discuss the implications of our findings.MethodsA Medline search was performed using each of the terms “central retinal artery occlusion”, “retinal infarction”, “retinal ischemia”, and “cherry red spot” from 1970 to the present including articles in French and German. All retrieved references as well as their reference lists were screened for relevance. An Internet search using these terms was also performed to look for additional references.ResultsWe find that the experimental evidence showing that inner retinal infarction occurs after 90–240 min of total CRAO, which is the interval generally accepted in the medical literature and practice guidelines, is flawed in important ways. Moreover, the retinal ganglion cells, supplied by the CRA, are part of the central nervous system which undergoes infarction after non-perfusion of 12–15 min or less.ConclusionsRetinal infarction is most likely to occur after only 12–15 min of complete CRAO. This helps to explain why therapeutic maneuvers for CRAO are often ineffective. Nevertheless, many CRAOs are incomplete and may benefit from therapy after longer intervals. To try to avoid retinal infarcton from inadvertent ocular compression by a headrest during prone anesthesia, the eyes should be checked at intervals of less than 15′.
Highlights
The critical time from onset of complete occlusion of the central retinal artery (CRA) to functionally significant inner retinal infarction represents a window of opportunity for treatment and has medical-legal implications, when central retinal artery occlusion (CRAO) complicates therapeutic interventions
We find that this clinically important time limit for inner retinal non-perfusion has been greatly overestimated for several reasons. It is based on a series of experiments on nonhuman primates by Hayreh and coworkers [11, 12, 14] which are inappropriate for extrapolation to human CRAO because: a) The experiments were performed on barbiturate anesthetized monkeys
B) The experiments were not controlled for the presence of hypothermia in the experimental animals which was likely to have had an additional neuro-protective effect prolonging retinal ganglion cell survival [17]. c) Clamping of the CRA just before its entrance into the optic nerve sheath was performed in all the monkey experiments but is not an appropriate model for complete CRAO because there is collateral circulation to the CRA distal to the clamp in the monkey derived mostly from posterior ciliary artery branches of the ophthalmic artery [4, 21]
Summary
The critical time from onset of complete occlusion of the central retinal artery (CRA) to functionally significant inner retinal infarction represents a window of opportunity for treatment and has medical-legal implications, when central retinal artery occlusion (CRAO) complicates therapeutic interventions. Central retinal artery occlusion (CRAO) of sufficient duration causes a stroke, infarction of the inner retina including the retinal ganglion cells and their axons which form the optic nerve, central nervous system tissue [1, 2]. Retinal stroke from CRAO typically presents as acute, catastrophic, permanent visual loss in one eye, about 80% of the time with a visual acuity of 20/400 or worse, an afferent pupillary defect, a classic retinal cherry red spot on ophthalmoscopy from opacification of the infarcted ganglion cell layer surrounding the fovea, and sometimes a visible CRA embolus or other retinal arterial emboli [1, 3, 5]. The outer retina including the photoreceptors and underlying retinal pigment epithelium is supplied with oxygen by the lush choroidal circulation derived from the long and short posterior
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