Central retinal artery occlusion or retinal stroke: a neurosonologist's perspective.

In central retinal artery occlusion (CRAO) or retinal stroke, which is usually a vision-threatening condition, timely diagnosis is imperative to improve the chances of retinal preservation and to establish adequate secondary prevention measures. Even though retinal strokes have been traditionally assigned to the field of ophthalmology, while considering reperfusion therapy as the only way to avoid permanent vision loss, we suggest prompt evaluation of CRAO causes (primarily related to cardiovascular risk factors) performed by a well-organized interdisciplinary team (ophthalmologist and neurologist) in a neurovascular center with stroke expertise. Therefore, the most suitable adjunct method for rapidly diagnosing non-arteritic CRAO could be target transorbital ultrasound, performed by an experienced neurologist/neurosonologist in the stroke unit. Consequently, after an ophthalmological assessment, a final decision on thrombolytic therapy could be made. We accept that further research is obviously needed to determine whether transorbital ultrasound could replace ophthalmological investigation in the case of a suspected acute retinal stroke. We assert that retinal stroke requires interdisciplinary treatment in cooperation with neurologists and ophthalmologists, with an additive value for each to achieve the best results for the patient.

Implementation of a retinal stroke-code protocol results in visual recovery in patients receiving reperfusion therapies.

INTRODUCTION: Reperfusion therapies represent promising treatments for patients with Central Retinal Artery Occlusion (CRAO), but access is limited due to low incidence and lack of protocols. We aimed to describe the benefit of implementing a Retinal Stroke-Code protocol regarding access to reperfusion, visual acuity and aetiological assessment. PATIENTS AND METHODS: Prospective cohort study performed at a Comprehensive Stroke Centre. Criteria for activation were sudden monocular, painless vision loss within 6 h from onset. Eligible patients received IAT when immediately available and IVT otherwise. All patients were followed by ophthalmologists to assess best-corrected visual acuity (BCVA) and visual complications, and by neurologists for aetiological workup. Visual amelioration was defined as improvement of at least one Early Treatment Diabetic Retinopathy Study (ETDRS) letter from baseline to 1 week. RESULTS: Of 49 patients with CRAO, 15 (30.6%) received reperfusion therapies (12 IVT, 3 IAT). Presentation beyond 6 h was the main contraindication. Patients receiving reperfusion therapies had better rates of visual improvement (33.3% vs 5.9%, p = 0.022). There were no complications related to reperfusion therapies. Rates of neovascular glaucoma were non-significantly lower in patients receiving reperfusion therapies (13.3% vs 20.6%, p = 0.701). Similar rates of atherosclerotic, cardioembolic and undetermined aetiologies were observed, leading to 10 new diagnosed atrial fibrillation and five carotid revascularizations. CONCLUSION: A comprehensive acute management of CRAO is feasible despite low incidence. In our study, reperfusion therapies were safe and associated with higher rates of visual recovery. A similar etiological workup than ischemic stroke led to of high proportion of underlying aetiologies.

Retinal stroke: research models, targets and experimental drugs.

INTRODUCTION: Retinal artery occlusion (RAO), often caused by a microembolus and resulting in inner retinal ischemia, could be considered as the retinal analog to cerebral stroke. Although several therapeutic targets have been suggested in animal models of retinal ischemia and several potential treatments have been evaluated on small series of patients, central retinal artery occlusion (CRAO) is still rarely treatable in clinical practice. AREAS COVERED: Here, we review several animal models of RAO, including increased intraocular pressure, laser, vasoconstriction, embolization and clamp. We also review the pathogenic mechanisms that contribute to cell death cascades during ischemia, and the therapeutic strategies targeting these events. These strategies aim to restore blood flow by fibrinolysis, increase the oxygen or glucose supply, decrease the energy demands, restrict ionic leak fluxes or reduce the detrimental effects of glutamate, calcium and free radicals. The current literature suggests that tPA treatment could be effective for CRAO. EXPERT OPINION: Eye care professionals must make a rapid and accurate diagnosis and immediately refer patients with acute retinal stroke to specialized centers. CRAO management should also be facilitated by developing local networks to encourage collaboration among ophthalmologists, retina specialists and stroke neurologists.

Central retinal artery occlusion-A new, provisional treatment approach.

The retinal ganglion cells infarcted in central retinal artery occlusion (CRAO) are the somata of the optic nerve axons, part of the central nervous system. Consequently, CRAO with inner retinal infarction is a small vessel stroke, usually with the devastating consequence of severe visual loss in the affected eye. At present, there is no generally accepted, evidence-based therapy of nonarteritic CRAO in contrast to ischemic cerebral stroke that has well-accepted treatment protocols. Widely divergent and controversial therapeutic options for CRAO reflect the desperation of treating physicians and disparate conflicting studies. We examine reasons why treatment of nonarteritic CRAO remains problematic and then suggest a provisional new approach to treatment based on updated understanding of CRAO pathophysiology and analysis of current therapeutic options and their rationales.

Central retinal artery occlusion - rethinking retinal survival time.

BACKGROUND: 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 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. METHODS: A 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. RESULTS: We 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. CONCLUSIONS: Retinal 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'.

Low endogenous recanalization in embolic central retinal artery occlusion--the retrobulbar "spot sign".

BACKGROUND AND PURPOSE: Central retinal artery occlusion (CRAO) is most often indirectly diagnosed by lack of retinal perfusion. Direct embolus characterization may help to understand the natural course and low response to treatment. In a previous study we identified a hyperechoic signal within the optic nerve and in the central retinal artery ("spot sign"). METHODS: In this study we performed a follow-up investigation in 7 patients with CRAO and positive spot sign indicating the embolic cause of the occlusion after a median interval of 17 months (range 11-38 months) using a battery of tests (ocular color-coded sonography, optic coherence tomography [OCT], fundoscopy, amongst others). RESULTS: The spot sign persisted in all patients, none had high-grade internal carotid artery stenosis, stroke or transient ischemic attacks. Four patients were completely blind, 3 patients were able to recognize hand movements. OCT demonstrated retinal atrophy, and fundoscopy revealed only minimal arterial perfusion. CONCLUSIONS: The hyperechoic spot sign may be an important predictive prognostic marker for persistent loss of vision. Its persistence may indicate calcified or cholesterol emboli and may explain the low therapeutic success rate to thrombolysis. Further studies on their origin and significance in atherosclerotic disease are warranted.