Retinal Artery Occlusion with Multiple Emboli: An Alarm for Serious Systemic Implications
Retinal Artery Occlusion with Multiple Emboli may indicate Severe Carotid Artery Occlusion Disease with Haemodynamic Changes
In a recent study published in BMJ Open Ophthalmology, researchers have reported an association between a rare subgroup of retinal artery occlusion presenting with multiple emboli and severe carotid artery occlusion disease which may have serious systemic implications.
The study was conducted by researchers from Changhua Christian Hospital, Taiwan and University of Neurosciences, Ontario, Canada.
Retinal artery occlusion (RAO), generally caused by embolus arising from carotid artery or cardiac lesions results in severe and permanent vision loss. Atherosclerotic plaques in the carotid artery, carotid stenosis and carotid artery occlusion with haemodynamically significant intracranial blood flow changes are associated with retinal artery occlusion. Literature regarding the association of ocular symptoms and clinical findings of RAO with the severity of carotid artery occlusion disease is however, limited.
The researchers reviewed the records of patients who had presented to Changhua Christian Hospital with acute RAO from 2004 to 2017. Out of 208 eyes which had presented with acute RAO, 12 eyes (5.7%) of 11 patients who had multiple emboli were recruited in the study. In this retrospective cohort, the researchers studied the records of clinical findings along with ophthalmic, carotid and cerebral artery flow evaluation done by any of the following methods: Carotid Arteriography, Carotid Doppler, CT Angiography, Magnetic Resonance Angiography. The presence of plaque, the degree of stenosis in the common carotid artery, internal carotid artery and external carotid artery were studied along with data on compensatory or collateral blood flow pattern in intracranial circulation, if available.
The results of the study were as follows
1.All the patients had typical features of sudden vision loss, retinal whitening and multiple visible retinal emboli. Two cases had branch RAO whereas the others had central RAO. In six eyes (50%), an embolus was seen at the optic disc. The number of emboli exceeded ten in nine eyes (75%).
2. Eleven eyes (91.6%) had ipsilateral carotid plaques and atherosclerosis, of which six had high-grade carotid stenosis (58%–95%) and the other five had total carotid occlusion. Carotid evaluations for the non-RAO side revealed no stenosis in two cases, and low-grade stenosis (<50%) in the others.
3. Flow studies demonstrated decreased or diminished cerebral flow where internal carotid artery stenosis was 60% or more. Increased vertebral flow which may contribute to compensate the intracranial circulation was demonstrated bilaterally in three cases and unilaterally in five cases.
4. Significant haemodynamic changes like decreased cerebral blood perfusion with responsive compensatory flows for intracranial redistributions were found in nine patients of RAO (81.8%) with carotid stenosis 60% or greater.
5. The authors postulate that most intracranial circulations were re-established via the circle of Willi by compensatory flows from the internal carotid artery of the other side laterally or from the vertebral artery posteriorly. However, reversal of the ophthalmic flow was noted in three eyes, indicating that compensatory flow may also arise from external carotid artery and ophthalmic artery anastomosis, probably when the flow through the circle of Willis is inadequate
According to the authors, the pathogenesis of RAO with multiple emboli and ipsilateral carotid artery occlusion may be more complicated than previously described. The classical method of multiple emboli formation is that blood flow through a stenotic vessel may cause turbulence resulting in a part of an unstable plaque getting dislodged from the vessel wall. This may possibly act like a nucleus on which further adherence of debris takes place. However, this mechanism is possible only in cases where the carotid arteries are stenotic, but not totally occluded. In cases of severe or total carotid artery occlusion having compensatory flow mechanism, indirect embolism from the collateral pathways may explain the pathogenesis of multiple emboli. In these collateral pathways, haemodynamic changes like blood flow in abnormal direction, dilatation of the collaterals and establishment of reperfusion may all contribute to scaling of debris from the vessel wall and formation of microemboli.
The authors postulate that multiple emboli may therefore represent the existence of haemodynamic changes and compensatory flow to redistribute the intracranial circulation in cases of severe carotid artery occlusion. Hence, the presentation of RAO with multiple emboli may be considered an alarm of a possible impending stroke, similar to amaurosis fugax and transient ischaemic attacks.
Therefore, the important message conveyed by the authors in this article is: RAO with multiple emboli is an uncommon entity but on diagnosis, urgent evaluation by a physician and initiation of appropriate medication to prevent further progression is advisable.