Central Retinal ArteryEdit
The central retinal artery is the principal blood vessel that sustains the inner layers of the retina, the light-sensitive tissue at the back of the eye. It is a small yet critically important branch that arises from the ophthalmic artery, itself a branch of the internal carotid system, and it travels within the optic nerve to enter the eye at the optic disc. In most people, the central retinal artery supplies the inner retinal layers via end-artery branches, with the macula sometimes receiving additional input from a cilioretinal artery. The integrity of this artery is essential for normal vision, and its occlusion or severe narrowing can result in rapid and often permanent visual impairment.
The central retinal artery's role sits at the intersection of vascular biology and ocular physiology. Because the retina has high metabolic needs, the CRA’s uninterrupted perfusion is crucial for maintaining retinal neurons and supporting cells. When blood flow is compromised, retinal ischemia can follow quickly, making timely recognition and understanding of this vessel and its path important for clinicians and researchers alike.
Anatomy and microvasculature
The central retinal artery originates from the ophthalmic artery, which in turn stems from the internal carotid system. After entering the orbit, the CRA travels within the optic nerve and pierces the lamina cribrosa to reach the retina, where it divides into superior and inferior branches that radiate across the nerve fiber layer to perfuse the inner retina. The outer retina, by contrast, is primarily supplied by the choroidal circulation supplied by the posterior ciliary arteries. In some individuals, a cilioretinal artery provides an additional route of perfusion to the macular region, which can influence visual outcomes when the CRA is compromised. retina ophthalmic artery internal carotid artery optic disc cilioretinal artery choroid
The CRA’s status as an end artery—lacking substantial collateral supply in many regions of the retina—helps explain why occlusive events can produce sudden, focal deficits. Vascular autoregulation and the severity of ischemia interact with patient-specific factors to determine the extent of retinal injury. The anatomy of the CRA is also studied in the context of systemic vascular disease, including carotid atherosclerosis and hypertensive changes, which can predispose individuals to embolic or thrombotic events. embolism thrombosis carotid artery disease
Function and blood supply
The inner retinal layers, including the ganglion cell layer and inner nuclear layer, rely predominantly on the CRA for oxygen and nutrients. The retinal architecture and the high metabolic demand of photoreceptors and associated neurons make this circulation vital for sustained function. When blood flow is intact, the retina maintains normal cellular activity; when it is reduced or interrupted, retinal cells can die or become dysfunctional, leading to visual symptoms. retina ischemia
Because the macula—responsible for sharp central vision—may receive supplementary supply from a cilioretinal artery in some people, the impact of CRA compromise can vary. In cases where the cilioretinal circulation is absent or limited, central vision is typically affected more severely. Understanding these vascular relationships is important in both clinical evaluation and imaging interpretation. cilioretinal artery macula central retinal artery occlusion
Pathology
The most common clinically significant pathology involving the central retinal artery is central retinal artery occlusion (CRAO). CRAO is an emergency in many settings, presenting most often as a sudden, painless loss of vision in one eye. A characteristic fundoscopic finding is a pale retina with a cherry-red spot at the fovea, where the underlying choroidal circulation remains visible. These signs reflect inner retinal ischemia due to obstructed flow in the CRA. Other findings may include attenuation of retinal arteries and edema of the inner retina on imaging. central retinal artery occlusion fundoscopy cherry-red spot retinal ischemia
Etiologies of CRAO are diverse and include embolic sources (such as atherosclerotic debris from the carotid arteries or cardiac sources), thrombotic events in situ, inflammatory or vasculitic processes (for example, giant cell arteritis), vasospasm, and, less commonly, iatrogenic causes related to procedures near the ocular vasculature. Systemic cardiovascular risk factors—age, hypertension, diabetes mellitus, dyslipidemia, and smoking—heighten the likelihood of CRAO through atherothrombotic mechanisms. embolic thrombosis giant cell arteritis hypertension diabetes mellitus smoking carotid artery disease
Diagnosis typically involves urgent ophthalmologic assessment supplemented by imaging. Fundoscopy can confirm retinal pallor and the cherry-red spot; fluorescein angiography may show delayed or absent perfusion in the retina. Optical coherence tomography (OCT) can reveal inner retinal thickening and edema in the acute phase. Systemic evaluation for stroke risk and cardiovascular disease is common, including carotid ultrasound and cardiac workup. fundoscopy fluorescein angiography optical coherence tomography carotid ultrasound ischemia
Management remains a topic of clinical debate. Because CRAO is an ocular analog of acute vascular occlusion, some aggressive interventions used in stroke care have been explored, including thrombolytic therapy, intra-arterial or IV approaches, and hyperbaric oxygen therapy. However, high-quality evidence supporting a singularly effective treatment is lacking, and results from different studies are mixed. Consequently, guidelines emphasize rapid assessment and individualized care, with emphasis on screening for underlying etiologies and mitigating systemic risk factors. Patients with suspected inflammatory etiologies (such as giant cell arteritis) require prompt systemic steroids and specialist evaluation. thrombolysis hyperbaric oxygen therapy stroke giant cell arteritis
Prognosis after CRAO is highly dependent on the speed of recognition and treatment, as well as the presence of any residual macular perfusion. In many cases, vision remains significantly impaired or is permanently reduced, although some patients regain partial function, particularly if collateral pathways or cilioretinal supply preserve macular perfusion. Long-term outcomes are influenced by the management of cardiovascular risk factors and adherence to medical follow-up. prognosis macula collateral circulation retina
Diagnosis and imaging
Comprehensive assessment blends ophthalmologic examination with vascular and neurologic evaluation. Color fundus photography documents retinal appearance; fluorescein angiography assesses perfusion dynamics; OCT provides structural details of retinal layers and edema patterns. Systemic workups may include blood tests, cardiovascular risk assessment, and imaging of the carotid arteries to identify potential embolic sources. fundoscopy fluorescein angiography OCT retina carotid ultrasound embolism
Management and prognosis
Timely management hinges on rapid evaluation by ophthalmology and, when appropriate, neurology. Elevating awareness of CRAO as an ocular emergency is important, given the potential for vision loss to progress if untreated. In suspected inflammatory etiologies, prompt immunosuppressive treatment is essential. For noninflammatory CRAO, the best-supported strategies focus on rapid workup, control of vascular risk factors, and consideration of trial therapies within the bounds of current evidence and patient-specific risk. ophthalmology neurology giant cell arteritis stroke thrombolysis