Central Retinal Artery Occlusion (CRAO) is a critical eye condition similar to a stroke in the brain, requiring urgent medical attention. Patients with CRAO experience sudden, painless, monocular vision loss, and the visual prognosis is poor, with a low chance of spontaneous recovery. The condition is associated with an increased risk of ischemic heart disease and cerebral stroke due to underlying atherosclerotic risk factors. Currently, there is no officially recommended treatment for CRAO. This review covers the anatomy, pathophysiology, clinical features, and management approaches for CRAO. CRAO is an ocular emergency, and its clinical presentation depends on the site and degree of occlusion. Patients typically present with sudden, painless, monocular vision loss, and the visual prognosis is poor, with 61% of patients having vision of counting fingers or worse. The incidence of CRAO is relatively rare, estimated at one patient per 100,000 in a calendar year, with higher rates in certain populations, such as those over 80 years old. CRAO occurs when the central retinal artery (CRA) or its branches are occluded. The CRA originates from the ophthalmic artery and supplies blood to the optic nerve surface and the inner retina. Thromboembolism is the most common cause, often resulting from thrombi formed in the carotid artery. Arteritic CRAO, associated with inflammatory conditions like giant cell arteritis, accounts for a smaller proportion of cases. Patients with CRAO present with sudden, severe vision loss, often within minutes. Common fundus examination findings include a cherry-red spot, retinal opacity, disc pallor, retinal artery attenuation, disc oedema, and boxcar ring. Visual field defects are also common, typically central or centrocecal scotomas. Paracentral acute middle maculopathy (PAMM) is a related entity, characterized by hyperreflective parafoveal bands on spectral-domain optical coherence tomography (SD-OCT). CRAO is classified into transient monocular vision loss (TMVL), branch retinal artery occlusion (BRAO), and CRAO. CRAO can be further divided into transient non-arteritic CRAO, arteritic CRAO, and non-arteritic CRAO. The classification is based on anatomy and pathophysiology. Prompt, extensive ocular and systemic clinical workup is essential for patients with suspected CRAO. This includes a detailed history, visual acuity assessment, pupillary examination, and fundus examination. Additional investigations such as optical coherence tomography (OCT), OCT angiography (OCT-A), and fluorescein angiography (FFA) are used to evaluate retinal ischemia and disease progression. Management of CRAO involves three phases: acute, subacute, and chronic. The acute phase focuses on determining if reperfusion is possible,Central Retinal Artery Occlusion (CRAO) is a critical eye condition similar to a stroke in the brain, requiring urgent medical attention. Patients with CRAO experience sudden, painless, monocular vision loss, and the visual prognosis is poor, with a low chance of spontaneous recovery. The condition is associated with an increased risk of ischemic heart disease and cerebral stroke due to underlying atherosclerotic risk factors. Currently, there is no officially recommended treatment for CRAO. This review covers the anatomy, pathophysiology, clinical features, and management approaches for CRAO. CRAO is an ocular emergency, and its clinical presentation depends on the site and degree of occlusion. Patients typically present with sudden, painless, monocular vision loss, and the visual prognosis is poor, with 61% of patients having vision of counting fingers or worse. The incidence of CRAO is relatively rare, estimated at one patient per 100,000 in a calendar year, with higher rates in certain populations, such as those over 80 years old. CRAO occurs when the central retinal artery (CRA) or its branches are occluded. The CRA originates from the ophthalmic artery and supplies blood to the optic nerve surface and the inner retina. Thromboembolism is the most common cause, often resulting from thrombi formed in the carotid artery. Arteritic CRAO, associated with inflammatory conditions like giant cell arteritis, accounts for a smaller proportion of cases. Patients with CRAO present with sudden, severe vision loss, often within minutes. Common fundus examination findings include a cherry-red spot, retinal opacity, disc pallor, retinal artery attenuation, disc oedema, and boxcar ring. Visual field defects are also common, typically central or centrocecal scotomas. Paracentral acute middle maculopathy (PAMM) is a related entity, characterized by hyperreflective parafoveal bands on spectral-domain optical coherence tomography (SD-OCT). CRAO is classified into transient monocular vision loss (TMVL), branch retinal artery occlusion (BRAO), and CRAO. CRAO can be further divided into transient non-arteritic CRAO, arteritic CRAO, and non-arteritic CRAO. The classification is based on anatomy and pathophysiology. Prompt, extensive ocular and systemic clinical workup is essential for patients with suspected CRAO. This includes a detailed history, visual acuity assessment, pupillary examination, and fundus examination. Additional investigations such as optical coherence tomography (OCT), OCT angiography (OCT-A), and fluorescein angiography (FFA) are used to evaluate retinal ischemia and disease progression. Management of CRAO involves three phases: acute, subacute, and chronic. The acute phase focuses on determining if reperfusion is possible,