If available, consider intravenous fluorescein angiography and/or electroretinography to confirm the diagnosis.To revisit the concept of retinectomy and the theory of mechanical forces on the retina occurring in rhegmatogenous retinal detachment (RRD) and to describe the potential application of radial retinectomy in RRD with advanced proliferative vitreoretinopathy (PVR). This may include hemoglobin A1c, lipid profile, Rh factor, antinuclear antibody, fluorescent treponemal antibody absorption test, hypercoagulability labs, carotid artery duplex, electrocardiogram, echocardiogram, and outpatient Holter monitoring. Other workup should be considered based on individual risks factors and history. If symptom onset is less than 6 hours, a CT head without contrast should be obtained to rule out intracranial hemorrhage and determine if the patient is a candidate for thrombolytic therapy. If inflammatory markers are elevated and the history and physical are consistent with giant cell arteritis, then high dose steroids should be initiated immediately. Initial blood work should include point-of-care glucose, complete blood count with differential, and coagulation assays (PT/INR, PTT).Īn erythrocyte sedimentation rate and C-reactive protein should be obtained to rule out giant cell (temporal) arteritis. As such, workup for CRAO closely parallels the workup for stroke or transient ischemic attacks. Other conditions may present with a cherry red spot on fundoscopic exams (commotio retinae, Tay-Sachs, Niemann-Pick disease) but should be easy to differentiate based on clinical presentation.ĬRAO is analogous to a cerebral vascular accident involving the retina. Rarely, arteriolar emboli may be visualized. Narrowing, "boxcarring" or segmentation of the arterioles also may be appreciated. This spot results from the preserved choroidal circulation visible beneath the thin fovea. On fundoscopy, the retina will appear diffusely pale with a cherry red central spot. A thorough fundoscopic exam is crucial for accurate diagnosis of CRAO, and a dilated exam should be performed on any patient without contradictions to mydriatic medications who presents with symptoms concerning for CRAO. Typically, intraocular pressures, anterior chamber exam, and extraocular eye movements are within normal limits. However, visual acuity can vary from loss of light perception to finger counting. Patients with CRAO often present with monocular loss of light perception and an afferent pupillary defect. Patients may report an antecedent transient visual loss (amaurosis fugax) and often have a history of atherosclerotic disease. Rapid differentiation between thromboembolic versus arteritic processes is important as optimal therapy differs and the rapid administration of steroids for vasculitic causes of CRAO is associated with improved outcomes.ĬRAO typically presents with sudden, painless, monocular vision loss that occurs over seconds. Predisposing conditions include but are not limited to polycythemia vera, sickle cell anemia, multiple myeloma, systemic lupus erythematosus, factor V Leiden, prothrombin III mutation, hyperhomocysteinemia, polyarteritis nodosa, giant cell (temporal) arteritis, antiphospholipid syndrome, activated protein C resistance, Behcet disease, and syphilis. Thrombi may be due to atherosclerotic disease, collagen-vascular disease, inflammatory states, and/or hypercoagulable states. In-situ thrombosis also may cause retinal artery occlusion. On fundoscopy, calcium emboli appear white, cholesterol emboli (Hollenhorst plaques) appear orange, and platelet-fibrin emboli appear dull white. Calcium emboli typically arise from cardiac valves. Both cholesterol and platelet-fibrin emboli typically arise from atheromas in the carotid arteries. The three main types of emboli are cholesterol, calcium, and platelet-fibrin. An embolism is the most common cause of CRAO.
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