Central retinal artery occlusion

Amaurosis fugax is transient, painless monocular vision loss from retinal ischemia, most often microembolic from an ipsilateral carotid or a cardiac source, and it is treated as a TIA-equivalent with urgent carotid/cardiac workup and immediate aspirin 81 mg daily plus a high-intensity statin.

Central retinal vein occlusion causes sudden, painless, variable monocular vision loss from thrombosis of the central retinal vein, is treated with intravitreal anti-VEGF for macular edema, and carries a real risk of neovascular glaucoma in the ischemic subtype.

Branch retinal vein occlusion is caused by secondary thrombosis at an arteriovenous crossing, where a sclerotic, hypertension- or diabetes-damaged arteriole compresses the adjacent venule, producing sectoral hemorrhage that is treated with intravitreal anti-VEGF injection when it causes macular edema.

Giant cell arteritis is a granulomatous large- and medium-vessel vasculitis of patients over 50 that threatens irreversible blindness through ischemic optic neuropathy. Diagnosis is clinical and must not delay treatment: start high-dose glucocorticoids immediately on suspicion, intravenous methylprednisolone pulse for visual loss, then confirm with temporal artery biopsy within 1 to 2 weeks and add tocilizumab as glucocorticoid-sparing therapy.

Sudden painless monocular vision loss from occlusion of the posterior ciliary artery by giant cell arteritis infarcts the optic nerve head and threatens the fellow eye within days. Treatment with high-dose glucocorticoids must begin on clinical suspicion, before biopsy confirmation, because established blindness is usually permanent.

Carotid artery stenosis is atherosclerotic narrowing of the extracranial internal carotid artery that raises ischemic stroke risk, graded by percent luminal narrowing on duplex ultrasound. Symptomatic stenosis of at least 50% warrants urgent revascularization; asymptomatic stenosis under 80% is managed with best medical therapy alone, including a high-intensity statin and antiplatelet agent.

Bacterial infection of the endocardial surface, usually a heart valve, producing vegetations that destroy the valve and embolize; diagnosis rests on the modified Duke criteria (blood cultures plus echocardiography) and treatment is a prolonged organism-directed intravenous antibiotic course, with valve surgery for heart failure, uncontrolled infection, or embolic recurrence.

Antiphospholipid syndrome is an acquired autoimmune thrombophilia in which antiphospholipid antibodies cause recurrent venous and arterial thrombosis and pregnancy morbidity, paradoxically prolonging the aPTT in vitro while promoting clotting in vivo. Diagnosis requires a qualifying clinical event plus a laboratory antibody confirmed positive on two occasions at least 12 weeks apart, and thrombotic disease is treated with indefinite warfarin rather than a DOAC.

Cholesterol embolization syndrome is showering of cholesterol crystals from atherosclerotic plaques into small arteries, typically after an arterial procedure or anticoagulation. It causes livedo reticularis, blue toes with preserved pulses, and acute kidney injury; management is supportive with aggressive statin therapy and avoiding further arterial insult.

Ischemic stroke is sudden focal neurologic deficit from arterial occlusion confirmed by infarction on neuroimaging. Diagnosis relies on urgent noncontrast head CT to exclude hemorrhage; treatment is IV alteplase within 4.5 hours and mechanical thrombectomy for large-vessel occlusion within an extended window, followed by antiplatelet therapy and risk-factor control.

Rhegmatogenous retinal detachment is a surgical emergency in which a full-thickness retinal break lets liquefied vitreous separate the neurosensory retina from the retinal pigment epithelium, presenting with flashes, floaters, and an advancing visual field curtain. Diagnosis is by dilated indirect ophthalmoscopy with scleral depression, and treatment is prompt surgical reattachment, most urgent while the fovea is still spared.

Acute angle-closure glaucoma is a pupillary-block emergency in which sudden closure of the iridocorneal angle blocks aqueous outflow, causing severe eye pain, halos, and rapidly rising intraocular pressure that can blind the eye within hours if not treated. Diagnosis is clinical plus tonometry and gonioscopy; treatment is immediate topical and systemic IOP-lowering therapy followed by laser peripheral iridotomy.

Optic neuritis is inflammatory demyelination of the optic nerve, usually a presenting event of multiple sclerosis, causing subacute painful monocular vision loss with a relative afferent pupillary defect. Confirm with MRI orbits/brain and treat with IV methylprednisolone followed by an oral prednisone taper, never oral prednisone alone.