Central retinal vein occlusion

Central retinal artery occlusion is sudden, painless, profound monocular vision loss from embolic or thrombotic occlusion of the central retinal artery, an ocular stroke equivalent in which irreversible retinal infarction begins around 90 minutes after complete occlusion. Diagnosis is clinical on dilated fundoscopy, and management pairs time-critical reperfusion attempts with an emergency embolic and giant-cell-arteritis workup to protect the fellow eye and prevent a subsequent stroke.

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.

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.

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.

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.

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.

Age-related macular degeneration is a leading cause of irreversible blindness in older adults in resource-rich countries, presenting as painless central vision loss from drusen and retinal pigment epithelium change (dry AMD) or choroidal neovascularization (wet AMD). Dry AMD is managed with AREDS2 supplementation and risk-factor control; wet AMD is treated with intravitreal anti-VEGF injection.

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.

Primary open-angle glaucoma is a chronic, usually asymptomatic optic neuropathy with a normal iridocorneal angle, progressive cupping of the optic disc, and characteristic peripheral-before-central visual field loss. Diagnosis rests on tonometry, gonioscopy to confirm the open angle, dilated funduscopy with cup-disc ratio, and perimetry, and treatment is lifelong topical IOP-lowering therapy escalating to laser or incisional surgery for uncontrolled disease.