Sudden Vision Loss

Sudden visual loss is a common complaint among patients of different ages with variable presentations. Some patients describe it as a gray-black curtain that gradually descends or as blurring, fogging, or dimming of vision. It usually lasts a few minutes but can persist for hours. The frequency varies from a single episode to many episodes during a day; it may continue for years but more often lasts from seconds to hours. Ischemia is the most common mechanism of acute visual dysfunction, and it can affect any aspect of the visual system.

Eye ischemia is claasified as the following:

Transient visual obscuration – Episodes lasting seconds that are associated with papilledema and increased intracranial pressure
Amaurosis fugax – Brief, fleeting attack of monocular partial or total blindness that lasts seconds to minutes
Transient monocular visual loss or transient monocular blindness – A more persistent vision loss that lasts minutes or longer
Transient bilateral visual loss – Episodes affecting one or both eyes or both cerebral hemispheres and causing visual loss
Ocular infarction – Persistent ischemic damage to the eye, resulting in permanent vision loss

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Transient monocular visual loss in a person younger than 45 years may be benign; many attacks are probably vasospastic or due to migraine.

Transient bilateral visual loss is almost always associated with severe occlusive disease of the internal carotid artery, aortic arch, or bilateral occipital lobe ischemia.

Patients with ICA disease often have other systemic evidence of atherosclerosis, such as coronary and peripheral vascular disease. Smoking, hypercholesterolemia, and hypertension are also risk factors.

Transient Bilateral Vision Loss

Wray has classified TMVL into 3 different groups based mostly on pathogenesis; they include the following:

Type 1 is characterized by loss of all or a portion of vision in one eye, lasting seconds to minutes, with full recovery. It is usually secondary to an embolic phenomenon. The attacks have been related to an ICA origin associated with ulceration but not critical narrowing.
Type 2 includes visual loss due to hemodynamically significant, occlusive, low-flow lesions in the ICAs or ophthalmic arteries. Symptoms are more frequent, less rapid in onset, and longer in duration than type 1 attacks, with gradual vision recovery.
Type 3 is thought to be due to vasoconstriction or vasospasm.

Angle Closure Glaucoma

The diagnosis is not difficult when the presentation is typical—a painful, red eye with increased intraocular pressure that is accompanied by diaphoresis, nausea, and vomiting. Atypical presentations include chronic angle closure or an acute closure without pain. The presence of a midposition, fixed pupil in an eye with reduced vision can suggest unrecognized angle-closure glaucoma. Treatment consists of topical miotics and beta-blockers, systemic carbonic anhydrase inhibitors, hyperosmotic agents, and perhaps analgesics and antiemetics. Ophthalmologic consult is warranted.

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Medical care for patients with sudden visual loss includes the following:

Aspirin is believed to be beneficial in patients with no hemodynamically significant disease of the carotid artery (ie, greater than 1 mm residual lumen) or those who are poor surgical candidates.
- In general, aspirin together with modification of risk factors (eg, decreasing serum cholesterol level, controlling systemic hypertension) reduces the likelihood of myocardial infarction. It is also very effective in reducing the risk of stroke.
Advise patients with frequent or severe headaches to stop smoking.
Inferior retinal detachment is treated with the patient sitting up. Superior detachment is treated with the patient lying prone.