Step 2 CK · Ophthalmology & ENT

Acute Vision Loss

Name: Acute Vision Loss
Creator: Veli Bakalov, MD

Painful or painless — the fork that drives the workup

Ophthalmology & ENT·Urgent Eye Conditions·5 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

Study materialsNo account needed

Card deckActive-recall cards · quick checks · quiz

High-yield

Split acute monocular loss by pain: painless = CRAO, CRVO, retinal detachment, vitreous hemorrhage, amaurosis fugax; painful = optic neuritis (eye movement), GCA (headache), angle closure.
CRAO: sudden painless severe loss, pale retina, cherry-red macula, RAPD; a retinal stroke (about 90–100 minutes of tolerance) needing a stroke workup and immediate ESR/CRP for GCA.
Amaurosis fugax is a retinal TIA (descending shade lasting minutes, carotid embolus): carotid duplex, antiplatelet, statin, endarterectomy for symptomatic 70–99% stenosis (50–69% in selected patients); a Hollenhorst plaque means carotid disease.
CRVO: blood-and-thunder fundus (four-quadrant hemorrhages, tortuous veins, cotton-wool spots, disc edema) with hypertension, glaucoma, or hyperviscosity; anti-VEGF for macular edema.
Retinal detachment: flashes, new floaters, then a curtain (high myopia, trauma, cataract surgery) is a same-day surgical emergency; vitreous hemorrhage: floaters with a lost red reflex, classically diabetic neovascularization (B-scan if no fundus view).
GCA (age over 50, jaw claudication, scalp tenderness, PMR, ESR often over 50): start high-dose steroids immediately, biopsy within 1–2 weeks, because the fellow eye is at risk.
Arteritic AION = GCA, pale swollen disc, high ESR/CRP, urgent steroids; non-arteritic AION = disc at risk plus vasculopathy, painless altitudinal defect, no proven treatment.
Optic neuritis: subacute painful loss with eye movement, central scotoma, red desaturation, RAPD in a young woman; MRI brain and orbits for MS; IV methylprednisolone speeds recovery (oral prednisone alone raises recurrence).
An RAPD (swinging-flashlight test) means optic nerve or severe retinal disease (optic neuritis, CRAO, large detachment), never cataract or uncomplicated vitreous hemorrhage.

Framework: painful or painless?

Ask first whether it hurts. Painless sudden monocular loss points to the retina and its vessels: central retinal artery occlusion (CRAO), central retinal vein occlusion (CRVO), retinal detachment, vitreous hemorrhage, or amaurosis fugax. Painful loss points to optic neuritis (pain with eye movement), giant cell arteritis (headache), or angle-closure glaucoma. Check acuity, the red reflex, the fundus, and the pupils, then refer emergently.

Acute monocular vision loss

Cause	Pain	Key symptom	Key finding
CRAO	None	Sudden, severe loss	Pale retina, cherry-red macula, RAPD
Amaurosis fugax	None	Descending shade lasting minutes	Often normal; ± Hollenhorst plaque
CRVO	None	Sudden loss	Hemorrhages in all four quadrants, tortuous veins
Retinal detachment	None	Flashes, floaters, then a curtain	Detached retina; RAPD if large
Vitreous hemorrhage	None	Sudden floaters and haze	No red reflex; fundus not visible
Arteritic AION (GCA)	Headache	Severe loss after age 50	Pale swollen disc, high ESR and CRP
Optic neuritis	On eye movement	Subacute loss, washed-out colors	RAPD, central scotoma
Angle closure	Severe eye pain	Halos, vomiting	Fixed mid-dilated pupil, hard eye

Relative afferent pupillary defect (RAPD, Marcus Gunn pupil). On the swinging-flashlight test, the affected pupil paradoxically dilates when the light swings onto it. An RAPD signals asymmetric optic nerve or severe retinal disease: optic neuritis, CRAO, or a large retinal detachment. It is absent with media problems such as cataract or an uncomplicated vitreous hemorrhage.

A homonymous field defect localizes behind the optic chiasm (for example, an occipital stroke), and a bitemporal defect localizes to the chiasm itself; neither points to the eye.

Retinal vascular occlusion

CRAO is a retinal stroke. Sudden, painless, severe monocular loss with a pale, edematous retina, a cherry-red macula, and an RAPD. The cherry-red spot is intact choroid showing through the thin fovea while the surrounding ischemic retina turns pale. The retina tolerates only about 90–100 minutes of ischemia, so the prognosis is poor.

Check ESR and CRP immediatelyExclude giant cell arteritis, which threatens the other eye.
Emergent stroke workupCarotid duplex and a search for a cardiac embolic source.
Acute measuresOcular massage, lowering IOP, and high-flow oxygen have limited benefit; some centers give IV thrombolysis within an early window, though benefit is unproven; intra-arterial fibrinolysis showed no benefit and more complications (EAGLE trial).

Managing CRAO

A Hollenhorst plaque (a bright cholesterol embolus lodged at a retinal arteriole bifurcation) points to carotid disease.

Amaurosis fugax is a retinal TIA. Transient, painless monocular loss described as a curtain or shade descending over the eye and lasting minutes, from a carotid embolus. Work it up with carotid duplex and manage it like a TIA: antiplatelet therapy, a statin, and carotid endarterectomy for symptomatic 70–99% stenosis (considered for 50–69% in selected patients).

CRVO: "blood and thunder." Sudden painless loss with diffuse retinal hemorrhages in all four quadrants, dilated tortuous veins, cotton-wool spots, and disc edema. Risk factors are hypertension, glaucoma, and hyperviscosity. Macular edema is treated with intravitreal anti-VEGF injections.

CRAO versus CRVO

Feature	CRAO	CRVO
Fundus	Pale retina, cherry-red spot	Four-quadrant hemorrhages, tortuous veins, disc edema
Cause	Embolus or arteritis (GCA)	Venous thrombosis (hypertension, glaucoma, hyperviscosity)
Behaves like	A stroke	A chronic macular problem
Management	Stroke workup plus ESR and CRP	Anti-VEGF for macular edema

Both cause sudden, painless monocular vision loss.

Ischemic CRVO can drive iris neovascularization and a painful neovascular glaucoma months later, so these patients need follow-up.

Retinal detachment and vitreous hemorrhage

Retinal detachment. Painless photopsias (flashes) and a shower of new floaters, then a curtain or shadow advancing across the visual field, sometimes with an RAPD. Risk factors include high myopia, trauma, and prior cataract surgery. It is a surgical emergency, most urgent while the macula is still attached; refer the same day.

Vitreous hemorrhage. Sudden painless floaters and haze, with loss of the red reflex and no view of the retina. The classic cause is neovascularization from proliferative diabetic retinopathy; retinal tears and trauma also cause it. When the fundus cannot be seen, B-scan ultrasound looks for a detachment behind the blood.

A diabetic with sudden floaters and an obscured fundus has a vitreous hemorrhage from neovascularization until proven otherwise.

Giant cell arteritis and ischemic optic neuropathy

Giant cell (temporal) arteritis. Age over 50 with headache, jaw claudication, scalp tenderness, and polymyalgia rheumatica. Vision loss comes from arteritic anterior ischemic optic neuropathy (AION), with a pale, swollen disc. ESR is often over 50 (frequently over 100), and CRP is high.

SuspectAge over 50, jaw claudication, high ESR and CRP.
Treat nowHigh-dose corticosteroids immediately, without waiting for the biopsy.
ConfirmTemporal artery biopsy within 1–2 weeks; skip lesions mean a negative biopsy does not exclude GCA.
ProtectWithout treatment, the fellow eye can be lost within days.

GCA with vision loss

Arteritic versus non-arteritic AION

Feature	Arteritic (GCA)	Non-arteritic
Patient	Over 50 with systemic symptoms	Crowded "disc at risk" plus hypertension, diabetes, sleep apnea, nocturnal hypotension
Labs	High ESR and CRP	Normal
Vision loss	Severe; pale, swollen disc	Painless, often noticed on waking; altitudinal field defect
Treatment	Urgent high-dose steroids	Control risk factors; no proven treatment

Optic neuritis

The painful optic neuropathy of the young. Subacute monocular loss over days with pain on eye movement, a central scotoma, red desaturation (dyschromatopsia), and an RAPD, typically in a young woman. It is classically the presenting event of multiple sclerosis, and the disc often looks normal because the inflammation is behind the eye.

Workup and treatment. Obtain MRI of the brain and orbits; periventricular white-matter lesions predict progression to MS. IV methylprednisolone speeds visual recovery but does not change the final outcome, and oral prednisone alone increases recurrence.

Uhthoff phenomenon: vision transiently worsens with heat or exercise (a hot shower, a workout) in demyelinating optic neuritis.