Retinal Vascular Occlusions & Related Hemorrhage

Central Retinal Artery Occlusion (CRAO)

Central retinal artery occlusion is an ophthalmic emergency and a direct stroke equivalent: sudden, painless, profound vision loss from acute interruption of the retina's arterial blood supply. Fundoscopy shows diffuse retinal whitening from ischemic edema of the inner, ganglion-cell-bearing retina, with a cherry red spot at the fovea. The spot is not a lesion. It is a contrast effect: the fovea has no inner retinal layer to swell, and the choroid, not the occluded retinal vessels, nourishes it directly, so it keeps its normal color against the pale, edematous retina around it. Pale retinal edema with a cherry red spot is the key finding that separates CRAO from CRVO on fundoscopy, which instead shows diffuse hemorrhage without that whitening.

On fluorescein angiography, CRAO shows delayed or patchy filling of the retinal arteries and a dark, nonperfused macula, a direct reflection of the obstructed arterial inflow. Because the embolic mechanism is the same as in cerebral stroke, management follows a stroke protocol. A patient seen within the first few hours of onset may benefit from ocular massage, anterior chamber paracentesis, or another IOP-lowering maneuver meant to dislodge the embolus and restore perfusion, alongside urgent referral for stroke workup given the shared risk of concurrent cerebral ischemia.

Branch and Central Retinal Vein Occlusion

Vein occlusions differ from CRAO in both mechanism and distribution. Branch retinal vein occlusion (BRVO) occurs at an arteriovenous crossing, where the artery and vein share a common adventitial sheath. Chronic arteriolar thickening, most often from systemic hypertension and arteriosclerosis, compresses the adjacent vein enough to trigger thrombus formation and downstream venous congestion. Only the venous drainage of one retinal sector is affected, so the resulting flame-shaped and dot-blot hemorrhages, along with dilated, tortuous vessels, stay confined to a wedge following that vein's distribution. This sectoral pattern is what separates BRVO from a central occlusion, which involves the entire retina rather than one quadrant.

Macular edema is the main vision-threatening complication of both BRVO and CRVO. Intravitreal anti-VEGF injection is the current first-line treatment, lowering vascular permeability and improving visual outcomes, the same mechanism used for diabetic macular edema but applied here to a different underlying vasculopathy.

Central retinal vein occlusion splits into two forms with very different prognoses. Nonischemic CRVO is more common and typically preserves vision better than 20/200, with mild venous dilation and a mild or absent pupillary defect. Ischemic CRVO causes severe vision loss, a relative afferent pupillary defect, and extensive four-quadrant hemorrhage with widespread capillary nonperfusion on angiography. The distinction matters past the initial exam: roughly a third of ischemic eyes develop iris and angle neovascularization, driven by VEGF released from the chronically hypoxic retina, and go on to neovascular glaucoma with markedly elevated intraocular pressure. This complication is nicknamed "90-day glaucoma" because it tends to appear eight to fifteen weeks after the occlusive event, though the window can run from the first month out to several years later. Nonischemic CRVO can also convert to the ischemic form over time, so both types warrant ongoing monitoring rather than a single early classification.

Terson Syndrome & Subhyaloid Hemorrhage

Preretinal, or subhyaloid, hemorrhage occurs when blood collects in the potential space between the retina and the posterior vitreous face, or under the internal limiting membrane, rather than within the retinal layers themselves. That space is gravity-dependent, so the blood settles into a "boat-shaped" configuration: a flat, horizontal fluid level on top with a curved, rounded margin below. This shape is the key feature separating it from a flame-shaped intraretinal hemorrhage or a round, well-demarcated subretinal hemorrhage.

The association most often tested for preretinal hemorrhage near the optic disc is rupture of fragile neovascular vessels in proliferative diabetic retinopathy. The same boat-shaped hemorrhage also occurs in Valsalva retinopathy, where a sudden rise in intrathoracic or venous pressure ruptures a superficial retinal capillary, and in Terson syndrome, where subarachnoid hemorrhage raises intracranial pressure sharply enough to transmit along the optic nerve sheath and rupture peripapillary retinal vessels. In Terson syndrome, the preretinal or vitreous hemorrhage appears in the setting of a known intracranial bleed.

Related Topics

Continue exploring Retina & Vitreous: