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Resuscitation Quick Actions • First 2 Minutes

High-Acuity

CRAO is an Ocular Stroke

Activate Code Stroke/notify neurology; workup mirrors acute ischemic stroke (carotid ultrasound, echocardiogram, telemetry)

Cherry-Red Spot (CRAO)

Pale, milky, ischemic edematous retina + prominent bright 'cherry-red spot' in fovea + segmentation/boxcarring of arterioles

Giant Cell Arteritis (GCA)

Age > 50 with CRAO: check STAT ESR and CRP; if elevated, give Methylprednisolone 1g IV daily stat to save the contralateral eye!

Emergent CRAO Maneuvers

Digital ocular massage (cycles of 10s pressure/5s release), Timolol 0.5% drops, Acetazolamide 500 mg IV (dislodges embolus downstream)

CRVO 'Blood and Thunder'

Massive retinal venous thrombosis: diffuse flame hemorrhages in all 4 quadrants + tortuous dilated veins + cotton wool spots

Amaurosis Fugax Warning

Transient monocular vision loss lasting 5–15 minutes ('curtain pulled down and up') = CAROTID ATHEROEMBOLISM herald before major stroke

Bottom-Line Clinical Pearl

Central Retinal Artery Occlusion (CRAO) is an OPHTHALMIC ISCHEMIC STROKE characterized by sudden, catastrophic, painless monocular vision loss (often counting fingers or light perception only). Fundoscopy reveals a pale, milky, edematous ischemic retina with a pathognomonic 'CHERRY-RED SPOT' at the fovea (where the thin fovea allows underlying vascular choroid to shine through) and 'boxcarring' of retinal arterial blood columns. In elderly patients (> 50 years), always check ESR and CRP to rule out arteritic CRAO from GIANT CELL ARTERITIS (GCA); if suspected, administer IV Methylprednisolone (1,000 mg/day) immediately to save the contralateral eye! Embolic non-arteritic CRAO requires immediate stroke center transfer, 12-lead ECG (atrial fibrillation), carotid ultrasound, and acute IOP-lowering maneuvers (ocular massage, Timolol, IV acetazolamide). Central Retinal Vein Occlusion (CRVO) presents with subacute, painless vision loss; fundoscopy reveals the classic 'BLOOD AND THUNDER' appearance (diffuse retinal hemorrhages and optic disc edema).

1. Central Retinal Artery Occlusion (CRAO): Ocular Stroke

The central retinal artery is the primary branch of the ophthalmic artery (derived from the internal carotid artery), providing end-arterial perfusion to the inner two-thirds of the retina. The fovea, however, receives additional dual circulation from the deeper short posterior ciliary arteries (choroid).

Occlusion occurs due to: (1) Calcific/cholesterol emboli (Hollenhorst plaques) originating from ipsilateral internal carotid stenosis, (2) Fibrin-platelet cardioembolism from atrial fibrillation or endocarditis, or (3) Arteritic vasculitis (Giant Cell Arteritis/Temporal Arteritis) in elderly patients. Retinal neurons suffer irreversible ischemic necrosis within 90 to 240 minutes of complete circulatory cessation.

Physical & Fundoscopic ExamDiagnostic Findings in CRAOPathophysiologic Rationale
Visual AcuitySevere, profound drop in vision (typically limited to counting fingers, light perception, or total darkness)Complete ischemia of retinal ganglion cells and inner nuclear layers.
Pupillary ExamProminent Relative Afferent Pupillary Defect (RAPD/Marcus Gunn pupil)Defective sensory input from the infarcted retina.
Retinal ParenchymaDiffuse pale, opaque, milky-white, ground-glass retinaAcute intracellular cytotoxic axonal edema of the ganglion cell layer obscuring underlying choroid.
Fovea CentralisPathognomonic 'Cherry-Red Spot'The fovea lacks the ganglion cell layer and is nourished entirely by the deeper choroidal circulation, allowing the bright red vascular choroid to show through.
Retinal Arterioles'Boxcarring'/cattle-trucking of blood columns; visible bright refractile Hollenhorst plaques at arterial bifurcationsStasis and segmentation of red blood cell columns within narrowed, non-pulsatile arterioles.

2. Central Retinal Vein Occlusion (CRVO): 'Blood & Thunder'

Central Retinal Vein Occlusion (CRVO) is caused by thrombosis of the central retinal vein at or near the lamina cribrosa of the optic nerve, where the artery and vein share a common adventitial sheath. Risk factors include advanced age, hypertension, diabetes mellitus, hypercoagulable disorders, and glaucoma. Outflow obstruction causes massive hydrostatic venous backpressure, producing vascular engorgement, diffuse retinal edema, and capillary rupture.

Clinical ParameterCentral Retinal Artery Occlusion (CRAO)Central Retinal Vein Occlusion (CRVO)
Speed of Vision LossInstantaneous/Hyperacute (seconds to minutes)Subacute/Rapid over hours to days (often noticed upon waking in morning)
Fundoscopic AppearancePale, milky-white retina with Cherry-Red Spot and thin thread-like arterioles'Blood and Thunder' fundus: widespread diffuse flame-shaped and blot hemorrhages across all 4 retinal quadrants, massive optic disc edema, and engorged tortuous veins
Emergency ManagementAcute stroke workup; emergent IOP lowering; rule out Giant Cell Arteritis (ESR/CRP)Urgent ophthalmology referral for anti-VEGF intraocular injections and panretinal photocoagulation to prevent neovascular glaucoma ('90-day glaucoma')
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