Central retinal artery occlusion: Difference between revisions
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==Background==
==Background==
*Abbreviation: CRAO
*Acute interruption of blood flow to the retinal artery causing retinal ischemia
*The first branch of internal carotid artery is the ophthalmic artery.  Visual loss from CRAO is usually painless and is more common in the elderly with carotid artery disease
*A stroke equivalent — 15-25% of patients will have an acute stroke or TIA within 1 week<ref name="lee">Lee J, et al. Risk of stroke in patients hospitalized with central retinal artery occlusion. ''Stroke''. 2013;44(4):967-971. PMID 23399955.</ref>
*Cherry red spot (fundoscopy)
*'''Ophthalmologic emergency''' — retinal tolerance for ischemia is approximately 90-100 minutes
**Macula is thinnest portion of retina
*Permanent vision loss occurs in most patients despite treatment
**Intact underlying choroidal circulation remains visible through this section
*Average age: 60-65 years
***Macular area maintains normal color (red) versus surrounding ischemic, pale retina due to differing blood supplies
*Most common cause: thromboembolism from carotid artery atherosclerosis or cardiac source
*Restoration of blood flow within 100min may lead to complete recovery
**Occlusion &gt;240min leads to irreversible damage
*5-10% of CRAO is associated with giant cell arteritis<ref>Miller N, Newman N. Walsh & Hoyt’s Clinical Neuro-ophthalmology. 5th Edition. Baltimore: Williams and Wilkins 1998. pp. 3758-9.</ref>


===Etiology===
==Etiology==
*Embolism
*Carotid artery atherosclerosis (most common)
*Thrombosis
*Cardiac embolism (atrial fibrillation, valvular disease, endocarditis)
*[[Temporal Arteritis]]
*Giant cell arteritis (GCA) — '''must be excluded in patients >50'''
*Vasculitis
*Hypercoagulable states
*[[Sickle Cell Disease]]
*Vasculitis
*[[Blunt orbital trauma|Trauma]]
*Dissection of carotid or ophthalmic artery
*Vasospasm (migraine)
*[[Acute_Angle-Closure_Glaucoma|Glaucoma]]
*Low retinal blood flow ([[carotid stenosis]] or hypotension)


==Clinical Features==
==Clinical Features==
*Sudden, [[Acute vision loss (noninflamed)|painless, monocular vision loss]]
*Sudden, painless, monocular vision loss — often described as "lights went out"
**Often preceded by episodes of amaurosis fugax
*Typically develops over seconds
*Severe visual acuity loss (often counting fingers or light perception only)
*Relative afferent pupillary defect (APD / Marcus Gunn pupil)
*Fundoscopy:
**Pale/white retina with cherry-red spot at fovea (pathognomonic)
**Box-car segmentation of retinal vessels (intermittent blood flow)
**Retinal edema
*Branch RAO: visual field defect corresponding to affected branch


==Differential Diagnosis==
==Differential Diagnosis==
{{Acute vision loss noninflamed DDX}}
*[[Central retinal vein occlusion]] (hemorrhages on fundoscopy, less acute)
*[[Retinal detachment]]
*[[Optic neuritis]] (painful with eye movement)
*[[Vitreous hemorrhage]]
*[[Giant cell arteritis]] (GCA) with anterior ischemic optic neuropathy
*[[Stroke (main)|Stroke]] affecting visual cortex


==Evaluation==
==Evaluation==
*APD
*'''ESR and CRP''' — '''stat''' to evaluate for giant cell arteritis (ESR >50 in GCA)
*[[Fundoscopy]]
**If GCA suspected: start treatment immediately (see below)
**Pale retina, cherry red macula
*Fundoscopic exam — cherry-red spot diagnostic
**Boxcar segmentation of blood column
*Intraocular pressure (IOP) — rule out [[Acute angle-closure glaucoma|acute glaucoma]]
*Etiology work-up
*CT/CTA head and neck — evaluate for stroke, carotid stenosis
**ESR and CRP
**May also obtain CTA to look for embolic source
**Carotid US
*ECG — evaluate for atrial fibrillation
**ECG
*Echocardiogram — evaluate for cardiac embolic source
**Echo for embolus or atrial shunt
*Labs: CBC, BMP, coagulation studies, lipid panel, HbA1c
**CBC, coags, ANA, syphilis
*MRI with DWI — assess for concurrent acute stroke


==Management==
==Management==
;Consult ophtho with goals for reducing itraocular pressure, dislodging  the embolus or increasing arterial flow
*'''No proven treatment''' reliably restores vision; most interventions have limited evidence<ref name="mac">Mac Grory B, et al. Management of Central Retinal Artery Occlusion: A Scientific Statement From the American Heart Association. ''Stroke''. 2021;52(6):e282-e294. PMID 33843236.</ref>
 
*Traditional temporizing measures (limited evidence):
;Start high dose systemic corticosteroids if high ESR/CRP (especially high CRP) and sudden vision loss
**Ocular massage — intermittent digital pressure over closed eyelid (10-15 seconds on, 5 seconds off)
*Median starting PO [[prednisone]] 80mg/day, with 40% of patients on > 100mg/day
**Attempt to dislodge embolus distally
*Treat until BOTH ESR and CRP stabilize (~2-3 wks)<ref>Hayreh SS. Anterior Ischemic Optic Neuropathy. [Internet]. 2013 Available from: http://www.medicine.uiowa.edu/eye/AION-part2/.</ref>
*Emergent ophthalmology consultation
 
*If GCA suspected (age >50, elevated ESR, headache, jaw claudication):
No evidence supporting or refuting the following treatments: <ref>Rudkin A et al. Clinical characteristics and outcome of current standard management of central retinal artery occlusion. Clin Experiment Ophthalmol 2010; 38:496-501</ref>
**Methylprednisolone 1 g IV daily x 3 days or Prednisone 1 mg/kg PO
#Ocular massage  
**Do NOT wait for temporal artery biopsy to start treatment
#*Intermittent direct digital pressure applied through closed eyelid x 10-15 sec with rapid release to create pressure gradient to dislodge embolism
*Stroke workup: same as [[TIA]] / [[Stroke (main)|stroke]]
#[[Timolol]] ophthalmic 0.5% to decrease intraocular pressure
**Dual antiplatelet therapy, statin, carotid imaging
#*Alternative [[acetazolamide]] 500mg IV or PO<ref>Gerstenblith BI, Fecarotta CM. The Wills Eye Manual. Lippincott 2012.</ref>
*Consider emergent catheter-directed intra-arterial thrombolysis (tPA) at specialized centers if <6 hours (experimental)
#Increase PCO2 leading to retinal artery vasodilation/increased retinal blood flow 
#*Rebreathe into paper bag x10 min q hr
#*Inhale 95% O2 and 5% CO2 (Carbogen)<ref>Atebara N. Efficacy of anterior chamber paracentesis and carbogen in treating nonarteritic central retinal artery occlusion. Ophthalmology 1995; 102:2029-2038</ref>
#Anterior chamber paracentesis
#*Causes acute drop in IOP to dislodge embolism
#Intraarterial fibrinolysis or low dose systemic thrombolytics<ref>Schumacher M, et al: Central retinal artery occlusion: Local intraarterial fibrinolysis versus conservative treatment, a multicenter
randomized trial. Ophthalmology 2010; 117:1367-1375</ref><ref>Chen C et al: Efficacy of intravenous tissue-type plasminogen activator in central retinal artery occlusion: Report from a randomized, controlled trial. Stroke 2011; 42:2229-2234.</ref>
#[[Acetazolamide]], 500mg IV or PO
#[[Mannitol]]


==Disposition==
==Disposition==
 
*Admit for stroke workup (telemetry, vascular imaging, echocardiography)
*Discharge with ophtho follow up in 1-4wk
*Emergent ophthalmology consultation
*If GCA suspected: admit for IV steroids and temporal artery biopsy within 1-2 weeks
*Treat as stroke equivalent with aggressive risk factor modification


==See Also==
==See Also==
 
*[[Central retinal vein occlusion]]
*[[Acute Vision Loss (Noninflamed)]]
*[[Retinal detachment]]
*[[Stroke (main)]]
*[[Giant cell arteritis]]
*[[Acute angle-closure glaucoma]]


==References==
==References==
<references/>  
<references/>


[[Category:Ophthalmology]]
[[Category:Ophthalmology]]
[[Category:Vascular]]
[[Category:Neurology]]

Latest revision as of 09:26, 22 March 2026

Background

  • Acute interruption of blood flow to the retinal artery causing retinal ischemia
  • A stroke equivalent — 15-25% of patients will have an acute stroke or TIA within 1 week[1]
  • Ophthalmologic emergency — retinal tolerance for ischemia is approximately 90-100 minutes
  • Permanent vision loss occurs in most patients despite treatment
  • Average age: 60-65 years
  • Most common cause: thromboembolism from carotid artery atherosclerosis or cardiac source

Etiology

  • Carotid artery atherosclerosis (most common)
  • Cardiac embolism (atrial fibrillation, valvular disease, endocarditis)
  • Giant cell arteritis (GCA) — must be excluded in patients >50
  • Hypercoagulable states
  • Vasculitis
  • Dissection of carotid or ophthalmic artery

Clinical Features

  • Sudden, painless, monocular vision loss — often described as "lights went out"
  • Typically develops over seconds
  • Severe visual acuity loss (often counting fingers or light perception only)
  • Relative afferent pupillary defect (APD / Marcus Gunn pupil)
  • Fundoscopy:
    • Pale/white retina with cherry-red spot at fovea (pathognomonic)
    • Box-car segmentation of retinal vessels (intermittent blood flow)
    • Retinal edema
  • Branch RAO: visual field defect corresponding to affected branch

Differential Diagnosis

Evaluation

  • ESR and CRP — stat to evaluate for giant cell arteritis (ESR >50 in GCA)
    • If GCA suspected: start treatment immediately (see below)
  • Fundoscopic exam — cherry-red spot diagnostic
  • Intraocular pressure (IOP) — rule out acute glaucoma
  • CT/CTA head and neck — evaluate for stroke, carotid stenosis
    • May also obtain CTA to look for embolic source
  • ECG — evaluate for atrial fibrillation
  • Echocardiogram — evaluate for cardiac embolic source
  • Labs: CBC, BMP, coagulation studies, lipid panel, HbA1c
  • MRI with DWI — assess for concurrent acute stroke

Management

  • No proven treatment reliably restores vision; most interventions have limited evidence[2]
  • Traditional temporizing measures (limited evidence):
    • Ocular massage — intermittent digital pressure over closed eyelid (10-15 seconds on, 5 seconds off)
    • Attempt to dislodge embolus distally
  • Emergent ophthalmology consultation
  • If GCA suspected (age >50, elevated ESR, headache, jaw claudication):
    • Methylprednisolone 1 g IV daily x 3 days or Prednisone 1 mg/kg PO
    • Do NOT wait for temporal artery biopsy to start treatment
  • Stroke workup: same as TIA / stroke
    • Dual antiplatelet therapy, statin, carotid imaging
  • Consider emergent catheter-directed intra-arterial thrombolysis (tPA) at specialized centers if <6 hours (experimental)

Disposition

  • Admit for stroke workup (telemetry, vascular imaging, echocardiography)
  • Emergent ophthalmology consultation
  • If GCA suspected: admit for IV steroids and temporal artery biopsy within 1-2 weeks
  • Treat as stroke equivalent with aggressive risk factor modification

See Also

References

  1. ↑ Lee J, et al. Risk of stroke in patients hospitalized with central retinal artery occlusion. Stroke. 2013;44(4):967-971. PMID 23399955.
  2. ↑ Mac Grory B, et al. Management of Central Retinal Artery Occlusion: A Scientific Statement From the American Heart Association. Stroke. 2021;52(6):e282-e294. PMID 33843236.
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