Rosen & Barkin's 5-Minute Emergency Medicine Consult (142 page)

DIAGNOSIS

• Sudden, painless, monocular loss of vision
  
• Prior episodes of sudden visual loss:
  
  • May last a few seconds to minutes (amaurosis fugax)
    
  • Caused by transient embolic phenomena or decreased ocular blood flow
    

• Significantly decreased visual acuity
  
• Afferent pupillary defect usually present
  
• Retinal appearance:
  
  • Emboli visualized within vascular tree of the retina
    
  • Appears as glinting white or yellow flecks (Hollenhorst plaques) within the vessels
    
  • Ischemic edema visible within 15–20 min of occlusion
    
  • “Cherry-red spot” remains over the fovea (only area where there is very thin retina allowing the vascular choroids to show through).
    
  • Affected arteries empty or showing dark red stationary or barely pulsatile segmented rouleaux (“box-carring”)
    
  • Within 1–2 hr opacification of the usually transparent infarcting retinal nerve layer occurs.
    
• Partial field deficits:
  
  • Occur only if branch of central retinal artery involved
    

• Visual acuity and visual field testing
  
• Fundoscopic exam
  
• Intraocular pressure measurements
  
• Emergent ophthalmologic consultation
  

Directed toward evaluating underlying etiology of occlusion:

• CBC with differential and platelet count
  
• PT/PTT
  
• Electrolytes, BUN/creatinine, glucose
  
• Electronic spin resonance for giant cell arteritis (in patients >55 yr old)
  
• ANA, RF, CRP, ESR
  
• Rapid plasma reagin (RPR)
  
• Hemoglobin electrophoresis
  
• Serum protein electrophoresis
  

Directed toward evaluating underlying etiology of occlusion:

• Carotid artery ultrasound/Doppler
  
• Possibly echocardiography
  
• Fluorescein angiography or electroretinography to confirm the diagnosis
  

• Acute angle-closure glaucoma
  
• Central retinal vein occlusion
  
• Giant cell arteritis (temporal arteritis)
  
• Optic neuritis
  
• Retinal detachment
  

TREATMENT

• Immediate global massage in an attempt to dislodge the embolus:
  
  • Lay patient flat and apply digital global massage bolus.
    
  • On closed eyelid, apply constant pressure for 15 sec and remove for 15 sec. Repeat for 5 cycles.
    
• Initiate high-flow oxygen via 100% nonrebreather:
  
  • Consider transfer to a facility capable of providing hyperbaric oxygen (HBO) if <24 hr from symptom onset
    
  • May use inhaled carbogen (a mixture of carbon dioxide and oxygen gas) if available
    
• Administer IV acetazolamide to decrease intraocular pressure.
  
• Apply topical timolol maleate to reduce intraocular pressure.
  
• Administer aspirin and IV heparin for prevention of clot propagation.
  
• Obtain emergent ophthalmology consultation for:
  
  • Anterior chamber paracentesis to help reduce intraocular pressure
    
  • Possible intra-arterial fibrinolysis for clot lysis
    
• Administer high-dose systemic steroids in suspected cases of inflammatory arteritis.
  

• Acetazolamide: 500 mg IV or PO
  
• Carbogen: Inhalation of 95% oxygen and 5% carbon dioxide mixture
  
• Heparin: 80 U/kg IV bolus then 18 U/kg/h continuous infusions (rate adjusted based on PTT level)
  
• Timolol maleate 0.5% solution: 1 drop topically to affected eye
  

• Methylprednisolone: 250 mg IV in suspected cases of inflammatory arteritis
  
• Aspirin: 325 mg PO
  
• Mannitol
  
• Sublingual nitroglycerin
  

FOLLOW-UP

Required for workup of proximal cause in acute cases (source of embolism, thrombosis, or inflammatory)

Chronic retinal artery occlusion with no evidence of active disease can be worked up as an outpatient.

All suspected cases warrant emergent ophthalmology consultation.

Most cases will require carotid ultrasound to exclude atherosclerotic disease.

• Amaurosis fugax (transient, possibly resolved retinal artery occlusion) is a sentinel event and may lead to complete occlusion or stroke. Do not ignore these symptoms and urgent workup is required.
  
• Retinal artery occlusion is a medical emergency requiring immediate treatment to prevent loss of the eye.
  
• It is important to document a full eye exam including visual acuity and evaluation of the optic fundus.
  

• Arnold M, Koerner U, Remonda L, et al. Comparison of intra-arterial thrombolysis with conventional treatment in patients with acute central retinal artery occlusion.
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  . 2005;76(2):196–199.
  
• Fraser SG, Adams W. Interventions for acute non-arteritic central retinal artery occlusion.
  Cochrane Database Syst Rev
  . 2009;(1):CD001989.
  
• Hazin R, Daoud YJ, Khan F. Ocular ischemic syndrome: Recent trends in medical management.
  Curr Opin Ophthalmol
  . 2009;20:430–433.
  
• Murphy-Lavoie H, Butler F, Hagan C. Central retinal artery occlusion treated with oxygen: a literature review and treatment algorithm.
  Undersea Hyperb Med.
  2012;39(5):943–953.
  
• Vortmann M, Schneider JL. Acute monocular visual loss.
  Emerg Med Clin North Am
  . 2008;26(1):73–96.
  

See Also (Topic, Algorithm, Electronic Media Element)

• Central Retinal Venous Occlusion
  
• Visual Loss
  

CODES

362.31 Central retinal artery occlusion

BASICS

Disease characterized by decreased visual acuity resulting from venous occlusion of any etiology

• Ischemic CRVO:
  
  • 20–25% of cases
    
  • Blocked venous return leads to backflow in capillaries, hemorrhage, and macular edema.
    
  • Limited space at lamina cribrosa predisposes to thrombosis due to slow flow and vessel wall changes
    
  • Theorize that arteriosclerotic changes in the adjacent artery may impinge upon the vein.
    
  • Blood viscosity also thought to play a role
    
• Nonischemic CRVO:
  
  • Milder, incomplete occlusion