Rosen & Barkin's 5-Minute Emergency Medicine Consult (143 page)

DIAGNOSIS

Classic description:

• Acute, unilateral, painless vision loss
  
• “Blood and thunder” appearance on fundoscopy
  

• Painless, unilateral vision loss
  
• If nonischemic, may be incomplete and intermittent vision loss
  

• Decreased visual acuity:
  
  • Usually worse than 20/200
    
• Afferent pupillary defect
  
• Dilated tortuous veins
  
• Retinal hemorrhages:
  
  • If central, findings in all 4 quadrants
    
  • Extensive hemorrhages give a dramatic look to fundus classically described as “blood and thunder appearance.”
    
• Disk edema
  
• Cotton wool spots
  

• BP
  
• Visual acuity:
  
  • Hand movements typically is all that is seen.
    
• Visual fields
  
• Fundoscopy
  
• Tonometry:
  
  • Normal pressures are between 10 and 21 mm Hg.
    

• CBC
  
• PT/PTT
  
• ESR
  
• ANA
  
• Serum protein electrophoresis
  

Fluorescein angiography:

• Ophthalmologists use this to map areas of nonperfusion.
  
• Differentiates between ischemic and nonischemic
  

Gonioscopy:

• Measure iris or angle neovascularization.
  

• Amaurosis fugax/transient ischemic attack
  
• Cavernous sinus thrombosis
  
• DM
  
• HTN/hypertensive retinopathy
  
• Hyperviscosity syndromes:
  
  • Sickle cell, polycythemia, leukemia, multiple myeloma
    
• Hysterical blindness
  
• Ocular ischemia syndrome
  
• Papilledema
  
• Retinal artery occlusion
  
• Retinal detachment
  
• Severe anemia with thrombocytopenia
  
• Temporal arteritis
  
• Vitreal hemorrhage
  

TREATMENT

No specific interventions need occur prior to arrival at the hospital in regard to the eye.

• Initiate steps to lower intraocular pressure (IOP) if it is elevated.
  
• Treat underlying medical problems.
  

• Recognition and prompt ophthalmologic referral is the cornerstone of ED treatment.
  
• Though not proven, the following may be tried in consultation with an ophthalmologist:
  
  • Aspirin
    
  • Anti-inflammatory agents
    
  • Systemic steroids
    
  • Systemic anticoagulation
    
  • Fibrinolytics (controversial)
    
  • Laser chorioretinal anastomosis
    

There is no proven treatment for CRVO, ophthalmologists may treat with the following:

• Intravitreal triamcinolone
  
• Antivascular endothelial growth factor:
  
  • Bevacizumab
    

Use of oral contraceptives can increase the risk of CRVO.

FOLLOW-UP

Patients may be admitted for surgical intervention, depending upon the ophthalmologist.

Patients can be discharged from the ED as long as they have immediate follow-up with an ophthalmologist.

• If no ophthalmologist is available, treatment should be initiated for concomitant conditions and patient transferred to nearest hospital with ophthalmologic consultation.
  
• Ophthalmologists often perform panretinal photocoagulation if neovascularization is found.
  

• Patients with ischemic CRVO need prolonged follow-up to catch neovascularization and glaucoma that typically develop.
  
• Patients with CRVO likely have other vascular diseases and need complete medical workups.
  
• Patients should also follow with an internist to manage comorbidities and risk factors.
  

• Increased IOP resulting from neovascularization and edema can cause vascular insufficiency and with delayed treatment vision loss can be permanent.
  
• When patients present with bilateral CRVOs or CRVO at a young age, workup must search for hyperviscosity syndromes.
  

• Beran DI, Murphy-Lavoie H. Acute painless vision loss.
  J La State Med Soc
  . 2009;161(4):214–223.
  
• Di Capua M, Coppola A, Albisinni R, et al. Cardiovascular risk factors and outcome in patients with retinal vein occlusion.
  J Thromb Thrombolysis
  . 2009.
  
• Khare GD, Symons RC, Do DV, et al. Common ophthalmologic emergencies.
  Int J Clin Pract
  . 2008;62(11):1776–1784.
  
• Marx JA, Hockberger RS, Walls RM, eds.
  Rosen’s Emergency Medicine: Concepts and Clinical Practice
  . 7th ed. St. Louis, MO: Mosby; 2010.
  
• McAllister IL. Central retinal vein occlusion: A review.
  Clin Experiment Ophthalmol.
  2012;40(1):48–58.
  
• Turello M, Pasca S, Daminato R, et al. Retinal vein occlusion: Evaluation of “classic” and “emerging” risk factors and treatment.
  J Thromb Thrombolysis
  . 2009.
  
• Yanoff M, Duker J.
  Ophthalmology
  . 3rd ed. St. Louis, MO: Mosby; 2008.
  

See Also (Topic, Algorithm, Electronic Media Element)

• Central Retinal Artery Occlusion
  
• Visual Loss
  

CODES

362.35 Central retinal vein occlusion

BASICS

• Abnormal, localized dilation or outpouching of cerebral artery wall:
  
  • Occurs in 5–10% of population
    
• Rupture of saccular aneurysms account for 5–15% of strokes
  
• Of those that rupture:
  
  • 40% occur at anterior communicating artery (ACA)
    
  • 30% at internal carotid (IC)
    
  • 20% in middle cerebral artery (MCA)
    
  • 5–10% in vertebrobasilar artery (VBA) system
    

• Asymptomatic in 3.2% of population
  
• “Congenital,” saccular, or berry aneurysms most common (90%):
  
  • Develop at weak points in arterial wall and bifurcations of major cerebral arteries
    
  • Incidence increases with age
    
  • Multiple in 20–30%
    
  • Increased incidence:
    
    • Polycystic kidney disease
      
    • Cerebral arteriovenous malformation
      
    • Type III collagen deficiency
      
    • Fibromuscular dysplasia
      
    • Ehlers–Danlos syndrome
      
    • Marfan syndrome
      
    • Pseudoxanthoma elasticum
      
    • Neurofibromatosis
      
    • Moyamoya syndrome
      
    • Coarctation of the aorta
      
    • Tuberous sclerosis
      
    • Sickle cell disease
      
    • Osler–Weber–Rendu syndrome
      
    • α1-Antitrypsin deficiency
      
    • Systemic lupus erythematosus
      
    • Glucocorticoid remediable hyperaldosteronism
      
• Arteriosclerotic, fusiform, or dolichoectatic (7%):
  
  • More common in peripheral arteries
    
• Inflammatory (mycotic):
  
  • 10% of patients with bacterial endocarditis
    
• Traumatic, associated with severe closed head injury
  
• Neoplastic, embolized tumor fragments
  
• Familial correlation: 1st-degree relative with history of aneurysm essentially doubles lifetime risk