Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Retinal Vein Occlusion

  • Author: Jesse Borke, MD, FACEP, FAAEM; Chief Editor: Robert E O'Connor, MD, MPH  more...
 
Updated: Jan 22, 2015
 

Background

Retinal vein occlusion (RVO) is a common vascular disorder of the retina and one of the most common causes of vision loss worldwide. Specifically, it is the second most common cause of blindness from retinal vascular disease after diabetic retinopathy. RVO has been recognized as an entity since 1855, but many aspects of the pathogenesis and management of this disorder remain uncertain. In the Canadian Journal of Ophthalmology in 2007, it was noted that "Research into CRVO is fraught with challenges, from accurate disease classification to its treatment; even the most prestigious trials have become controversial."[1]

RVO is classified according to where the occlusion is located. Occlusion of the central retinal vein at the level of the optic nerve is referred to as central retinal vein occlusion (CRVO). Occlusion at the primary superior branch or primary inferior branch involving approximately half of the retina is referred to as hemiretinal vein occlusion (HRVO). Obstruction at any more distal branch of the retinal vein is referred to as branch retinal vein occlusion (BRVO). The location of the occlusion influences the pathogenesis, clinical presentation, and management of RVO.

RVO is further subdivided into nonischemic and ischemic types, according to the amount of retinal capillary ischemia seen by the ophthalmologist on fluorescein angiography. Such a distinction is relevant to the clinician, since two thirds of patients with the ischemic type develop the dreaded complications of macular edema, macular ischemia, and neovascularization that lead to blindness. However, the two subtypes cannot always be reliably distinguished based on physical examination alone and have little bearing on the initial management in the emergency department (ED). For these reasons, the emergency physician should focus on diagnosis and recognition of the clinical scenario, so that prompt management can commence and urgent ophthalmologic evaluation obtained.

Next

Pathophysiology

RVO is essentially a blockage of a portion of the venous circulation that drains the retina. With blockage, pressure builds up in the capillaries, leading to hemorrhage and leakage of fluid and blood. This can lead to macular edema with leakage near the macula. Macular ischemia occurs when these capillaries, which supply oxygen to the retina, manifest leakage and nonperfusion. Neovascularization, new abnormal blood vessel growth, then occurs, which can result in neovascular glaucoma, vitreous hemorrhage, and, in late or severe cases, retinal detachment. Visual morbidity and blindness in RVO result from macular edema, retinal hemorrhage, macular ischemia, and neovascular glaucoma.

Intraluminal thrombus formation in RVO is associated with the venous stasis, endothelial injury, and hypercoagulability of the Virchow triad. In CRVO, the vein is typically occluded by thrombus formation consisting of fibrin and platelets at or posterior to the level of the lamina cribrosa. The inciting factor in BRVO is often compression of the adjacent vein by atherosclerotic retinal arteries at the site of AV crossing, leading to turbulent flow and venous stasis.[35, 32, 33, 34]

In both ischemic and nonischemic CRVO, blockage of the retinal vein occurs, but the nonischemic type is able to maintain better relative blood flow to the retina through collaterals. The nonischemic type of CRVO is the milder clinical presentation and accounts for 75%-80% of cases. Neovascularization is rare. Unfortunately, conversion to the ischemic type is common. The ischemic type is associated with marked decreased vision, as ischemic CRVO predisposes to anterior neovascularization called rubeosis irides, which leads to high-pressure neovascular glaucoma. Neovascularization in the posterior eye can lead to vitreous hemorrhage and retinal detachment.

Previous
Next

Epidemiology

Frequency

United States

Central retinal vein occlusion

Most patients with CRVO are older than 65 years. Most cases are unilateral, with approximately 6%-14% of cases bilateral. A study in Taiwan in 2008 noted a seasonal variation of CRVO, with a peak incidence occurring during the month of January.[2]

Branch retinal vein occlusion

BRVO is 3 times more common than CRVO. Men and women are affected equally, with the bulk of presentations between age 60 and 70 years.

International

A large population-based study in Israel reported a 4-year incidence of RVO of 2.14 cases per 1000 of general population older than 40 years and 5.36 cases per 1000 of general population older than 64 years.

In Australia, the prevalence of RVO ranges from 0.7% in patients aged 49-60 years to 4.6% in patients older than 80 years.

Mortality/Morbidity

The primary concern is vision loss; the morbidity of this disorder depends on the location of the occlusion and the degree of ischemia.

Neovascularization can result in neovascular glaucoma, vitreous hemorrhage, and, in late or severe cases, retinal detachment. Visual morbidity and blindness in RVO result from macular edema, retinal hemorrhage, macular ischemia, and neovascular glaucoma.

Central retinal vein occlusion/hemiretinal vein occlusion

The Central Venous Occlusion Study (CVOS) has helped to define visual loss morbidity in CRVO. Visual recovery in the study was found to vary, with the presenting visual acuity the best predictor of final visual acuity.[39] Sixty-five percent of eyes with an initial acuity of 20/40 or higher had the same or better visual acuity on final evaluation. In contrast to this, only 20% of patients who presented with an initial acuity of less than 20/200 had any significant improvement in final visual acuity. HRVO generally has an outcome similar to that of CRVO.

Patients with ischemic CRVO are much more likely to have poor visual acuity, both at initial presentation and final visual acuity, compared to those with the nonischemic type.[36]

Branch retinal vein occlusion

Patients with nonmacular BRVO may be asymptomatic, and normal visual acuity is the rule. Patients with macular involvement or edema from BRVO may have mild to (rarely) severely decreased visual acuity that may spontaneously improve within the first 3 months or so after the episode.

Race

A large 2010 study reported the prevalence of BRVO to be 2.8 per 1000 in whites, 3.5 in blacks, 5.0 in Asians, and 6.0 in Hispanics and the prevalence of CRVO to be 0.88 per 1000 in whites, 0.37 in blacks, 0.74 in Asians, and 1.0 in Hispanics.[37]

Sex

A population cohort study showed no significant difference between men and women in terms of incidence.[38]

Age

The prevalence of all types of RVO increases with age. Most CRVOs are seen in patients older than 65 years. Most BRVOs are seen in patients greater than 50 years old, with the highest rate of occurrence during the seventh and eighth decades of live. This age stratification is likely due to the association of age with atherosclerosis. When RVO is seen in younger patients, they are more likely to have an underlying coagulopathy, and patients younger than 45-50 years who lack identifiable cardiovascular risk factors should be screened for coagulopathy.

Previous
 
 
Contributor Information and Disclosures
Author

Jesse Borke, MD, FACEP, FAAEM Medical Director, Emergency Department, Lakeview Hospital; Director of Process Improvement and Throughput, Kaleida Health Millard Fillmore Suburban

Jesse Borke, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Audrey Tai, DO, MS Resident Physician, Department of Ophthalmology, University of Buffalo State University of New York School of Medicine and Biomedical Sciences

Audrey Tai, DO, MS is a member of the following medical societies: American Academy of Ophthalmology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Douglas Lavenburg, MD Clinical Professor, Department of Emergency Medicine, Christiana Care Health Systems

Douglas Lavenburg, MD is a member of the following medical societies: American Society of Cataract and Refractive Surgery

Disclosure: Nothing to disclose.

Chief Editor

Robert E O'Connor, MD, MPH Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Association for Physician Leadership, American Heart Association, Medical Society of Delaware, Society for Academic Emergency Medicine, Wilderness Medical Society, American Medical Association, National Association of EMS Physicians

Disclosure: Nothing to disclose.

Acknowledgements

Mark Fonrose, MD, FACEP Assistant Professor of Emergency Medicine, Kings County Hospital Center/State University of New York

Mark Fonrose, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Richard J Spitz, MD Staff Physician, Assistant Professor of Emergency Medicine, Department of Surgery, Division of Emergency Medicine, University Of Texas Health Science Center

Disclosure: Nothing to disclose.

Loice Swisher, MD Assistant Professor, Department of Emergency Medicine, Mercy Hospital of Philadelphia

Disclosure: Nothing to disclose.

References
  1. Madhusudhana KC, Newsom RS. Central retinal vein occlusion: the therapeutic options. Can J Ophthalmol. 2007 Apr. 42(2):193-5. [Medline].

  2. Ho JD, Tsai CY, Liou SW, et al. Seasonal variations in the occurrence of retinal vein occlusion: a five-year nationwide population-based study from Taiwan. Am J Ophthalmol. 2008 Apr. 145(4):722-728. [Medline].

  3. D'Amico DJ, Lit ES, Viola F. Lamina puncture for central retinal vein occlusion: results of a pilot trial. Arch Ophthalmol. 2006 Jul. 124(7):972-7. [Medline].

  4. Jonas JB, Harder B. Ophthalmodynamometric differences between ischemic vs nonischemic retinal vein occlusion. Am J Ophthalmol. 2007 Jan. 143(1):112-6. [Medline].

  5. Ascaso FJ, Padgett E, Núñez E, Villén L, Grzybowski A, Cristóbal JA. Branch retinal vein occlusion and vitreovascular traction: a preliminary spectral domain OCT case-control study. Graefes Arch Clin Exp Ophthalmol. 2014 Mar. 252(3):375-81. [Medline].

  6. Weis E, Gan KD, Hinz BJ, et al. A retrospective cohort study of radial optic neurotomy for severe central retinal vein occlusions. Can J Ophthalmol. 2008 Feb. 43(1):73-8. [Medline].

  7. Raja MS, Goldsmith C. Interventions for CRVO. Ophthalmology. 2008 Jan. 115(1):219; author reply 219-20. [Medline].

  8. Vitreous-Retina-Macula Consultants of New York. Retinal Venous occlusive Disease: Branch Retinal Occlusion/Central Retinal Occlusion. Available at www.vrmny.com. Accessed: April 2008.

  9. Kinge B, Stordahl PB, Forsaa V, Fossen K, Haugstad M, Helgesen OH, et al. Efficacy of ranibizumab in patients with macular edema secondary to central retinal vein occlusion: results from the sham-controlled ROCC study. Am J Ophthalmol. 2010 Sep. 150(3):310-4. [Medline].

  10. Yamamoto T, Kamei M, Sayanagi K, Matsumura N, Nishida K, Sakaguchi H. Simultaneous intravitreal injection of triamcinolone acetonide and tissue plasminogen activator for central retinal vein occlusion: a pilot study. Br J Ophthalmol. 2011 Jan. 95(1):69-73. [Medline].

  11. Farahvash MS, Moghaddam MM, Moghimi S, et al. Dalteparin in the management of recent onset central retinal vein occlusion: a comparison with acetylsalicylic acid. Can J Ophthalmol. 2008 Feb. 43(1):79-83. [Medline].

  12. Wright JK, Franklin B, Zant E. Clinical case report: treatment of a central retinal vein occlusion with hyperbaric oxygen. Undersea Hyperb Med. 2007 Sep-Oct. 34(5):315-9. [Medline].

  13. Ozdek S, Deren YT, Gurelik G, et al. Posterior subtenon triamcinolone, intravitreal triamcinolone and grid laser photocoagulation for the treatment of macular edema in branch retinal vein occlusion. Ophthalmic Res. 2008. 40(1):26-31. [Medline].

  14. Kawaji T, Takano A, Inomata Y, et al. Trans-Tenon's retrobulbar triamcinolone acetonide injection for macular oedema related to branch retinal vein occlusion. Br J Ophthalmol. 2008 Jan. 92(1):81-3. [Medline].

  15. Papadia M, Misteli M, Jeannin B, Herbort CP. The influence of anti-VEGF therapy on present day management of macular edema due to BRVO and CRVO: a longitudinal analysis on visual function, injection time interval and complications. Int Ophthalmol. 2014 Sep 23. [Medline].

  16. Sarao V, Bertoli F, Veritti D, Lanzetta P. Pharmacotherapy for treatment of retinal vein occlusion. Expert Opin Pharmacother. 2014 Sep 5. 1-12. [Medline].

  17. Batioglu F, Astam N, Ozmert E. Rapid improvement of retinal and iris neovascularization after a single intravitreal bevacizumab injection in a patient with central retinal vein occlusion and neovascular glaucoma. Int Ophthalmol. 2008 Feb. 28(1):59-61. [Medline].

  18. Binder S, Aggermann T, Brunner S. Long-term effects of radial optic neurotomy for central retinal vein occlusion consecutive interventional case series. Graefes Arch Clin Exp Ophthalmol. 2007 Oct. 245(10):1447-52. [Medline].

  19. Ferrara DC, Koizumi H, Spaide RF. Early bevacizumab treatment of central retinal vein occlusion. Am J Ophthalmol. 2007 Dec. 144(6):864-71. [Medline].

  20. Gandhi JS. Natural history of non-ischemic central retinal vein occlusion versus iatrogenic intervention. J Postgrad Med. 2007 Oct-Dec. 53(4):270; author reply 270-1. [Medline].

  21. Gumus K, Kadayifcilar S, Eldem B, et al. Assessment of the role of thrombin activatable fibrinolysis inhibitor in retinal vein occlusion. Retina. 2007 Jun. 27(5):578-83. [Medline].

  22. Hasselbach HC, Ruefer F, Feltgen N, et al. Treatment of central retinal vein occlusion by radial optic neurotomy in 107 cases. Graefes Arch Clin Exp Ophthalmol. 2007 Aug. 245(8):1145-56. [Medline].

  23. Keith S, Humphries R. Current Diagnosis & Treatment of Emergency Medicine. 6th ed. McGraw-Hill Co; 2008.

  24. Koizumi H, Ferrara DC, Brue C, et al. Central retinal vein occlusion case-control study. Am J Ophthalmol. 2007 Dec. 144(6):858-863. [Medline].

  25. Kreutzer TC, Alge CS, Wolf AH, et al. Intravitreal bevacizumab for the treatment of macular oedema secondary to branch retinal vein occlusion. Br J Ophthalmol. 2008 Mar. 92(3):351-5. [Medline].

  26. Leoncini G, Bruzzese D, Signorello MG, et al. Platelet activation by collagen is increased in retinal vein occlusion. Thromb Haemost. 2007 Feb. 97(2):218-27. [Medline].

  27. Mohamed Q, McIntosh RL, Saw SM, et al. Interventions for central retinal vein occlusion: an evidence-based systematic review. Ophthalmology. 2007 Mar. 114(3):507-19, 524. [Medline].

  28. Morley M, Heier J. Ophthalmology. Part 8; Section 5. 2nd ed. Mosby; 2004.

  29. Recchia FM, Chen E, Li C, et al. Use of cox-2 inhibitors in patients with retinal venous occlusive disease. Retina. 2008 Jan. 28(1):134-7. [Medline].

  30. Sodi A, Giambene B, Marcucci R, et al. Atherosclerotic and thrombophilic risk factors in patients with recurrent central retinal vein occlusion. Eur J Ophthalmol. 2008 Mar-Apr. 18(2):233-8. [Medline].

  31. Bowers DK, Finkelstein D, Wolff SM, Green WR. Branch retinal vein occlusion. A clinicopathologic case report. Retina. 1987. 7(4):252-9. [Medline].

  32. Zhao J, Sastry SM, Sperduto RD, Chew EY, Remaley NA. Arteriovenous crossing patterns in branch retinal vein occlusion. The Eye Disease Case-Control Study Group. Ophthalmology. 1993 Mar. 100(3):423-8. [Medline].

  33. Green WR, Chan CC, Hutchins GM, Terry JM. Central retinal vein occlusion: a prospective histopathologic study of 29 eyes in 28 cases. Retina. 1981. 1(1):27-55. [Medline].

  34. Newman-Casey PA, Stem M, Talwar N, Musch DC, Besirli CG, Stein JD. Risk factors associated with developing branch retinal vein occlusion among enrollees in a United States managed care plan. Ophthalmology. Oct. 121:1939-48.

  35. Hayreh SS, Podhajsky PA, Zimmerman MB. Natural history of visual outcome in central retinal vein occlusion. Ophthalmology. 2011 Jan. 118(1):119-133.e1-2. [Medline]. [Full Text].

  36. Rogers S, McIntosh RL, Cheung N, Lim L, Wang JJ, Mitchell P. The prevalence of retinal vein occlusion: pooled data from population studies from the United States, Europe, Asia, and Australia. Ophthalmology. 2010 Feb. 117(2):313-9.e1. [Medline].

  37. Klein R, Klein BE, Moss SE, Meuer SM. The epidemiology of retinal vein occlusion: the Beaver Dam Eye Study. Trans Am Ophthalmol Soc. 2000. 98:133-41; discussion 141-3. [Medline]. [Full Text].

  38. Natural history and clinical management of central retinal vein occlusion. The Central Vein Occlusion Study Group. Arch Ophthalmol. 1997 Apr. 115(4):486-91. [Medline].

  39. Mohamed Q, McIntosh RL, Saw SM, Wong TY. Interventions for central retinal vein occlusion: an evidence-based systematic review. Ophthalmology. 2007 Mar. 114(3):507-19, 524. [Medline].

 
Previous
Next
 
A: Central retinal vein occlusion (CRVO). B: Hemiretinal retinal vein occlusion (HRVO). C: Branch retinal vein occlusion (CRVO).
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.