eMedicine Specialties > Ophthalmology > Retina

Branch Retinal Vein Occlusion: Treatment & Medication

Author: Lihteh Wu, MD, Consulting Surgeon, Department of Ophthalmology, Vitreo-Retinal Section, Instituto De Cirugia Ocular, Costa Rica
Coauthor(s): Teodoro Evans, MD, Retina Fellow, Vitreo-Retinal Section, Instituto De Cirugia Ocular, Costa Rica
Contributor Information and Disclosures

Updated: Jul 20, 2007

Treatment

Medical Care

Medical treatment is not effective in this condition. In the past, anticoagulants, fibrinolytic agents, clofibrate capsules (Atromid-S), and carbogen inhalation have been used but without success.

Hemodilution has been proposed as an alternative treatment for BRVO by lowering the hematocrit and plasma viscosity and by improving retinal perfusion. However, the true benefit of hemodilution has not been established because published reports have used combination therapy in the hemodilution group.

Intravitreal injection of triamcinolone has been used to treat macular edema of different etiologies because of its potent antipermeability and anti-inflammatory properties. A few cases of macular edema secondary to BRVO treated with an intravitreal triamcinolone injection have been reported. The exact dose remains unclear. Doses from 4 mg to 25 mg have been reported to be effective. Multiple doses appear to be needed. Therefore, a biodegradable, longer-acting intravitreal implant of dexamethasone is currently under investigation. Preliminary results are promising. Complications resulting from corticosteroid therapy include cataract formation, elevation of intraocular pressure, infectious endophthalmitis, noninfectious endophthalmitis, and retinal detachment. Further study is warranted to define what role, if any, intravitreal corticosteroids have in the management of macular edema secondary to BRVO.

Vascular endothelial growth factor (VEGF) is a potent inductor of vascular permeability and intraocular neovascularization. In humans, the aqueous levels of VEGF and interleukin 6 (IL-6) are correlated with the degree of retinal ischemia and the severity of macular edema in BRVO. Therefore, VEGF inhibition appears to be a promising treatment modality for macular edema.  

Two small prospective case series of 7 eyes and 12 eyes, respectively, with macular edema secondary to BRVO were treated with a single intravitreal injection of 1.25 mg of bevacizumab. All eyes had decreased central macular thickness and improvement of visual acuity 1 month after the injection. However, the effect was not sustained, and, by 6 weeks, recurrence of the edema was noted in most eyes.

Schaal and colleagues injected 22 eyes with 2.5 mg of bevacizumab and followed them prospectively for an average of 23 weeks.44 Eyes with recurrent or persistent macular edema were reinjected. At the last follow-up visit, 76% of eyes gained greater than or equal to 3 lines of visual acuity. The central macular thickness improved from 678 µm at baseline to 236 µm at the last follow-up visit. They reported an average of 2.5 injections per eye.

In a retrospective review of 27 patients that had a mean of 5.3 months of follow-up, Rabena and colleagues reported that eyes were injected with 1.25 mg of bevacizumab at baseline and reinjected if recurrent or persistent edema was present.40 They found that the mean visual acuity improved from 20/200 to 20/100 at the last follow-up visit. The mean central 1-mm macular thickness decreased from 478 µm at baseline to 332 µm at the last follow-up visit. The average number of injections in their study was 2.

Surgical Care

BRVOs have a relatively benign course. Nevertheless, certain complications that lead to visual loss may occur. These complications include macular edema and the sequelae from retinal neovascularization (eg, vitreous hemorrhage, tractional retinal detachment, neovascular glaucoma). Several surgical and laser techniques are available to deal with these situations.

  • Macular grid laser photocoagulation

    • Macular grid laser photocoagulation was mildly effective in the treatment of macular edema in a small prospective trial, the BVOS.
    • The current recommendation is to wait 3 months to see if the patient's vision spontaneously improves.
    • If no improvement occurs and if the hemorrhages have mostly cleared from the macular area, a fluorescein angiogram is obtained. If the angiogram shows leakage in the macular area that is responsible for the decrease in vision, treatment with a macular grid laser is recommended. After 3 years of follow-up care, 63% of laser treated eyes improved by 2 or more lines of vision compared with 36% of control eyes.
    • Despite macular photocoagulation, eyes gained on average 1.33 lines of vision with respect to baseline. At the 3-year follow-up, 40% of eyes had a visual acuity of less than 20/40 and 12% of eyes had a visual acuity of less than 20/200.
    • If the fluorescein angiogram reveals macular nonperfusion, laser therapy is not warranted, and observation is recommended. Finkelstein reported that eyes with macular nonperfusion have a good visual prognosis.14 In his series, the median visual acuity was 20/30.
  • Scatter photocoagulation

    • The BVOS also demonstrated that scatter photocoagulation reduces the prevalence of neovascularization from 40% to 20%.
    • However, if all eyes with nonperfusion were treated, 60% of patients who would never develop neovascularization would be treated.
    • If only the eyes that develop neovascularization were treated, the events of vitreous hemorrhage would decrease from 60% to 30%.
    • Therefore, the recommendation is to wait until neovascularization actually develops before scatter photocoagulation is considered.
  • Laser-induced chorioretinal anastomosis

    • Bypass of the normal retinal venous drainage channels is attempted by creating a communication between the obstructed vessel and the choroid.
    • Problems with this technique are the lack of reliability in creating an anastomosis (most groups report a 30-50% success rate) and its complications. Complications from the procedure include tractional retinal detachment and vitreous hemorrhage.
  • Vitrectomy and arteriovenous decompression

    • Virtually all cases of BRVO occur at arteriovenous crossings.
    • Because arterial compression is believed to be the major cause of this condition, some have recommended lifting the artery from the underlying vein to relieve the compression.
    • Several small, uncontrolled series have shown good results in improving macular edema and macular perfusion. However, others have reported a lack of efficacy of this procedure. Planning of a multicenter controlled trial is currently underway.
  • Several surgeons have reported resolution of macular edema secondary to BRVO after vitrectomy with or without peeling of the internal limiting membrane.
  • Pars plana vitrectomy techniques with or without scleral buckling may be necessary in eyes with tractional and rhegmatogenous retinal detachments.

Consultations

  • Consult a vitreoretinal specialist if complications arise.
  • In atypical cases where a thrombophilic condition is suspected, consultation with a hematologic specialist is recommended.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Corticosteroids

Have potent anti-inflammatory and antipermeability properties.


Triamcinolone (Kenalog-40)

Through its antipermeability properties secondary to its anti-VEGF effects, strengthens blood retinal barrier and prevents its disruption.

Adult

4 mg Intravitreally is most common dose because easy to aliquot and inject 0.1 cc from commercially available 40 mg/mL vial; apart from convenience of dosing, no studies support this dose over any other dose

Pediatric

Not established

Documented hypersensitivity; fungal, viral, and bacterial skin infections

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Complications include progression of nuclear sclerosis, increased intraocular pressure, retinal detachments, sterile endophthalmitis, and infective endophthalmitis; after 4-6 wk of topical corticosteroid use, 5% of eyes develop elevated intraocular pressure >16 mm Hg, and 30% develop intraocular pressure elevation of 6-15 mm Hg; unclear how long it takes for intraocular pressure to rise following initial intravitreal injection; unknown what effect initial dose, frequency of reinjection, or cumulative corticosteroid dose has on intraocular pressure; all reported studies show that 4-mg dose and 25-mg dose appear to have similar effect on intraocular pressure; most treated eyes respond to topical antiglaucoma medication but few may require filtering procedures; cataract formation appears to be associated with rise in intraocular pressure (most cataracts develop slowly; posterior subcapsular cataracts appear to be more common); to avoid endophthalmitis, use one vial per eye and sterile technique (endophthalmitis occurs in approximately 0.1% of injections)

Antineoplastic Agent, Monoclonal Antibody

Nonspecific monoclonal anti-VEGF angiogenesis that targets and inhibits vascular endothelial growth factor (VEGF) activity.


Bevacizumab (Avastin)

Murine derived monoclonal antibody that inhibits angiogenesis by targeting and inhibiting VEGF. Inhibiting new blood vessel formation denies blood, oxygen, and other nutrients needed for tumor growth.

Adult

Not established; 1.25-2.5 mg reported in literature

Pediatric

Not established

Coadministration with 5-fluorouracil increases incidence (2-fold) of serious and fatal arterial thromboembolic events (ie, CVA, MI, TIAs, angina)

Pregnancy

C - Safety for use during pregnancy has not been established

Precautions

Common adverse effects include hypertension, fatigue, thrombosis, diarrhea, leukopenia, proteinuria, headache, anorexia, and stomatitis; may cause serious or fatal, but rare events, including gastrointestinal perforation, intra-abdominal infections, impaired wound healing, hemoptysis (particularly with lung cancers), reversible posterior leukoencephalopathy syndrome (RPLS), nasal septum perforation, and internal bleeding; increases risk of serious and fatal arterial thrombotic events with 5-fluorouracil; do not initiate treatment for at least 28 days following major surgery, the surgical incision should be fully healed; breastfeeding should be discontinued during and for at least 20 d following treatment with bevacizumab; all women with child bearing potential have to have a negative pregnancy test prior to treatment

More on Branch Retinal Vein Occlusion

Overview: Branch Retinal Vein Occlusion
Differential Diagnoses & Workup: Branch Retinal Vein Occlusion
Treatment & Medication: Branch Retinal Vein Occlusion
Follow-up: Branch Retinal Vein Occlusion
Multimedia: Branch Retinal Vein Occlusion
References
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Further Reading

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Keywords

BRVO, branch retinal vein obstruction, retinal tributary vein occlusion, retinal vein occlusions, retinal vascular diseases, retinal endothelial vascular damage, arterial compression, central retinal vein occlusions, hemiretinal vein occlusions

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Contributor Information and Disclosures

Author

Lihteh Wu, MD, Consulting Surgeon, Department of Ophthalmology, Vitreo-Retinal Section, Instituto De Cirugia Ocular, Costa Rica
Lihteh Wu, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Association for Research in Vision and Ophthalmology, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

Coauthor(s)

Teodoro Evans, MD, Retina Fellow, Vitreo-Retinal Section, Instituto De Cirugia Ocular, Costa Rica
Disclosure: Nothing to disclose.

Medical Editor

Vytautas A Pakainis, MD, Chief of Ophthalmology, Dorn Veterans Administration Medical Center, Professor of Ophthalmology, Ophthalmology, University of South Carolina School of Medicine
Vytautas A Pakainis, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and South Carolina Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Steve Charles, MD, Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine
Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Macula Society, and Retina Society
Disclosure: Alcon Laboratories Consulting fee Consulting

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

 
 
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