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Symptoms ⬇

Blind spot in the visual field or loss of vision, usually unilateral.

Signs ⬆ ⬇

(See Figure 11.9.1.)

Critical

Superficial hemorrhages in a sector of the retina along a retinal vein. The hemorrhages usually do not cross the horizontal raphe (midline).

Other

CWSs, retinal edema, a dilated and tortuous retinal vein, narrowing and sheathing of the adjacent artery, retinal neovascularization, VH.

11-9.1 Branch retinal vein occlusion.

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Differential Diagnosis ⬆ ⬇

  • Diabetic retinopathy: Dot-blot hemorrhages and microaneurysms extend across the horizontal raphe. Nearly always bilateral. See 11.12, DIABETIC RETINOPATHY.
  • Hypertensive retinopathy: Narrowed retinal arterioles. Hemorrhages are not confined to a sector of the retina and usually cross the horizontal raphe. Bilateral in most. See 11.10, HYPERTENSIVE RETINOPATHY.

Etiology ⬆ ⬇

Disease of the adjacent arterial wall (usually secondary to HTN, arteriosclerosis, or diabetes) compresses the venous wall at a crossing point.

Reference(s) ⬆ ⬇

Campochiaro PA, Heier JS, Feiner L, et al. Ranibizumab for macular edema following branch retinal vein occlusion: six-month primary end point results of a phase III study. Ophthalmology. 2010;117(6):1102-1112.Varma R, Bressler NM, Suñer I, et al. Improved vision-related function after ranibizumab for macular edema after retinal vein occlusion: results from the BRAVO and CRUISE trials. Ophthalmology. 2012;119(10): 2108-2118.

Work Up ⬆ ⬇

Workup
  1. History: Systemic disease, particularly HTN or diabetes?
  2. Complete ocular examination, including dilated retinal examination with indirect ophthalmoscopy to look for retinal neovascularization and ME.
  3. OCT: Used to help detect presence and extent of ME as well as monitor response to therapy.
  4. Check blood pressure.
  5. Blood tests: Fasting blood sugar and hemoglobin A1c, lipid profile, CBC with differential and platelets, PT/PTT. If clinically indicated, consider a more comprehensive workup. See 11.8, CENTRAL RETINAL VEIN OCCLUSION.
  6. Medical examination: Performed by an internist to check for cardiovascular disease.
  7. An IVFA is obtained after the hemorrhages clear or sooner if neovascularization is suspected.

Treatment ⬆ ⬇

  1. Retinal neovascularization: Sector PRP to the ischemic area, which corresponds to area of capillary nonperfusion on IVFA.
  2. Prompt and appropriate treatment of underlying medical conditions (e.g., HTN).

BRVO-Related Macular Edema

  1. Anti-VEGF treatment is now the gold standard. Intravitreal ranibizumab 0.5 mg and aflibercept 2 mg are FDA-approved for treating RVO-associated ME. Intravitreal bevacizumab has also been used off-label. Risks of intravitreal injection are low but include VH and endophthalmitis.
  2. Focal retinal laser photocoagulation has historically been the gold-standard treatment if edema is present for 3 to 6 months duration, and visual acuity is below 20/40 with macular capillary perfusion. However, anti-VEGF treatment is now largely favored. Limitations of focal laser include length of time before effect (often several months) and the need to wait until retinal hemorrhages clear.
  3. Dexamethasone intravitreal implant or off-label intravitreal steroid (e.g., triamcinolone 40 mg/mL, inject 1 to 4 mg). See 11.8, CENTRAL RETINAL VEIN OCCLUSION.
NOTE:

There is an evolving trend, particularly in cases of severe edema, to initiate treatment with pharmacologic agents for rapid visual recovery followed by focal laser for better durability of effect. Multiple pharmacologic trials (BRAVO and CRUISE) have validated that early anti-VEGF treatment leads to better visual outcomes.

Follow Up ⬆

In general, every month initially, with gradual interval taper based on vision, presence of ME, and treatment response. At each visit, the patient should be checked for neovascularization and ME.