Branch Retinal Vein Occlusion

DR.SHAH-NOOR HASSAN FCPS,FRCS
Consultant, Vitreo-Retina
Bangladesh Eye Hospital & Institute

1. branch Retinal Vein Occlusion Dr. Shah-Noor Hassan FCPS,FRCS Consultant, Vitreo -Retina Bangladesh Eye Hospital & Institute

2. INTRODUCTION First described by LEBER in 1877. KOYANAGI first described more incidence in UT branch. 2 nd most common cause of vision d/t retinal vascular disease (after diabetic retinopathy) BRVO accounts for 69.5% of total RVO .

3. Demography Age: 5 th – 6 th decade Sex: males = females Incidence : 0.7% between 50 – 60 4.6% after 80 yrs

4. Risk factors Systemic hypertension Diabetes Hyperlipidemia Glaucoma Smoking Age related atherosclerosis

5. Others risk factors– Eyes with shorter axial lengths Anti- phospholipid antibody syndrome Elevated plasma homocysteine levels Low serum folate levels Inflammatory disease( Sarcoidosis, Bechet’s disease) Acquired & inherited thrombophilic conditions Hyper viscosity state ( polycythemia , myeloma, etc.)

6. Protective factors Higher serum HDL Moderate alcohol consumption

7. Pathogenesis Almost always occurs at AV crossings Retinal artery and vein share a common adventitial sheath & in some cases a common medium Artery located anterior to the vein at the obstructed site; lumen of the vein compressed upto 33 % at the obstruction site Role of vitreous – eyes with decreased axial length and and higher likelihood of vitreomacular attachment at AV crossings

8. Turbulent flow at the crossing site causes focal swelling of the endothelium and deeper vein wall leading to venous obstruction Actual venous thrombus at the point of occlusion

9. Venous occlusion stagnation hypoxia Edema & hemorrhage Increased tissue pressure perfusion pressure = art. pres.-vein. pres . Venous obstruction Venous pressure Overloading of collateral drainage capacity Macular edema & ischemia Unrelieved venous pressure Rupture of vein wall & intraretinal hemorrhage

10. CLASSIFICATION 1 ) Major BRVO : -occlusion of 1 st order temporal branch at disc. -occlusion of 1 st order temporal branch away from disc, but involving branch to macula. 2 ) Minor macular BRVO – involving only a macular branch 3 ) Peripheral BRVO – not involving the macular circulation

11. INCIDENCE OF TYPES Upper temporal quadrant : 49 - 63 % Lower temporal quadrant : 29 – 51 % Macular : 24 % Nasal : 0.5 – 2.6 %

12. CLINICAL FEATURES PRESENTATION *macular involvement : sudden blurred vn,metamorphopsia ,relative V F defect. *peripheral involvement : asymptomatic. VISUAL ACUITY -depends on macular involvement - Orth & Patz : farther the site of occlusion from disc better is prognosis.

13. EYES VISION 50 % 6/12 or better 25 % 6/60 or worse

14. Fundus examination EARLY STAGE : Dilatation and tortuosity of the venous segment distal to the site of occlusion and attenuation proximally Flame shaped and dot-blot hemorrhages, retinal oedema and cotton wool spots : usually in triangular pattern, apex of which lies towards the site of obstruction.

15. Macular edema 5 – 15 % of eyes over 1 year period 18 % resolve by 4.5 months, 41% by 7.5 months

16. Course Resolve within 6 – 12 months Segmental distribution of retinal vascular abnormalities pers Hard exudates, venous sheathing and sclerosis peripheral to the site of obstruction

17. Apparent on FA Capillary non-perfusion Microaneurysms Collateral vessel formation

18. Neovascularization NVD – 10 % NVE – 25 % in cases with extensive ischemia, >1/3 fundus Serious complication – leads to recurent pre-retinal and vitreous hemorrhage

19. Fellow eye involvement Bilateral involvement 4.5 - 6.5 %

20. OCT

21. Fluorescein angiography Delayed venous filling Blockage by blood Hyperfluorescence due to leakage

22. In late cases :in addition to nonfilling of the segment ( CNP) collaterals (non-leaking) may be seen or NV (leaking) Fluorescein column is narrowed at site of obstruction. Clemette’s sign of focal hyperfluorescence at AV crossing present from 6 th to 12th week.

23. COMPLICATIONS MACULAR CHANGES 1) Chronic macular oedema : 48% cases 1/3 rd edema regresses spontaneously 2) Macular non-perfusion : vision is unlikely to improve.

24. 3) Epiretinal membrane 4) Hard Exudates, pigment clumping at macula

25. NEOVASCULARIZATION : In major brvo : NVD 10%,NVE 36 % (if CNP areas > 5DD) develops at border of ischemic & non-ischemic retina. occurs max. upto 6-12 months, may occur upto 3 years. NV doesn't develop in macular brvo

26. VITREOUS & PRE-RETINAL H’GES:60 % (22-36% develop NVE if CNP areas >5DD, of them 40% develop VH)

27. Tractional RD Rhegmatogenous RD -Ischemia leads to atrophic hole formation. -secondary to tear formed due to fibrovascular traction Retinal detachment

28. ANT. SEGMENT NV : 1.6 %

29. INVESTIGATIONS BP, ECG CBC, ESR Fasting blood glucose & lipids In young patients Autoantibodies ACE Homocysteine Thrombophilia screen Plasma protein electrophoresis

30. Management 2 main objectives Identification of modifiable risk factors (example HT, DM, CVS) and their management – for other eye Recognition and management of sight-threatening complications

31. Anticoagulant therapy Not beneficial in either prevention or management Associated with systemic complications Theoretically, severity of intraretinal hemorrhage in acute phase

32. BRVO with perfused periphery & normal VA Favourable prognosis No therapy Monitored monthly for 1 st 3 months, then every 2 months for the 1 st year

33. BRVO with peripheral nonperfusion Laser treatment

34. Macular BRVO Involves a small vein draining a sector of the macular region Favourable natural course

35. Laser photocoagulation BVOS eligibility criteria Grid laser recommended in eyes with VA of 20/40 or less Persistent macular edema > 4 mths Resorption of macular hemorrhages

36. BVOS TREATED Gain of 2 or more lines-65% V/A of 6/12 or better-60% Mean gain of lines- 1.33 UNTREATED 37% 34% 0.23 MACULAR GRID LASER:

37. SCORE study Recommended grid photocoagulation for vision loss with macular edema secondary to BRVO However, leads to paracentral visual field defects

38. Ozurdex Sustained release biodegradable implant 0.7 mg Dexamethasone Received FDA & EU approval for treatment of macular edema secondary to RVO

39. Neovascularization According to BRVO study group: Scatter laser - if NVE is present (reduces chances of VH to 20%) may not treat all cases with CNP areas as 78% may not develop NVE & VH

40. BVOS TREATED VH incidence – 29% NVE incidence – 12%(CNP > 5DD) UNTREATED 61% 22% Thus 78% cases do not progress to NVE, hence laser not recommended till NVE develops. SECTORAL LASER

41. SURGICAL INTERVENTIONS Isovolaemic haemodilution tPA( tissue plasminogen activator) Chorio-retinal anastomosis Sheathotomy PVD Induction Steroids Anti-VEGF

42. LASER CHORIO-RETINAL ANASTOMOSIS Argon green(2.5-3.5W) Low success rate(30-40%) Complications : -VH -SRNVM -R.D -ERM

43. Surgical management SHEATHOTOMY OSTERLOH and CHARLES – 1988 Relieves the compression of artery on vein OPREMCAK and BRUCE – 1999, 85% had either same / improved V/A, 67 % improved Mester,Dillinger et al –ILM peeling gives better results Shah et al – 2000

44. BMV with PVD induction (+/- Sheathotomy) Proposed mechanisms : -removal of vitreo-macular traction -removal of cytokines that increase vascular permeability -improvement of oxygen tension in posterior retina -faster development of collaterals- 6 months (normally 6-24 months)

45. Pre-op Post-op

46. BMV+PVD(+/-Sheathotomy ??? ) No significant difference in improvement in VA in eyes with reperfusion of occluded vein and those without - indicating that the reopening of occluded vein is not essential for visual recovery. Improvement in macular oedema but no effect on macular function Yamamoto et al AJO 2004

47. Venous occlusion Retinal circulatory impedence Retinal oedema Cellular hypoxia Increased capillary permeability Angiogenic factor, VEGF Breakdown of inner blood retinal barrier Anti-VEGF

48. anti-VEGF Safe and efficacious. Unsustainad effect in some cases. Does not alter the perfusion status which determines the end result.

49. The benefit of any treatment has to be compared with the natural course of the disease. 50-60% maintain maintain initial V/A of 6/12 at 1-3 yrs followup. Thereafter natural course remains relatively stable. Conversely natural course of V/A<6/12 is unfavourable without treatment. ( at 3 yrs 23% had V/A of 6/60 or worse & only 37% gained 2 or more lines)

50. Treatment Focused on management of vision-limiting complications Macular edema Macular non-perfusion Vitreous hemorrhage from neovascularization

51. Treatment algorithm

52. Prognosis 33 – 50% regain 6/12 or better VA spontaneously.

53. THANK YOU

54. More similarities than dis -similarities in the risk factor profiles for BRVO, CRVO and HRVO Testing for patients with HT, DM and open-angle glaucoma should be part of the evaluation of patients with retinal vein occlusion

55. Favorable safety and tolerability profile over 12 months of follow-up. can be repeated with no new safety concerns after the second treatment with regard to IOP increases, although cataract progression does seem to increase

56. Edaravone (MCI-186) is effective as a free radical scavenger following arteriovenous sheathotomy for treatment of macular oedema associated with branch retinal vein occlusion T Maeno 1 , 2 ,  R Tano 1 , H Takenaka 1 ,  T Mano 1 + Author Affiliations 1 Tane Memorial Eye Hospital, Osaka, Japan 2 Department of Ophthalmology, Osaka Medical College, Takatsuki, Japan

57. Stabilization and increase in visual acuity after laser treatment did not correlate with an overall decrease in scotoma size. Improved central visual function seen in 25% of treated eyes appeared to be due to withdrawal of scotoma from the fovea.

58. Sheathotomy Principle steps Pars plana vitrectomy Overlying artery is separated from the vein by creating an incision in the adventitial sheath adjacent to the arteriovenous crossing and then separating the adhesions.

59. Although the study by Mason et al reported a benefi cial effect on VA in those patients undergoing surgery compared with those receiving laser or no treatment, the study was not randomized and was partly retrospective, introducing sources of potential bias. There is currently no evidence from RCTs supporting the routine use of adventitial sheathotomy to improve VA in eyes with BRVO

60. Intravitreal Tissue Plasminogen Activator to Treat Macular Edema Associated With Branch Retinal Vein Occlusion (Am J Ophthalmol 2006;142: 318–320 After topical anesthesia was applied and a paracentesis created tPA (40 k international units [IU]) injected into the vitreous bedrest in the supine position for four hours following treatment Mechanisms - PVD induction & development of collateral vessels

61. Multifocal ERG Responses from multifocal electroretinography demonstrate retinal dysfunction in branch retinal vein occlusion

62. Moreover, if repeat injections are required, the use of a sustained release steroid implant would obviate the need for multiple injections, but also magnify the risk of steroid related complications.

63. Although steroids have antiangiogenic, antifibrotic , and antipermeability properties, the principal effects of steroids are stabilization of the blood-retinal barrier, resorption of exudation, and down regulation of inflammatory stimuli. Whereas it is clear that there is a break-down in the blood retinal barrier in BVO, studies have shown that there may also be an inflammatory component that would respond to steroids.

64. Endophthalmitis, sterile endophthalmitis, pseudo- hypopyon , cataract, retinal tears, retinal detachment, and vitreous hemorrhage have all been described after intravitreal steroid injections. Additionally, steroid related complications including cataract and increased intraocular pressure (IOP) can occur. Increased IOP was seen in 33% of patients in the intravitreal injection group