Clinical Case Presentation. Branch Retinal Vein Occlusion. Sarita M. Registered Nurse Whangarei Base Hospital

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1 Clinical Case Presentation on Branch Retinal Vein Occlusion Sarita M. Registered Nurse Whangarei Base Hospital

2 Introduction Case Study Pathogenesis Clinical Features Investigations Treatment Follow-up Nurses Role Reference Content

3 Retinal Vein Occlusion 2nd most common retinal vascular disorder 2 main types: Central Retinal Vein Occlusion (CRVO) Branch Retinal Vein Occlusion (BRVO) one of the most common cause of sudden painless unilateral vision loss

4 History and Presentation Mrs. X, 72 y.o, healthy, fit and active >hx of distortion L eye for 1 yr > 1st clinic visit : Va R6/6 L6/24 IOP R15 L14 O/E: CMO left superotemporal area, R macula: normal

5 Plan: Bevacizumab x 2 doses Review + OCT 4/52

6 Clinic review after 2nd dose of Bevacizumab > VA 6/6 6/15-1 IOPs: normal O/E: slight blot hrge left ST macula OCT: persistent L superior macular oedema Plan: Bevacizumab x2 Review + OCT

7 Review after 4x doses of Bevacizumab VA: L 6/9 O/E: L old hrge or a small area of pigmentation OCT: nil swelling Plan: 2 months f/u + OCT

8 2/12 clinic review: VA : L 6/9 IOP: normal O/E: recurrence of L mac oedema OCT: recurrence of CMO Plan: 5th dose Avastin Review 6/52 + OCT

9 Review after 5x doses Bevacizumab VA: L 6/7.5+1 O/E: stable, no oedema noted OCT: nil CMO Plan: 2 months f/u + OCT

10 Clinic review 2/12 2/12 VA: L 6/7.5 O/E: some collaterals ST macula OCT: Slight thickening of RPE Plan: Discharge

11 Final Diagnosis: Left BRVO defined as a segmental intraretinal haemorrhage 4x more than CRVO Affects males and females equally Usually unilateral, 9% bilateral Risk factors: advancing age Classic trio : HTN, hyperlipidaemia, DM 50% of BRVO are hypertensive

12 Pathophysiology Usually occur at the arteriovenous (AV) junction arterial compression to adjacent vein -->partial obstruction inc intraluminal pressure transudation of blood to retina oedema perfusion Hypoxia Ischaemia ischaemia release of VEGF Mac Dec capillary tissue inc vascular permeability Tissue

13 Clinical Features Symptoms: Sudden onset of painless unilateral distortion or loss of vision Occasionally, floaters from vitreous haemorrhage Signs: Wedge-shape distribution of retinal haemorrhage retinal thickening & oedema cotton wool spots and hard exudates

14 Investigations: Optical Coherence Tomography - Best method - Measures macular oedema, and monitor the response to treatment - Findings Cystoid macular oedema, serous macular detachment, subretinal fluid

15 OCT angiography - newer technology can measure vascular density can observe the superficial and deep capillary networks, non flow areas, vascular dilation,and intraretinal oedema

16 Investigations: Fundal Fluorescein Angiographyinformation on the extent and location of the disease to study the choroidal and retinal vascular filling Findings - delayed venous filling in the area of occlusion - capillary nonperfusion - Dye extravasation from macular oedema or retinal

17 Treatment: is address to limit damage and progression of the disease Main purpose : is the resolution of the macular oedema before the foveal photoreceptor layer is damaged Treat the BRVO complications eg macular oedema, retinal neovascularization, vitreous hrge, and tractional retinal detachment

18 Treatment 1. Anti -VEGFs - treatment of choice for mac oedema and choroidal neovascularization Bevacizumab Ranibizumab Aflibercept

19 2. Laser photocoagulation Treatment

20 Treatment Mechanism: Destruction of photoreceptor of the ischaemic retina Decrease oxygen demand Increase oxygen influx Arteriolar constriction and inc resistance Dec capillary hydrostatic pressure Less transudation of fluid Less oedema

21 Treatment Corticosteroids Triamcinolone acetate Anti-inflammatory effect Antiangiogenic properties Inhibition of VEGF and other inflammatory cytokines Complications: inc IOP and cataract formation.

22 Treatment Surgery Arteriovenous sheathotomy (AVS) Pars plana vitrectomy + AVS Vitrectomy Retinal artery bypass

23 Treatment Medical Anti-platelet treatments - Ticlopidine - Beraprost - Heparin - Tissue plasminogen activator

24 Follow-up Initially, followed closely every month or 2 months to monitor macular oedema and neovascularization Anti-VEGF treatment with or without laser should be started if without spontaneous improvement With stable or resolved macular oedema, follow-up interval can be 3-6 months or even longer for stable chronic cases.

25 Northland DHB: Monthly intravitreal injections

26 Nurses Role Triage and history taking Monitor and assess stable BRVO cases Administer IV anti-vegf injection Education

27

28 References: [1] Jaulim,A.,Ahmed,B.,Khanam,T.,Chatziralli,I. (2013): Branch retinal vein occlusion:epidemiology,pathogenesis,risk factors, clinical features,diagnosis, and complications. An update of the literature. Retina,33(5), doi: /IAE.0b013e c15 [2] Patel, M., Prisant, L., & Marcus, D. (2003). Branch Retinal Vein Occlusion. The Journal of Clinical Hypertension, 5(4), doi: /j x [3] Karia, N. (2010). Retinal vein occlusion: pathophysiology and treatment options. Clinical ophthalmology, 4, Retrieved from [4] Chatziralli, I., Nicholson, L., Sivaprasad, S., & Hykin, P. (2015). Intravitreal steroid and anti-vascular endothelial growth agents for the management of retinal vein occlusion: Evidence from randomized trials. Expert Opinion on Biological Therapy.,15(12), [5] Duker, J., Waheed, N., & Goldman, D. (2014). Handbook of retinal OCT : Optical coherence tomography. Retrieved from [6] Biousse, V., & Newman, N. (2009). Neuro-ophthalmology Illustrated. New York, NY: Thieme Medical Publishers, Inc. [7] Lattanzio, R., Torres Gimeno, A., Battaglia Parodi, M., & Bandello, F. (2011). Retinal Vein Occlusion: Current Treatment. Ophthalmologica, 225(3), doi: / ) Li, J., Paulus, Y. M., Shuai, Y., Fang, W., Liu, Q., & Yuan, S. (2017). New Developments in the Classification, Pathogenesis, Risk Factors, Natural History, and Treatment of Branch Retinal Vein Occlusion. Journal of Ophthalmology, 2017.

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