Clinical Case Presentation on Branch Retinal Vein Occlusion · Clinical Case Presentation on Branch...

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

Transcript of Clinical Case Presentation on Branch Retinal Vein Occlusion · Clinical Case Presentation on Branch...

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

Clinical Case Presentation

on

Branch Retinal Vein Occlusion

Sarita M.Registered NurseWhangarei Base Hospital

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

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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

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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

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Plan:

Bevacizumab x 2 doses

Review + OCT 4/52

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Clinic review after 2nd dose of Bevacizumab

> VA 6/6 6/15-1 IOPs: normal

O/E: slight blot hrge left ST macula

Plan: Bevacizumab x2

Review + OCT

OCT: persistent L superior macular oedema

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Review after 4x doses of Bevacizumab

VA: L 6/9

O/E: L old hrge or a small area of pigmentation

Plan: 2 months f/u + OCT

OCT: nil swelling

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2/12 clinic review:

VA : L 6/9

IOP: normal

O/E: recurrence of L mac oedema

Plan: 5th dose Avastin

Review 6/52 + OCT

OCT: recurrence of CMO

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Review after 5x doses Bevacizumab

VA: L 6/7.5+1

O/E: stable, no oedema noted

Plan: 2 months f/u + OCT

OCT: nil CMO

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Clinic review 2/12

2/12

VA: L 6/7.5

O/E: some collaterals ST macula

OCT: Slight thickening of RPE

Plan: Discharge

2/12

VA: L 6/7.5

O/E: some collaterals ST macula

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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

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PathophysiologyUsually occur at the arteriovenous (AV) junction

arterial compression to adjacent vein -->partial obstruction → inc intraluminal

pressure → transudation of blood to retina

Mac

oedema

Dec capillary tissue

perfusion

Tissue

ischaemia release of VEGF → inc vascular permeability

Hypoxia

Ischaemia

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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

dilated and tortuous veins

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Investigations:

Optical Coherence Tomography

- Best method

- Measures macular oedema, and monitor the response to treatment

- Findings

Cystoid macular oedema, serous macular detachment, subretinal fluid

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OCT angiography - newer technology

can measure vascular density

can observe the superficial and deep capillary networks, non flow areas, vascular dilation,and intraretinal oedema

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Investigations:

Fundal Fluorescein Angiography-

information 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

neovascularization

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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

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Treatment

1. Anti -VEGFs - treatment of choice for mac oedema and choroidal

neovascularization

Bevacizumab

Ranibizumab

Aflibercept

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Treatment

2. Laser photocoagulation

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TreatmentMechanism:

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

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TreatmentCorticosteroids

Triamcinolone acetate

Anti-inflammatory effect

Antiangiogenic properties

Inhibition of VEGF and other inflammatory cytokines

Complications: inc IOP and cataract formation.

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Treatment

Surgery

Arteriovenous sheathotomy (AVS)

Pars plana vitrectomy + AVS

Vitrectomy

Retinal artery bypass

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Treatment

Medical

Anti-platelet treatments

- Ticlopidine

- Beraprost

- Heparin

- Tissue plasminogen activator

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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.

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Northland DHB: Monthly intravitreal injections

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Nurses’ Role

Triage and history taking

Monitor and assess stable BRVO cases

Administer IV anti-VEGF injection

Education

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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), 901-910. doi: 10.1097/IAE.0b013e3182870c15

[2] Patel, M., Prisant, L., & Marcus, D. (2003). Branch Retinal Vein Occlusion. The Journal of Clinical Hypertension, 5(4), 295-297. doi:

10.1111/j.1524-6175.2003.02469.x

[3] Karia, N. (2010). Retinal vein occlusion: pathophysiology and treatment options. Clinical ophthalmology, 4, 809-816. Retrieved from

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2915868/

[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),1685-1697.

http://dx.doi.org/10.1517/14712598.2015.1086744

[5] Duker, J., Waheed, N., & Goldman, D. (2014). Handbook of retinal OCT : Optical coherence

tomography. Retrieved from

https://www-clinicalkey-com-au.ezproxy.auckland.ac.nz:9443/#!/content/book/3-s2.0-B978032318884500032X

[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), 135-143. doi:10.1159/000314718)

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.